

GENERAL INFORMATION
Many different drugs and treatments have been used to treat alzheimer's disease. Some treatments are aimed at specific problems or symptoms of patients, while some are aimed at the disease itself. Click on a subject to see detailed information about that subject. Note: As each therapy is discussed, you may note numbers in brackets, like this [1]. The number in the bracket refers to the same number found under References. This means,in this example, that you can find more information in the original article,1, under 1, in the references at after the therapy listings. To see all the references, just click on References, after Zolpidem, the last therapy.
Acetominophen
Acetyl-L-Carnitine
Acupuncture
S-Adenosylmethionine
Animals
Anxiety, Aggression, Hostility--Treatments
Aromatherapy
Aspirin
Atropine
Benzodiazepines
Bingo
Carbamazepine
Citalopram
Deprenyl
Estrogen
Exercise
Gabapentin
Ginkgo Biloba
Huperzine A
Ibuprofen
Indomethacin
Lecithin
Light
Lithium
Massage
Music
Nicotinamide Adenine Dinucleotide [NADH]
Nerve Growth Factor
Nicotine
Olanzapine
Omentum Transplants
Oxygen
Phosphatidylserine
Photo Albums
Physostigmine
Piracetam
Propentofylline
Propranolol
Risperidone
Scopalamine
Sleep Apnea
Steroids
Therapeutic Touch
Thiamine
Ttranscranial Magnetic Stimulation
Transcutaneous Electrical Stimulation
Trazodone
Dr. Walsh's Anticoagulant Therapy
Zolpidem
References
ACETOMINOPHEN
    Acetominophen is a generic term for a drug,which many know better as the trade name Tylenol. One study has found that regular users of acetominophen seem to have a lower risk for developing alzheimer's disease [1]. Another study could not confirm this, and failed to find any risk reduction with acetominophen [2].
ACETYL-L-CARNITINE
    Acetyl-l-carnitine is a substance naturally found in cells. Acetyl-l-carnitine[ACL] helps transport fatty acids into the cells where the fats are burned for energy. Acetyl-l-carnitine is not a drug and can be found in health food stores. Acetyl-l-carnitine has been shown by many studies to protect brain cells from various kinds of insults [3-4].Is acetyl-l-carnitine effective? Some studies report good results. A study in 1990 shows that ACL increased name learning and digit recall in alzheimer patients [5]. A study in 1992,using 2.5 to 3.0 grams ACL daily, shows improved forward digit span recall and better verbal fluency in alzheimer patients [6]. Two studies gave alzheimer patients ACL for a year. ACL slowed the progression of the disease, as measured by the Blessed Dementia Scale and the Mini Mental State Exam [7-8]. ACL seems to be most effective for patients with early-onset alzheimer's disease [9] and in younger alzheimer patients [10].
Some studies have found ACL to be ineffective. One recent study gave 3.0 grams daily, and found no benefit for ACL [11]. One study finds that 10 milligrams of selegiline daily more effectively increases information processing and recall in patients than does 2.5 grams of acetyl-l-carnitine daily [12]. However, another study finds that acetyl-l-carnitine more effectively increases attention and recall in alzheimer patients than piracetam, which is a popular mind-enhancing drug [13]. The weight of evidence seems to suggest that for many patients, acetyl-l-carntine can be helpful, and it has the advantage of minimal side effects.
ACUPUNCTURE
    Acupuncture has been shown to increase learning and memory in animals [14]. Only one study, to my knowledge, has used acupuncture on dementia patients. This study used acupuncture combined with acupoint injection of acetylglutamate. Using the Hasegawa Dementia Scale and the Functional Activity Questionnaire as measures, more than 85% of patients show improvement [15]. Interestingly, the treatment also raised blood levels of high density lipoprotein,which is considered the " good cholesterol". High density cholesterol may be important because this kind of cholesterol seems to inhibit a protein called amyloid beta, which may be the cause of alzheimer's disease.
S-ADENOSYLMETHIONINE
    S-adenosylmethionine, popularly known as, SAMe,is sold in health food stores as a supplement.
SAMe, according to several studies, helps combat feelings of depression [16-17]. Only one study has tried SAMe on alzheimer patients. In that study, SAMe did not improve cognition or memory [18].
ANIMALS
    Pets may help calm alzheimer patients. One study of 64 alzheimer patients,residing in private homes, finds that patients exposed to pets have less anxiety and less verbal aggression toward their caregivers [19].
ANXIETY,AGGRESSION& HOSTILITY-- TREATMENTS
    A number of drugs and compounds have been used with varying effectiveness for the treatment of agitation and anxiety in alzheimer patients. Haloperidol or thioridazine have been widely used to control agitated patients. Both seem to work equally well, but haloperidol seems to cause more parkinson-like side effects,known as extrapyramidal symptoms [20]. Some studies have shown the haloperidol more effectively controls agitation when combined with other agents. For example, one study reports that carbamazepine and haloperidol controls agitation better than haloperidol by itself [21].
    Sometimes, behavior management techniques can control agitation. A very recent study finds that proper behavior managament by staff is just as effective in controlling agitation as haloperidol or trazodone [22]. What are behavior management techniques? When you have an anxious or agitated person, try to use some of the following
techniques:
1. Approach the patient in a gentle,calm manner.
2. Always try to orient a patient to his/ her room.
3. Use the patient's name frequently.
4. Approach patient from the front, not the side.
5. Reassure the patient that you understand their anxiety.
6. Don't tell patients what they should not do; instead focus on what they should do.
For example, don't say:"Don't go outside", but do say:"Please stay inside".Patients find it easier to understand a simple command.
    Some antidepressant compounds of the benzodiazepine class, such as trazodone, are quite effective at reducing agitation in alzheimer patients [23-24]. Twenty five milligrams,given three times daily, seems to decrease anxiety [25]. The major side effect at higher doses is dry mouth.
    Other less- used compounds have been shown to control agitation,sometimes when nothing else seems to work. Phosphatidylserine, sold in health food stores, decreases anxiety [26]. Propanolol, in daily doses from 10 to 80 milligrams daily, can control aggression in highly aggressive patients even after two weeks [27]. Medroxy-progesterone acetate,an anti-androgen, completed stopped
all physical and verbal aggression in 3 demented patients with extremely high aggression and hostility [28].
    Some drugs can actually increase hostility in alzheimer patients. Scopolamine, a cholinergic blocker, increases hostility more in alzheimer patients than in non-demented controls [29].
    Some drugs decrease anxiety, but come with additional costs to the patient. Benzodiazepines have been widely used to control anxiety. Diazepam is one drug in the benzodiazepine class. Benzodiazepines can actually worsen cognitive abilities [30-31] and increase the risk of falls [32-33]. Alzheimer patients,as you may know, are
more prone to falls because of a slowed gait and poor balance.
AROMATHERAPY
    Aromatherapy is the use of fragrances to achieve behavioral effects. I am aware of only one study of aromatherapy in alzheimer's disease.
In that study, only 1 of 4 patients benefited from the therapy [34].
ASPIRIN
    Regular use of aspirin seems to reduce the risk of alzheimer's disease [35-36]. The risk is reduced even more if aspirin is taken steadily more than a year [37]. Aspirin also seems to improve thinking in alzheimer patients. One study compared 239 alzheimer patients not taking aspirin with 206 alzheimer patients taking aspirin. The alzheimer patients who took aspirin did better on tests of word recognition. Aspirin-using patients also scored better on the cognitive subscale of the ADAS scale; aspirin-using alzheimer patients had a mean score of
19.7 on the ADAS-cognitive scale and non-aspirin using patients scored 21.3, a significant difference in favor of aspirin users [38].
ATROPINE
    Atropine should be used cautiously in alzheimer patients. Atropine worsens memory and thinking more in alzheimer patients than in non-demented elderly [39].
BENZODIAZEPINES
    Benzodiazepines are a class of drugs commonly use to relax anxious patients. Diazepam and lorazepam are examples of drugs in the benzodiazepine class. Lorazepam can produce transient memory impairment even in normal healthy volunteers [40]. A 1 milligram oral dose of lorazepam has been shown to impair cognition in alzheimer patients [41]. Benzodiazepines can also increase the risk of falls in demented patients. These compounds should be used cautiously in demented patients.
BINGO
    Bingo apparently is beneficial for alzheimer patients. One very recent study compared the benefits of physical exercise and bingo on thinking in alzheimer patients. Regular exercise did not improve cognition, but bingo increased the abilities of patients on the Boston Naming Test and Word List Recognition [42].
CARBAMAZEPINE
    Carbamazepine is an anticonvulsant,effective for seizures. However, carbamazepine effectively controls agitation and aggression in alzheimer patients, even in those with the most severe dementia [43-44]. One study reports that 100 to 300 milligrams of carbamazepine daily decreases agitation in
alzheimer patients not responding to other drugs [45]. Another study reports that doses of up to 480 milligrams daily are needed to control agitation and hostility in patients who do not respond to other drugs[46].
CITALOPRAM
    Citalopram is a selective serotonin uptake blocker. The drug tends to increase the action of serotonin in the brain,and serotonin tends to counter depression.
Citalopram is primarily used to treat depression.
Citalopram is especially useful in alzheimer patients who suffer from depression [47].Citalopram decreases anxiety, restlessness,irritability, and depression in alzheimer patients [48]. Citalopram does not have a pure antidepressant effect,but acts more like an emotional stabilizer. The drug reduces levels of blood cortisol [49].
DEPRENYL
    Deprenyl,also known as selegiline, is an inhibitor of the enzyme,monoamine oxidase B. Deprenyl can protect against radicals [50]and promotes nerve growth [51].
Deprenyl has been widely studied and used for the treatment of alzheimer's disease. Some studies show deprenyl has beneficial effects on alzheimer patients and an equal number of studies show no real benefit in alzheimer patients. At doses of 10 milligrams daily, deprenyl increases alertness [52],increases memory [53], and decreases depression and anxiety[54] in alzheimer patients.
Many studies of deprenyl have been for less than 6 months. Two longer term studies, for 6 months and 15 months, have shown no changes in cognition in alzheimer patients [55-56].
ESTROGEN
    Women who use estrogen regularly have a lower risk for alzheimer's disease [57-58]. Why does estrogen reduce risk? There may be multiple factors involved. Estrogen increases blood flow to the brain [59]. One very interesting study measured brain blood flow in healthy,non-demented,postmenopausal women. It turns out that these women have reduced blood flow to their brains, just like alzheimer patients do. When these same women are put on estrogen therapy, their brain blood flow returns to normal [60].
Estrogen may reduce risk by decreasing the toxicity of the amyloid beta protein, which is believed responsible for alzheimer's disease. Estrogen protects cultured brain cells from the toxic effects of amyloid beta [61]. Estrogen also encourages special brain cells, called microglia, to dispose of amyloid beta [62].
Estrogen has direct effects on memory and learning. Estrogen increases cognitive ability in healthy women without dementia [63-64]. Estrogen also has beneficial effects on cognition in alzheimer patients. Estrogen increases Mini Mental State Exam scores [65-66]. Estrogen also slows cognitive decline in alzheimer patients [67]. Estrogen can safely be given to alzheimer patients who take Aricept. In fact,the combination of Aricept and estrogen increases Mini Mental State Exam scores better in patients than either drug alone [68].
Estrogen effectively controls aggression when given to male alzheimer patients [69]. One study,using estrogen delivery via skin patches, reports that aggression is reduced by up to 50 percent in male alzheimer patients; in these males, estrogen works quickly in one to three days. Mood improves with minimal sedation. The only side effect is gynecomastia [70].
EXERCISE
    Exercise may help ward off alzheimer's disease. Many studies have shown that a lack of exercise significantly increases the risk of having alzheimer's disease [71-72]. On the other hand, those who regularly engage in physical exercise have a markedly reduced
risk of having alzheimer's disease[73-74]. Why does exercise reduce risk? No one knows for certain, but I suspect that exercise increases blood flow to the brain, and that the increased brain blood flow helps prevent alzheimer's disease.
    Exercise not only wards off alzheimer's disease, but it also helps those who already have the disease. Several studies have shown the regular physical activity increases Mini Mental State Exam scores in alzheimer patients [75-76]. Regular physical exercise also reduces agitation and aggression in alzheimer patients [77]. Exercise also helps patients communicate better [78].
GABAPENTIN
    Gabapentin is an anticonvulsant drug. It is being tested in various psychiatric conditions as a mood stablizer. In doses of 200 to 2,400 milligrams daily, the drug seems to decrease agitation in alzheimer patients who do not respond to conventional neuroleptics [79].
Approximately 40 percent of demented patients experience adverse effects,such as gait instability or sedation while on gabapentin [80]. Gabapentin is quite effective on agitation, with one study reporting 17 of 22 treated dementia patients as " much or greatly improved"[81].
GINKGO BILOBA
    Ginkgo biloba, an herbal extract,increases memory in demented and non-demented elderly [82].
How effective is ginkgo biloba? A recent study compared the ability of metrifonate, donepezil, tacrine, rivastigmine, and ginkgo biloba on cognitive ability in alzheimer patients. The study used the ADAS-cognitive subscale as a measure of cognition in patients. The study reports that ginkgo biloba improves cognitive scores as much
as the other drugs tested [83]. Two other studies find that 26 to 27 percent of alzheimer patients show more than 4 point improvements on the ADAS cognitive subscale,which is comparable to results found with cholinesterase inhibitors, such as donepezil [84-85].Ginkgo biloba also increases the abilities of alzheimer patients to perform routine activities of daily living and decreases
depression [86].
    How does ginkgo biloba work? Researchers are not certain how ginkgo biloba works. Ginkgo biloba is known to greatly increase blood flow. In fact, the extract has been used to treat painful intermittent claudication in the legs; this condition is partly caused by poor blood flow to the legs [87], which ginkgo biloba reverses.
In addition,ginkgo biloba protects cultured brain cells from the toxic effects of amyloid beta protein [88]. Ginkgo biloba also increases the frequency of brain waves, by promoting higher frequency alpha waves [89].
HUPERZINE A
    Huperzine A is derived from the common moss, Huperzia serrata. The extract has been used for years in China to treat fever and inflammation. Huperzine A increases memory and learning in animals [90] and in humans [91].
    Huperzine A potently inhibits acetylcholinesterase. Huperzine A increases acetylcholine levels in the brain [92]; as you may be aware, people with alzheimer's disease have low acetylcholine levels because
their disease destroys the cholinergic brain cells that make and use acetylcholine.
    I searched The National Library of Medicine to find clinical studies of huperzine A. Huperzine A has been studied mostly in China.
Chinese studies show that huperzine A enhances memory in healthy human volunteers [93]. One clinical study gave alzheimer patients huperzine, 0.2 milligrams (4 tablets)
daily. More than 58% of patients showed improvements in memory and cognition [94].
    How does huperzine A work? So far, research seems to show that huperzine A decreases oxidative stress. Free radicals cause oxidation of proteins, and this process is inhibited by huperzine A [95] Huperzine A also protects cultured brain cells from the toxic effects of amyloid beta protein[96].
IBUPROFEN
    Ibuprofen is an over the counter medication used to treat pain. Chemically, it is a non-steroidal,anti-inflammatory agent. Ibuprofen reduces the inflammation
associated with injury. Ibuprofen use reduces the risk for alzheimer's disease [97]. Another study finds that ibuprofen reduces the risk of getting alzheimer's disease up to 60 percent [98].
    Ibuprofen may reduce risk by its anti-inflammatory actions. This action is important because the brain of alzheimer patients seems to be characterized by a state of inflammation. For example, interleukin 6 and tumor necrosis factor, two inflammatory proteins, are found to be increased in alzheimer brains.
    Ibuprofen also seems to act as an antioxidant, since a recent study has shown that it can protect cells from peroxidation[99]. Ibuprofen has also been given to alzheimer mice. These mice have genes inserted in their DNA, which cause the deposition of amyloid deposits in the brain, similar to that seen in alzheimer brains. Ibuprofen reduces the deposition of amyloid in such mice [100].
INDOMETHACIN
    Indomethacin is a non-steroidal, anti-inflammatory drug used to treat pain. Indomethacin use has been shown to reduce the risk of alzheimer's disease. Indomethacin has been used clinically for alzheimer patients. One study gave patients 100 to 150 milligrams of indomethacin daily for six months. Patients receiving indomethacin increased their cognitive abilities 1.3 percent on a battery of tests; whereas, those patients not receiving indomethacin declined 8.4 percent [101].
    How does the drug work? Studies have shown the indomethacin does not alter the toxic effects of amyloid beta protein [102-103]. However,indomethacin does reduce the activation of brain microglia [104].
Microglia are the immune regulators in the brain, much like white blood cells are immune regulators in the bloodstream. In alzheimer patients, microglia become hyper-activated,
and may aggravate brain injury by secreting harmful chemicals,such as nitric oxide.
    Indomethacin should be used cautiously in alzheimer patients. One study reports that indomethacin can precipitate psychotic like episodes -including agitation, confusion,and aggression- in sensitive alzheimer
patients [105].
LECITHIN
    Choline is converted into acetylcholine,which brain cells use to transmit nerve messages. Lecithin is a rich dietary source of choline. In theory, lecithin should be good for alzheimer patients, who lack acetylcholine in their brains. However, studies have found no favorable effects of lecithin on cognition in alzheimer patients. A systemic review of all lecithin studies by the Cochrane Review concludes that lecithin is of no benefit for alzheimer patients [106].
LIGHT
    Light is an important nutrient for human beings. Light regulates our entire well-being through circadian rhythms. From the time you wake up to the time you go to bed again, your body functions are regulated according to a rigid schedule,and this schedule
revolves around the 24 hour day. For example, the normal daily rhythm of heart rate and blood pressure is to rise during the day and reach lows during the early night and morning. Alzheimer patients do not have normal circadian rhythms. Their blood pressure does not drop at night as is normal [107-108]. Further, their heart rate does not drop at night [109]. There are two reasons that might explain why daily rhythms are disturbed in alzheimer's disease.
First, mice that have high levels of amyloid beta have disturbed daily rhythms. Those without overexpressed amyloid beta have normal rhythms. Something about amyloid beta triggers disrupted rhythms [110].Second, the area of the brain that controls the daily rhythms of life, the suprachiasmatic nucleus, loses brain cells during the course of alzheimer's disease [111].
    External bright light can be very therapeutic for alzheimer patients. Because the daily rhythms of alzheimer patients are disrupted, many of these patients sleep during the day and stay awake at night. When these patients are exposed to bright light daily, their rhythms return to normal, and they sleep normally at night [112]. Bright light also reduces the incidence of agitation in alzheimer patients [113]. One study recently reported that bright light therapy increases Mini Mental State Exam scores in patients [114]. The best way to make sure patients get bright light is to take them outside in the sun daily, even if briefly. Studies have shown that alzheimer patients get far less exposure to the sun than do non-demented elderly [115].
LITHIUM
    Lithium has been investigated as a treatment for alzheimer's disease, based on the fact that lithium increases choline levels in cells. Choline synthesis may be impaired in alzheimer patients. Lithium does raise choline levels in the blood and red blood cells of patients, but this does not improve memory [116-117]. Lithium and lecithin does not improve cognition in alzheimer
patients [118]. Lithium was also noted to increase extrapyramidal symptoms in patients [119].
    Some studies have found that lithium impairs memory and thinking in alzheimer's disease [120]. In one study,lithium carbonate was given in doses of 400 to 600 milligrams daily for 5 weeks. Cognitive ability worsened in five patients out of nine studied. Overall, lithium does not seem to be of benefit for
alzheimer's disease.
MASSAGE
    Massage has not been well studied as a treatment for alzheimer's disease. One recent study of slow stroke massage by caregivers of community-dwelling
alzheimer patients shows that verbal agitation is not reduced by massage. However, slow stroke massage does decrease the incidence of wandering and pacing [121].
MUSIC
    Music is very beneficial for alzheimer patients. One study played big band music to alzheimer patients,each day, for six months. The patients were more alert,happy,and cooperative with staff [122]. Classical or favorite music decreases disruptive language [123]. However,music that is customized for each patient shows better results than generalized music [124].Music also seems to reduce the use of tranquilizers and hypnotics by alzheimer patients[125].
    Music has other beneficial effects. When alzheimer patients listen to relaxing music, the activity of their immune system increases. Natural killer cells, which degrade viruses, increase substantially in the bloodstream of patients who listen to music [126].
Music also seems to increase levels of melatonin in the blood of patients [127]. Melatonin is an important hormone that regulates sleep and body rhythms.
NICOTINAMIDE ADENINE DINUCLEOTIDE
    Nicotinamide adenine dinucleotide, commonly abbreviated as NADH, is an important compound found in all living cells. NADH is very important in the generation and transmission of energy within cells. NADH is located in mitochondria, which generate energy for cellular use.
Some researchers believe that alterations in mitochondria may be the cause of alzheimer's disease. Jorg Birkmayer,M.D.believes that NADH may work improperly in alzheimer patients. He tested his theory by giving 17 alzheimer patients 10 milligrams of NADH daily, 30 minutes before the first meal. He used the Mini Mental State Exam as one measure of cognitive ability in patients. The results were spectacular. All 17 patients showed improvements on the MMSE of more than
4 points; the average score increased by 8.35 points! The results do seem spectacular,when you consider the kind of results reported by cholinesterase inhibitors.
Cholinesterase inhibitors generally improve MMSE scores by more than 4 points in about one-third of patients. Dr.Birkmayer reported his study in 1996 [128]; a recent small trial of NADH, by other researchers, found no benefit of NADH for alzheimer patients.
    NADH, sold in health food stores,is also beneficial in the treatment of chronic fatigue syndrome.
NERVE GROWTH FACTOR
    Nerve growth factor,abbreviated as NGF, is found naturally in the brain, where it protects
brains cells [129]. Nerve growth factor may be inactivated by amyloid beta protein [130]. Therefore, attempts have been made to treat alzheimer patients with nerve growth factor.
    Nerve growth factor, infused into the brain of one alzheimer patient seemed to mildly stimulate
cognitive ability [131]. Another study infused nerve growth factor into the brains of 3 alzheimer patients. No patient showed cognitive improvement. In addition,diffuse back pain and pronounced weight loss were adverse effects seen [132].
    Gene therapy, using NGF, is currently in clinical trial at the University of California,San Diego.
Neurologist Mark H. Tuszynski, M.D., Ph.D., and his team on April 5, 2001, surgically implanted NGF-producing cells into the brain of a 60 -year- old woman with early stage alzheimer's disease. Previous work with monkeys has shown that the implantation of genetically-engineered cells
increases the survival of brain cells in primates by producing nerve growth factor after implantation. The current study is a Phase 1 clinical trial
to identify safety/toxicity. NICOTINE
    Nicotine, the main substance found in cigarettes,can increase or decrease the risk of
getting alzheimer's disease. Heavy smoking increases the risk of getting the disease [133-134]. The large Rotterdam Study reports that current smokers have more than four times the risk of getting alzheimer's disease,
compared with current non-smokers [135. Light cigarette smoking,however, seems to decrease risk. One study analyzed the reports of 18 studies of nicotine and alzheimer's disease; 15 of 18 studies found light smoking actually decreases alzheimer risk, on average, by 36 percent [136].
    Because mild nicotine seems to decrease risk of alzheimer's disease, some researchers have given alzheimer patients nicotine. One study gave 14 to 21 milligrams of nicotine daily to patients, via dermal plaster. Nicotine did not alter cognition [137].
Another study gave nicotine in skin patches. The treatment did not improve cognition, but did improve the alertness of patients [138].
OLANZAPINE
    Olanzapine is a drug normally used to treat psychosis,in particular,schizophrenia. It was approved by the FDA in 1996 and is marketed under the trade name Zyprexa,manufactured by Eli Lilly. The drug is now being used to treat alzheimer patients. The normal dose is 5 milligrams daily when used to control psychotic symptoms in alzheimer patients [139]. One recent study reports that 5 to 10 milligrams olanzapine daily effectively reduces aggression, hallucinations, and delusions in alzheimer patients. The most common side effects are a tendency to sleep more and a disturbed gait. Olanzapine does not alter cognition or produce extrapyramidal effects [140].
OMENTUM TRANSPLANTS
    Dr. Harry Goldsmith, a University of Nevada surgeon, has developed a procedure,which he feels may
truly benefit alzheimer patients. The surgery involves taking tissue, called omentum, from the abdomen, and inserting it into the scalp. Dr.Goldsmith believes that omentum, which is a blood- producing tissue, restores lost blood flow to the brain. Alzheimer patients, coincidentally, have markedly reduced brain flow. The omentum transplant was done on Bernie Weiss, who was in a nursing home before the transplant. According to a report, Bernie is home, taking care of himself, and even going out to lunch. Bernie is still having some signs of alzheimer's disease, but he is greatly improved.
OXYGEN
    Oxygen,under high pressure, has been given to demented patients with some success. In 1969, it was reported by Eleanor Jacobs that senile demented patients
who received 30 treatments of pure oxygen at 2.5 atmospheres of pressure, had remarkable memory gains.
The average score on the Wechsler Memory Scale before treatment was 76.0; after treatment with oxygen, the average score was 103.0 [141]. One study found that 28 of 59 patients showed good to excellent responses to oxygen [142]. However, later studies generally found
poor results with oxygen [143-144]. Oxygen fell into disuse, because the treatment was expensive and the cognitive effects lasted only 12 hours or so [145].
PHOSPHATIDYLSERINE
    Phosphatidylserine was first tried as a treatment for alzheimer's disease in the late 1980's. Italian studies found the substance increased alertness and mood in alzheimer patients. Phosphatidylserine, 300 grams daily, modestly improves memory and thinking[146-147]. Phosphatidylserine is most effective in the early stages of alzheimer's disease [148]. The effects of phosphatidylserine on cognition lastabout 8 to 16 weeks and then taper off [149]. However, phosphatidylserine improves the ability of patients to perform activities of daily living for periods up to 2 months [150]. Most studies have used phosphatidylserine in doses of 100 milligrams, given three times daily.
PHOTOGRAPH ALBUM
    A photograph album is a wonderful tool to promote and maintain cognitive abilities in alzheimer patients. The photo album is filled with pictures from the patient's life-pictures of friends, pictures of family, pictures of places traveled. Each day,the alzheimer patient and or caregiver uses a camera to take pictures of events and people during the day. Then the caregiver and patient sit down together and write notes in a journal, noting what each picture is about, and the names of persons in the picture. This is a wonderful cognitive tool [151].
PHYSOSTIGMINE
    Physostigmine is a cholinesterase inhibitor and preserves acetylcholine levels in brain cells.
Physostigmine, taken orally, is broken down rapidly in the blood, so that its effects are not very long-lasting [152].
Because physostigmine has such a short life in blood, it has not been found to be effective in alzheimer patients when given orally [153-154]. However, physostigmine is most effective orally when given for long periods of time,up to 6 weeks [155].
    Physostigmine effectively enhances cognitive ability when it is administered intravenously. Studies using intravenous physostigmine show good to excellent results in more than half of all patients [156-157]. When physostigmine is administered in transdermal patch,its effectiveness is comparable to the intravenous route[158].
    Physostigmine has been found to increase blood flow to the brains of alzheimer patients [159]. As you may recall, blood flow is reduced in the brains of
alzheimer patients.
PIRACETAM
    Piracetam is a popular remedy for dementia in Europe. One survey found that piracetam is the most common drug prescribed by German doctors for senile dementia [160]. Piracetam increases glucose use by the brain and has general cognitive-enhancing effects
even in non-demented people.
    Piracetam is not generally effective in alzheimer patients. A review by the Cochrane Database System Review summarized the results of all clinical studies that used piracetam to treat alzheimer patients[161]. In most studies, the dose given has ranged from 2.4 to 9.9 grams of piracetam daily. There are no significant side effects to the drug. Although piracetam does not seem to enhance cognitive abilities in patients, it does increase alertness [162].
PROPENTOFYLLINE
    Propentofylline is a relatively new drug that markedly slows the progression of alzheimer's disease for up to 56 weeks [166]. The drug increases Mini Mental State Exam scores in patients noticeably within 3 months and the effects last for up to one year [167-168].
The drug also substantially reduces home care and caregiving costs [169].
    Propentofylline is usually taken in doses of 300 milligrams, three times daily, one hour before meals. Meals seem to interfere with the
absorption of the drug [170]. The drug is well tolerated and has no severe side effects.
    How does the drug work? Propentofylline is an adenosine A2 receptor agonist and protects brain cells from injury [171]. Propentofylline decreases the toxic effects of amyloid beta protein [172]. The drug also increases the synthesis of nerve growth factor [173]. Propentofylline is a promising new drug for the treatment of alzheimer's disease with different modes of action than cholinesterase inhibitors.
PROPRANOLOL
    Propranolol,a drug used to treat high blood pressure, effectively controls agitation in alzheimer patients [163]. One study used 80 to 560 milligrams of propranolol daily to treat agitated alzheimer patients,who were not responding to conventional drugs. The agitation was effectively controlled without sedation [164].
   Another study reports that more than 67 percent of agitated alzheimer patients respond within two weeks on 10 to 80 milligrams of propranolol daily. Agitation is controlled for as long as 14 months [165].
RISPERIDONE
    Risperidone is an antipsychotic drug used to treat delusions,hallucinations, and agitation. Risperidone is more effective than haloperidol, a traditional antipsychotic drug [174]. Risperidone also causes far less extrapyramidal side effects, compared with haloperidol [175-176].
    Risperidone is given in doses of 0.25 to 2.5 milligrams daily. In one study, alzheimer patients who were highly aggressive and violent, were effectively calmed, without sedation, when they were given up to 2.5 milligrams of risperidone daily [177]. Approximately 64 percent of all demented patients show decreases in agitation and anxiety with doses as low as 0.25 to 0.5 milligrams of risperidone daily [178].
    Risperidone does have side effects. At doses greater than 1 milligram daily, the following side effects have been noted: insomnia, agitation, headache,
tremors, dizziness, constipation, and rapid heartbeat . Sedation is experienced by less than 2 percent of patients [179]. Risperidone can also cause peripheral edema [180].
SCOPOLAMINE
    Scopolamine is an anticholinergic drug. The drug tends to decrease memory equally in demented and non-demented patients [181-182]. Scopolamine also tends to aggravate feelings of hostility, especially in alzheimer patients [183]. Scopolamine should, therefore, be used cautiously in alzheimer patients.
SLEEP APNEA
    Sleep apnea is a condition that is more common in aging and dementia. Sleep apnea occurs when a person momentarily stops breathing while still sound asleep. Because the breath is held longer than normal, oxygen levels fall in the bloodstream. The condition, can, in fact, be diagnosed by monitoring oxygen levels with a device called a pulse oximeter.
    What are the signs and symptoms of sleep apnea? Excessive nighttime snoring and daytime sleepiness, despite adequate hours asleep, are tell-tale signs [184]. Daytime sleepiness, caused by sleep apnea, has been implicated as a cause of many auto accidents.
Awakening excessively at night to go to the bathroom is often precipitated by an episode of sleep apnea [185].
Sleep apnea also increases mental confusion and impairs memory, in demented and non-demented elderly [186-187].
Sleep apnea can also raise nightime systolic blood pressure [188]. Less common effects of sleep apnea are hallucinations, headaches, and sexual difficulties [189].
    Sleep apneas occur more frequently in alzheimer patients than in non-demented elderly [190-191]. Episodes of sleep apnea are also longer. Sleep apnea also becomes more severe as the underlying dementia becomes more severe [192]. Sleep apnea can aggravate existing memory defects and confusion in alzheimer patients. Snoring at night, a sign of sleep apnea, is twice as prevalent in alzheimer patients as in elderly controls [193].
    Sleep apnea is relatively easy to treat, once it is correctly diagnosed by a physician. Some patients are given special appliances to wear to create positive airway pressure, and this positive pressure corrects the underlying sleep apnea. Sometimes, conservative treatment can solve sleep apnea. Avoid caffeine, since that can precipitate sleep apnea in sensitive people. Sleeping on the back instead of the side or stomach can sometimes alleviate a minor sleep apnea.
STEROIDS
    Steroids may be expecially dangerous for alzheimer patients. Steroid use can reduce memory and cause confusion even in non-demented adults [194-195]. A recent study gave prednisone to alzheimer patients, based on the belief that prednisone might reduced the inflammation found in alzheimer brains. Prednisone, a steroid, was not found to be harmful or helpful to alzheimer patients [196].
    Interestingly, some research reports have found that steroids can benefit some kinds of demented patients. One researcher gave 100 milligrams of hydrocortisone intramuscularly three times daily for two days,and then 50 milligrams daily of oral prednisone, to two senile demented patients. The cognition of the patients markedly improved [197]. The two patients who responded to the steroid therapy had elevated blood alpha globulins and a raised erythrocyte sedimentation rate, co-existing with their dementia. Another researcher found steroids of
remarkable benefit in four demented patients [198].
THERAPEUTIC TOUCH
    Therapeutic touch is a nursing procedure where trained practitioners perform healing movements without actually touching the patient's body. Therapeutic touch was pioneered by Dolores Krieger, R.N. Therapeutic touch practitioners try to heal by altering disturbed energy fields around the patient.>br>
    To the best of my knowledge, only one study has used therapeutic touch to treat alzheimer patients. In that study, therapeutic touch was shown to reduce rocking motions, fist clenching, and verbal anxiety in agitated alzheimer patients [199].
THIAMINE
    Thiamine is an important vitamin, critical as a cofactor in many enzyme reactions. Alzheimer patients generally have low levels of thiamine in their blood [200-201].
    Thiamine has been given to alzheimer patients clinically and it has been shown to be mildly beneficial. One study gave patients 3 grams daily. Patient Mini Mental State Scores improved +1.35 ,compared with placebo scores of +0.54, a significant improvement [202].
Another study ,using doses of 3 to 8 grams of thiamine daily,also found improvement in mental function of patients [203]. One study did not find any improvement [204].
TRANSCRANIAL MAGNETIC STIMULATION
    Certain kinds of magnetic fields may prove to be helpful for alzheimer patients. Reuven Sandyk, of NeuroCommunication Research Labs, has pioneered the use of magnetic fields to treat various diseases.
He uses very tiny magnetic fields, 5 to 8 hertz frequency, and of picotesla strength. Two alzheimer patients were treated with these fields, applied to the head region. Both patients showed remarkable improvements in drawing abilities,as measured by the Rey-Osterrieth Complex Figure test [205].
TRANSCUTANEUS ELECTRICAL STIMULATION
    Transcutaneous electrical stimulation,abbreviated as TENS, is used to treat pain. A tiny instrument delivers a small electric current through the skin to a nerve and disrupts the transmission of nerve impulses. TENS has been found useful for alzheimer patients. TENS improves the short term memory of patients with mild alzheimer's disease, but does not improve memory in mid-stage patients [206]. TENS also improves the altered circadian rhythms of patients, reducing night time activity and promoting more restful sleep [207]. TENS is not widely used as therapy and is still in the research stages.
TRAZODONE
    Trazodone was originally developed in Italy to treat depression. However, the drug has been found useful to manage agitation in demented patients. One 10-week study gave 13 alzheimer patients 25 milligrams of trazodone,three times daily. Patients were less irritable and anxious [208]. Another study compared trazodone,50 to 250 milligrams daily with haloperidol, 1 to 5 milligrams daily. Trazodone and haloperidol both work equally at controlling agitation; however, trazodone seems to work best on repetitive or verbal aggressive behavior, whereas haloperidol seems to work best on excess motor activity [209].
    Trazodone is not free of side effects. Trazodone may occassionally cause ventricular arrhythmia in patients with preexisting cardiac problems. Trazodone's most frequent side effects are drowsiness, headache, gastrointestinal upset, and postural hypotension . A rare but serious side effect is priapism in males, which may need
urologic intervention.
DR. WALSH'S ANTICOAGULANT THERAPY
    Arthur Walsh,M.D.,throughout the 1960-1995 period, published extensively about his work with anticoagulant therapy for dementia patients [210-211]. Dr. Walsh believes that the cause of many kinds of dementias, including alzheimer's disease, is a "sludging" of brain vessels. Blood flow to the brain becomes seriously reduced by aging,cholesterol deposits,and aggregated erthyrocytes. It is the reduced blood flow that causes dementia, in Dr. Walsh's view. Dr.Walsh has carefully documented how successful his anticoagulant therapy has been for dementia; yet, very few mainstream physicians have used the therapy for dementia.
    What is Dr. Walsh's procedure for anticoagulant therapy? Dr. Walsh prescribes a course of oral sodium warfarin, an anticoagulant, for the demented patient. Initial dosing may be 20 milligrams daily,
with 2.5 milligrams as a maintainence dose. Dr. Walsh records the baseline prothrombin time, a measure of blood clotting. To achieve clinical dementia relief, Dr. Walsh says the prothrombin time during therapy needs to be
about 2 times the baseline prothrombin time. Results are seen almost immediately and continue as long as the therapy is maintained, according to Dr.Walsh.
    How successful is the anticoagulant therapy? Dr. Walsh in 1992 wrote a report detailing his dementia work. Dr. Walsh selected 500 patients randomly from his treated cases and reported on them. Remember, most of the cases that Dr.Walsh saw were demented patients who others gave up on. Many of his cases were considered "hopeless". Dr. Walsh reports that more than 65 percent of such patients show a worthwhile response to therapy; more than 15 percent of these patients show dramatic and long-lasting improvement [212]. I will relate here a typical case report, cited by Dr.Walsh [213].
    Dr. Walsh treated a 74-year-old woman who was confused, talkative,and who had to be locked in a room at times; she was suffering from some sort of dementia. Her memory and thinking were bad. She could name only Bush and Carter as the last five presidents at the time. She could not do a simple arithmetic problem such as 4 x 16. She was started on a course of warfarin sodium by Dr. Walsh. Gradually, her memory and confusion improved. Two years later, the family reported that she was doing very well. She was able to help her husband with the income tax and to keep her checkbook again. The last two summers she also was able to enjoy a beach vacation with the family, going swimming and cooking as she used to.
    Dr. Jack Ratner, M.D. and others, in 1972, published an important confirming study of anticoagulant therapy in the Journal of the American Geriatrics Society [214]. Fourteen demented patients were treated with warfarin sodium, 20 milligrams orally to start, with maintainence dosage at 2.5 milligrams. Prothrombin time was kept at 2 times the control value. The Wechsler Memory Scale, expressed as a Memory Quotient, was one main measure of memory. Anticoagulant therapy was given for up to 12 months. Demented patients receiving therapy had baseline scores of 44.9 on the Wechsler Memory Test; twelve months later, their scores had declined just a bit to 38.0. The demented patients not receiving the anticoagulant therapy had a major decline on the Wechsler Memory Test. At baseline their score was 44.7; 12 months later, their scores on the Wechsler Memory Test had plummeted to 14.9.
With impressive results such as Dr.Walsh and Dr. Ratner report, one wonders why mainstream medicine has not paid more attention to their work.
ZOLPIDEM
    Zolpidem is a relatively new sleep-inducing drug. It is an imidazopyridine, a non-benzodiazepine drug.
Zolpidem shortens the time to fall asleep and prolongs the amount of time spent in restful sleep [215]. Zolpidem does not cause rebound insomnia or impair memory the next day [216].
    Zolpidem induces sleep at doses of 10 to 20 milligrams, taken just before going to bed. At lower doses, the drug controls anxiety and agitation in alzheimer
patients. One study reports on two highly-agitated alzheimer patients, whose agitation was not controlled by haloperidol or thioridazine. Doses of 2.5 milligrams, given before the morning routine of dressing and bathing, made these two patients calmer and easier to manage [217].
    Zolpidem is also effective for alzheimer patients who wander. A study finds that two alzheimer patients who spent the night hours wandering, instead of sleeping, had normal restful sleep restored when given zolpidem in doses of 10 to 15 milligrams at sleep time [218].
    Zolpidem has some adverse effects. Gastrointestinal upset, drowsiness, and orthostatic hypotension are known side effects of the drug.
Zolpidem can be given with other drugs, such as cimetidine,chlorpromazine,warfarin,and digoxin. Cimetidine and zolpidem can sometimes decrease alertness.
Zolpidem and imipramine can sometimes cause anterograde amnesia. Zolpidem does not have withdrawal effects and does not cause habituation [219].
REFERENCES
1. Breitner,JC.et.al.,Delayed onset of alzheimer's disease with nonsteroidal anti-inflammatory and histamine H2
blocking drugs. Neurobiol Aging, 1995, 16: 523-530.
2. Stewart,W.,et.al., Neurology,1997,48: 626-632.
3. Galli,G.,et.al., Activation of apoptosis by serum deprivation in a teratocarcinoma cell line: inhibition by
l-acetylcarnitine. Exp Cell Res, 204: 54-60.
4. Forloni, G.,et.al., Neuroprotective activity of acetyl-l-carnitine: studies in vitro.
J Neurosci Res, 1994, 37: 92-96.
5. Passeri,M., et.al., Acetyl-l-carnitine in the treatment of mildly demented elderly patients.
Int J Clin Pharmacol Res, 1990, 10: 75-79.
6. Sano,M., et.al., Double blind parallel design pilot study of acetyl levocarnitine in patients with alzheimer's disease.
Arch Neurol, 1992, 49: 1137-1141.
7. Spagnoli,A.,et.al., Long term acetyl-l-carnitine treatment in alzheimer's disease.
Neurology, 1991, 41:1726-1732.
8. Pettegrew,J.W.,et.al., Clinical and neurochemical effects of acetyl-l-carnitine in alzheimer's disease.
Neurobiol Aging, 1995, 16: 1-4.
9. Thal,L.J.,et.al., A l year multicenter placebo-controlled study of acetyl-l-carnitine in patients with alzheimer's disease.
Neurology, 1996, 47: 705-711.
10. Brooks, J.O.3rd,et.al., Acetyl-l-carnitine slows decline in younger patients with alzheimer's disease:
a reanalysis of a double-blind,placebo-controlled study using the trilinear approach. Int Psychogeriatr, 1998, 10: 193-203.
11. Thal,L.J.,et.al., A 1 year controlled trial of acetyl-l-carnitine in early-onset AD.
Neurology, 2000, 55: 805-810.
12. Campi,N., et.al., Selegiline versus acetyl-l-carnitine in the treatment of alzheimer type dementia.
Clin Ther, 1990, 12: 306-314.
13. Sinforiano, E.,et.al., Neuropsychological changes in demented patients treated with acetyl-l-carnitine.
Int J Clin Pharmacol Res, 1990, 10: 69-74.
14. Deng,Q.S.,et.al., Ionic mechanisms of acupuncture on improvement of learning and memory in aged animals.
Am J Chin Med, 1995, 23: 1-9.
15. Chen,Y., Clinical research on treating senile dementia by combining acupunture with acupoint-injection.
Acupuncture and Electro Therapeutics Res Int J, 1992, 17: 61-73.
16. Kagan,B.L.,et.al., Oral s-adenosylmethionine in depression: a randomized,double-blind,placebo-controlled trial.
Am J Psychiatry, 1990, 147:591-595.
17. Fugh-Berman,A.,et.al., Dietary supplements and natural products as psychotherapeutic agents.
Psychosom Med, 1999, 61: 712-728.
18. Cohen,B.M., et.al., S-adenosyl-l-methionine in the treatment of alzheimer's disease.
J Clin Psychopharmacol, 1988, 8:43-47.
19. Fritz,C.L., et.al., Association with companion animals and the expression of noncognitive symptoms in alzheimer's patients.
J Nerv Ment Dis, 1995, 183: 459-463.
20. Steele,C.,et.al., Haloperidol versus thioridazine in the treatment of behavioral symptoms in senile
dementia of the alzheimer's type: preliminary findings. J Clin Psychiatry, 1986, 47: 310-312.
21. Lemke,M.R.,Effect of carbamazepine on agitation in alzheimer's disease inpatients refractory to neuroleptics.
J Clin Psychiatry, 1995, 56: 354-357.
22. Teri,L.,et.al.,Treatment of agitation in AD: a randomized, placebo-controlled clinical trial.
Neurology, 2000, 55: 1271-1278.
23. Simpson,D.M.,Improvement in organically disturbed behavior with trazodone treatment.
J Clin Psychiatry,1996, 47: 191-193.
24. Lebert,F., Behavioral effects of trazodone in alzheimer's disease.
J Clin Psychiatry, 1994, 55: 536-538.
25. Gedye,A., Serotonergic treatment for aggression in a Down's syndrome adult showing signs of alzheimer's disease.
J Ment Defic Res, 1991,35: 247-258.
26. Feingeld,E.W.,et.al., Double-blind study with phospatidylserine in parkinsonian patients with senile dementia of alzheimer's type.
Prog Clin Biol Res, 1989, 317: 1235-1246.
27. Shankle,W.R.,et.al.,Low-dose propanolol reduces aggression and agitation resembling that associated with orbitofrontal dysfunction in elderly demented patients.
Alzheimer Dis Assoc Disord, 1995, 9: 233-237.
28. Amadeo,M.,Antiandrogen treatment of aggressivity in men suffering from dementia.
J Geriatr Psychiatry Neurol, 1996, 9: 142-145.
29. Sunderland,T.,Anticholinergic sensitvity in patients with dementia of the alzheimer type and age-matched controls. A dose-response study.
Arch Gen Psychiatry, 1987, 44: 418-426.
30. Larson,E.B., Adverse drug reactions associated with global cognitive impairment in elderly persons.
Ann Intern Med, 1987, 107: 169-173.
31. Ames,D.,et.al., Drugs used for psychiatric disorders.
Med J Aust, 1993, 159: 116-120.
32. Ames,D.,et.al., Drugs used for psychiatric disorders.
Med J Aus, 1993, 159: 116-120.
33. Schneider,L.S., Efficacy of treatment for geropsychiatric patients with severe mental illness.
Psychopharmacol Bull, 1993, 29: 501-514.
34. Brooker,D.J.,et.al., Single case evaluation of the effects of aromatherapy and massage on disturbed behavior in severe dementia.
Br J Clin Psychol, 1997, 36: 287-296.
35. Rich,J.B.,et.al., Nonsteroidal anti-inflammatory drugs in alzheimer's disease.
Neurology, 1995, 45: 51-55.
36. Doraiswamy,P.M.,et.al., NSAIDS and cognition in alzheimer's disease.
Neurology, 1996, 46: 1194.
37. Breitner,J.C.,et.al., Delayed onset of alzheimer's disease with nonsteroidal anti-inflammatory and histamine H2 blocking drugs.
Neurobiol Aging, 1995,16: 523-530.
38. Doraiswamy,P.M.,et.al., NSAIDS and cognition in alzheimer's disease.
Neurology, 1996, 46: 1194.
39. Inzelberg,R.,et.al.,Effects of atropine on learning and memory functions in dementia.
Clin Neuropharmacol,1990,13: 1-7.
40. Preston,G.C.,et.al.,Scopolamine and benzodiazepine models of dementia: cross-reversals by RO 15-1788 and physostigmine.
Psychopharmacology, 1989, 98: 487-494.
41. Pomara,N.,et.al., ApoE4 allele and susceptibility to drug-related memory impairment in the elderly.
J Clin Psychopharmacol, 1998, 18:179-181.
42. Sobel,B.P., Bingo vs. physical intervention in stimulating short-term cognition in alzheimer's disease patients.
Am J Alzheimers Dis Other Dement, 2001, 16: 115-120.
43. Lemke,M.R., Effect of carbamazepine on agitation in alzheimer's inpatients refractory to neuroleptics.
J Clin Psychiatry, 1995, 56: 354-357.
44. Lemke,M.R.,et.al.,Therapeutic use of carbamazepinefor treatment of agitations and affective disorders in geriatric psychiatry patients.
Psychiatr Prax, 1994, 21: 147-150.
45. Marin,D.B.,et.al.,Carbamazepine for aggressive agitation in demented patients.
Am J Psychiatry, 1989, 146: 805.
46. Gleason,R.P., et.al., Carbamazepine treatment of agitation in alzheimer's outpatients refractory to neuroleptics.
J Clin Psychiatry, 1990, 51: 115-118.
47. Raskind,M.A.,et.al., Alzheimer's disease and related disorders.
Med Clin North Am,2001, 85: 803-817.
48. Ragneskog,H.,et.al., Long-term treatment of elderly individuals with emotional disturbances: an open study with citalopram.
Int Psychogeriatr,1996, 8: 659-668.
49. Gottfries,C.G.,et.al., Effect of citalopram, a selective 5-HT reuptake blocker, in emotionally disturbed patients with dementia.
Ann Ny Acad Sci,1991, 640: 276-279.
50. Wu,R.M.,et.al., Suppression of hydroxyl radical formation and protection of nigral neurons by l-deprenyl.
Ann Ny Acad Sci, 1996, 786: 379-390.
51. Iwasaki,Y.,et.al., Deprenyl enhances neurite outgrowth in cultured rat spinal ventral horn neurons.
J Neurol Sci, 1994, 125: 11-13.
52. Martini,E.,et.al., Brief information on an early plase 2 study with deprenyl in demented patients.
Pharmacopsychiatry, 1987, 20: 256-257.
53. Tariot,P.N.,et.al., Cognitive effects of l-deprenyl in alzheimer's disease.
Psychopharmacology, 1987, 91: 489-495.
54. Schneider,L.S., et.al., A pilot study of low dose l-deprenyl in alzheimer's disease.
J Geriatr Psychiatry Neurol, 1991, 4: 143-148.
55. Burke,W.J.,et.al., L-deprenyl in the treatment of mild dementia of the alzheimer type: results of a 15 month trial.
J Am Geriatr Soc, 1993, 41: 1219-1225.
56. Freedman,M.,et.al., L-deprenyl in alzheimer's disease: cognitive and behavioral effects.
Neurology,1998, 50: 660-668.
57. Shepherd,J.E., Effects of estrogen on cognition,mood, and degenerative brain diseases.
J Am Pharm Assoc, 2001, 41: 221-228.
58. Greene,R.A., Estrogen and cerebral blood flow: a mechanism to explain the impact of estrogen on the incidence and treatment of alzheimer's disease.
Int J Fertil Womens Med, 2000, 45: 153-257.
59. Panidis,D.K.,et.al., The role of estrogen replacement therapy in alzheimer's disease.
Eur J Obstet Gynecol Reprod Biol, 2001, 95: 86-91.
60. Greene,R.A., Estrogen and cerebral blood flow: a mechanism to explain the impact of estrogen on the incidence and treatment of alzheimer's disease.
Int J Fertil Womens Med, 2000, 45: 153-257.
61. Kim,H.,et.al., Neuroprotective effects of estrogen against beta-amyloid toxicity are mediated by estrogen receptors in cultured neuronal cells.
Neurosci Lett, 2001, 302: 58-62.
62. Li,R.,et.al., Estrogen enhances the uptake of amyloid beta protein by microglia derived from the human cortex.
J Neurochem, 2000, 75: 1447-1454.
63. Kampen,D.L.,et.al., Estrogen use and verbal memory in healthy postmenopausal women.
Obstet Gynecol, 1994, 83: 979-983.
64. Robinson,D.,et.al., Estrogen replacement therapy and memory in olders women.
J Am Geriatr Soc, 1994, 12: 919-922.
65. Ohkura,T.,et.al., Long-term estrogen replacement therapy in female patients with dementia of the alzheimer type: 7 case reports.
Dementia, 1995, 6: 99-107.
66. Schneider,L.S., et.al., Effects of estrogen replacement therapy on response to tacrine in patients with alzheimer's disease.
Neurology, 1996, 46: 1580-1584.
67. Olichney,J.M.,et.al., Estrogen use and decline in cognition among alzheimer's disease patients.
Neurology, 1999, 52: A 395.
68. Relkin,N.,et.al., The effect of concomitant donepezil and estrogen treatment on the cognitive performance of women with alzheimer's disease.
Neurology,1999, 52: A397.
69. Kyomen,H.H.,et.al., The use of estrogen to decrease aggressive physical behavior in elderly men with dementia.
J Am Geriatr Soc, 39:1110-1112.
70. Kay,P.A., et.al., Transdermal estradiol in the management of aggressive behaviors in male patients with dementia.
Clin Gerontologist, 1995, 15: 54-58.
71. Kondo,K., et.al., A case-control study of alzheimer's disease in Japan- significance of life styles.
Dementia, 1994, 5: 314-326.
72. Broe,G.A.,et.al., A case-control study of alzheimer's disease in Australia.
Neurology,1990, 40: 1698-1707.
73. Shimamura,K.,et.al., Environmental factors possibly associated with onset of senile dementia.
Nippon Koshu Eisei Zasshi,1998, 45: 203-212.
74. Okamoto,K.,et.al., Sociomedical and lifestyle risk factors of senile dementia,determined in a nested case-control study.
Nippon Ronen Igakkai Zasshi, 1994,31: 604-609.
75. Rolland,Y.,et.al.,Feasibility of regular physical exercise for patients with moderate to severe alzheimer disease.
J Nutr Health Aging, 2000, 4: 109-113.
76. Lindemuth,G.F.,et.al., Improving cognitive abilites of elderly alzheimer's patients with intense exercise therapy.
Am J Alzheimer's Care Rel Dis Res, 1990,5: 31-33.
77. Namaxzi,K.H., et.al., A low intensity exercise/movement program for patients with alzheimer's disease: the TEMP-AD protocol.
J Aging Phys Act,1994, 2: 80-92.
78. Friedman,R.,et.al., The effects of planned walking on communication in alzheimer's disease.
J Am Geriatr Soc, 1991, 39: 650-654.
79. Roane,D.M., et.al., Treatment of dementia-associated agitation with gabapentin.
J Neuropsychiatry Clin Neurosci, 2000, 12: 40-43.
80. Herrmann, N.,et.al., Effectiveness of gabapentin for the treatment of behavioral disorders in dementia.
J Clin Psychopharmacol, 2000, 20: 90-93.
81. Hawkins,J.W.,et.al., A retrospective chart review of gabapentin for the treatment of aggressive and agitated behavior in patients with dementia.
Am J Geriatr Psychiatry, 2000, 8: 221-225.
82. Maurer,K.,et.al., Clinical efficacy of gingko biloba extract EGb 761 in dementia of the alzheimer type.
J Psychiatry Res, 1997, 31: 645-655.
83. Wettstein,A., Cholinesterase inhibitors and gingko extracts-- are they comparable in the treatment of dementia? Comparison of published placebo-controlled efficacy
studies of at least six months' duration. Phytomedicine, 2000, 6: 393-401.
84. Le Bars, P.L., et.al., A 26-week analysis of a double-blind, placebo-controlled trial of the gingko biloba extract EGb 761 in dementia.
Dement Geriatr Cogn Disord, 2000, 11: 230-237.
85. Le Bars,P.L., et.al., A placebo-controlled,double-blind, randomized trial of an extract of gingko biloba for dementia.
JAMA, 1997, 278: 1327-1332.
86. Haase,J.,et.al., Effectiveness of brief infusions with gingko biloba extracts EGb 716 in dementia of the vascular and alzheimer type.
Z Gerontol Geriatr, 1996, 29: 302-309.
87. Thomson,G.J., et.al., A clinical trial of gingko biloba extract in patients with intermittent claudication.
Int Angiol, 1990, 9: 75-78.
88. Yao,Z., et.al., The gingko biloba extract EGb 761 rescues the PC12 neuronal cells from beta-amyloid induced cell death by inhibiting the formation of
beta amyloid diffusible neurotoxic ligands. Brain Res, 2001, 889: 181-190.
89. Itil, T.M., et.al., The pharmacological effects of gingko biloba, a plant extract, on the brain of dementia patients in comparison with tacrine.
Psychopharmacol Bull, 1998, 34: 391-397.
90. Cheng, D.H.,et.al., Huperzine A, a novel promising acetylcholinesterase inhibitor.
Neuroreport, 1996, 8: 97-101.
91. Zhu, X.Z., et.al., Development of natural products as drugs acting on central nervous system.
Mem Inst Oswaldo Cruz, 1991, 86: 173-175.
92. Skolnick,A.A., Old chinese herbal medicine used for fever yields possible new alzheimer disease therapy.
JAMA, 1997, 277: 776.
93. Sun,Q.Q.,et.al., Huperzine A capsules enhance memory and learning peformance in 34 pairs of matched adolescent students.
Zhongguo Yao Li Xue Bao, 1999, 20: 601-603.
94. Xu,S.S., et.al., Efficacy of tablet huperzine A on memory,cognition,and behavior in alzheimer's disease.
Zhongguo Yao Li Xue Bao, 1995, 16: 391-395.
95. Zhang,H.Y., et.al., Huperzine B, a novel acetylcholinesterase inhibitor, attenuates hydrogen peroxide induced injury in PC 12 cells.
Neurosci Lett, 2000, 292: 41-44.
96. Xiao,X.Q.,et.al., Huperzine A and tacrine attenuate beta-amyloid induced oxidative injury.
J Neurosci Res, 2000, 61: 564-569.
97. Breitner,J.C., et.al., Delayed onset of alzheimer's disease with nonsteroidal anti-inflammatory and histamine H2 blocking drugs.
Neurobiol Aging, 1995, 16: 523-530.
98. Corrada,M., et.al., Nonsteroidal anti-inflammatory drugs and the risk of alzheimer's disease.
Neurology, 1996, 46: A433.
99. Lambat,Z., et.al., An investigation into the neuroprotective properties of ibuprofen.
Metab Brain Dis, 2000, 15: 249- 256.
100. Lim,G.P., et.al., Ibuprofen suppresses plaque pathology and inflammation in a mouse model for alzheimer's disease.
J Neurosci Res, 2000, 20: 5709-5714.
101. Rogers,J., et.al., Clinical trials of indomethacin in alzheimer's disease.
Neurology, 1993, 43: 1609-1611.
102. Lockhart,B.P., et.al., Inhibitors of free radical formation fail to attenuate direct beta-amyloid 25-35 peptide mediated neurotoxicity in rat
hippocampal cultures. J Neurosci Res, 1994, 39: 494-505.
103. Goodman, Y., et.al., Nordihydroquiacetic acid protects hippocampal neurons against amyloid beta peptide toxicity and attenuates free radical and calcium
accumulation. Brain Res, 1994, 654: 171-176.
104. Netland,E.E., et.al., Indomethacin reverses the microglial response to amyloid beta protein.
Neurobiol Aging, 1998, 19: 201-204.
105. Mallet,L., et.al., Indomethacin-induced behavioral changes in an elderly patient with dementia.
Annals of Pharmacotherapy,1998, 32: 201-203.
106. Higgins, J.P.T., et.al., Lecithin for dementia and cognitive impairment.
Cochrane Library, 2001, 2: Oxford.
107. Otsuka,A.,et.al., Absence of nocturnal fall in blood pressure in elderly persons with alzheimer type dementia.
J Am Geriatr Soc, 1990, 38: 973-978.
108. Otsuka,A., et.al., Circadian changes of blood pressure in the elderly with alzheimer's type dementia.
Nippon Ronen Igakkai Zaashi, 1990, 27: 570-572.
109. Reynolds,V.,et.al., Heart rate variation, age, and behavior in patients with senile dementia of alzheimer type.
Chronobiol Int, 1995, 12: 37-45.
110. Tate,B., et.al., Disruption of circadian regulation by brain grafts that overexpress alzheimer amyloid beta protein.
Proc Natl Acad Sci USA, 1992, 89: 7090-7094.
111. Swaab,D.F., et.al., The suprachiasmatic nucleus in the human brain in relation to age,sex, and senile dementia.
Brain Res, 1985, 342: 37-44.
112. Mishima,K.,et.al., Morning bright light therapy for sleep and behavior disorders in elderly patients with dementia.
Acta Psychiatr Scand, 1994, 89: 1-7.
113. Lovell,B.B.,et.al., Effect of bright light treatment on agitated behavior in institutionalized elderly subjects.
J Psychiatry Res, 1995, 57: 7-12.
114. Ito,T., et.al., Effects of bright light on cognitive disturbances in alzheimer-type dementia.
Nippon Ika Daigaku Zaashi, 1999, 66: 229-238.
115. Campbell,S.S., et.al., Exposure to light in healthy elderly subjects and alzheimer's patients.
Physiol Behav, 1988, 42: 141-144.
116. Brinkman,S.D., et.al., Lithium-induced increases in red blood cell choline and memory performance in alzheimer-type dementia.
Biol Psychiatry, 1984, 19: 157-164.
117. Pomara,N., et.al., Elevation of red blood cell glycine and choline levels in geriatric patients treated with lithium.
Am J Psychiatry, 1983, 140: 911-913.
118. Randels,P.M., et.al., Lithium and lecithin treatment in alzheimer's disease: a pilot study.
Hillside J Clin Psychiatry, 1984, 6: 139-147.
119. Kelwala,S.,et.al., Lithium-induced accentuation of extrapyramidal symptoms in individuals with alzheimer's disease.
J Clin Psychiatry, 1984, 45: 343-344.
120. Brinkman,S.D., et.al., Lithium induced increases in red blood cell choline and memory performance in alzheimer type dementia.
Biol Psychiatry, 1984, 19: 157-164.
121. Rowe,M., et.al., The effectiveness of slow-stroke massage in diffusing agitated behaviors in individuals with alzheimer's disease.
J Gerontol Nursing, 1999, 25: 22-34.
122. Lord,T.R., et.al., Effects of music on alzheimer patients.
Percept Mot Skills, 1993, 76: 451-455.
123. Casby,J.A.,et.al., The effect of music on repetitive disruptive vocalizations of persons with dementia.
Am J Occup Ther, 1994, 48: 883-889.
124. Gerdner,L.A., Effects of individualized versus classical relaxation music on the frequency of agitation in elderly persons with alzheimer's disease and related disorders.
Int Psychogeriatr, 2000, 12: 49-65.
125. Aldrige,D., Alzheimer's disease: rhythm,timing,and music as therapy.
Biomed Pharmacother, 1994, 48: 275-281.
126. Hasegawa,Y., et.al., Music therapy induced alterations in natural killer cell count and function.
Nippon Ronen Iggakai Zaashi, 2001, 38: 201-204.
127. Cattan,R., et.al., Music therapy increases serum melatonin levels in patients with alzheimer's disease.
Altern Ther Health Med, 1999, 5: 49-57.
128. Birkmayer,J.G., et.al., Coenzyme nicotinamide adenine dinucleotide: new
therapeutic approach for improving dementia of the alzheimer type. Ann Clin Lab Sci, 1996, 26: 1-9.
129. Lapchak,P.A., et.al., Effect of recombinant human nerve growth factor on presynaptic cholinergic function in rat hippocampal slices following partial
septohippocampal lesions: measures of acetylcholine synthesis, acetycholine release,and choline acetyltransferase activity.
Neurocience, 1991, 42: 639-649.
130. Castro,M., et.al., Does the Kunitz domain from the alzheimer's amyloid beta protein precursor inhibit a kallikrein responsible for post-translational
processing of nerve growth factor precursor? FEBS Lett,1990, 267: 207-212.
131. Olson,L., Grafts and growth factors in CNS. Basic science with clinical promise.
Stereotact Funct Neurosurg,1990, 54-55: 250-267.
132. Eriksdotter,M.,et.al.,Intracerebroventricular infusion of nerve growth factor in three patients with alzheimer's disease.
Dement Geriatr Cogn Disord, 1998, 9: 246-257.
133. Shalat,S.L., et.al., Risk factors for alzheimer's disease: a case-control study.
Neurology, 1987, 37: 1630-1633.
134. Wang,P.N., et.al., Risk factors for alzheimer's disease: a case-control study.
Neuroepidemiology, 1997, 16: 234-240.
135. Ott,A., et.al., Smoking and the risk of dementia and alzheimer's disease in a population-based cohort study: The Rotterdam Study.
Lancet, 1998, 351: 1840-1843.
136. Lee,P.N., et.al., Smoking and alzheimer's disease: a review of the epidemiological evidence.
Neuroepidemiology, 1994, 13: 131-144.
137. Snaedal,J., et.al., The effects of nicotine in dermal plaster on cognitive function in patients with alzheimer's disease.
Dementia, 1996, 7: 47-52.
138. White,H.K., et.al., Four week trial of nicotine skin patch treatment effects on cognitive performance in alzheimer's disease.
Psychopharmacology, 1999, 143: 158-165.
139. Raskind,M.A., et.al., Alzheimer's disease and related disorders.
Med Clin North Am, 2001, 85: 803-817.
140. Street,J.S., et.al., Olanzapine treatment of psychotic and behavioral symptoms in patients with alzheimer disease in nursing care facilities: a
double-blind, placebo-controlled trial. The HGEU Study Group.
Arch Gen Psychiatry, 2000, 57: 968-976.
141. Jacobs,E.A., et.al., Hyperoxygenation effect on cognitive functioning in the aged.
New England J Medicine, 1969, 281: 753-757.
142. Fraiberg,P.L., Oxygen inhalation in the control of psychogeriatric symptoms
in patients with long- term illness. J Am Geriatr Soc, 1973, 21: 321-328.
143. Goldfarb,A.I., et.al., Hyperbaric oxygen treatment of organic mental syndrome in aged persons.
J Gerontol, 1972, 27: 212.
144. Ben-Vishay,Y., et.al., Can oxygen reverse symptoms of senility?
NY State J Med, 1978, 78: 914-919.
145. Holdsworth,F., Hyperbaric oxygen and senile psychosis.
Lancet, 1969, 2: 1340.
146. Delwaide,P.J., et.al.,Double-blind, randomized controlled study of phosphatidylserine in senile demented patients.
Acta Neurol Scand, 1986, 73: 136-140.
147. Schreiber, S., et.al., An open trial of plant-source derived phosphatidylserine for treatment of age-related cognitive decline.
Isr J Psychiatry Relat Sci, 2000, 37: 302-307.
148. Crook,T.,et.al., Effects of phosphatidylserine in alzheimer's disease.
Psychopharmacol Bull, 1992, 28: 61-66.
149. Funfgeld,E.W., et.al., Double-blind study with phosphatidylserine in parkisonian patients with senile dementia of alzheimer's type.
Prog Clin Biol Res, 1989, 317: 1235-1246.
150. Naor,S., et.al., Phosphatidylserine effect on functioning and general condition of alzheimer's disease patients.
J Am Geriatr Soc, 1998, 46: S100.
151. Sandoz,C.J.,et.al.,Photographs as a tool in memory preservation for patients with alzheimer's disease.
Clinical Gerontologist, 1996, 17: 69-71.
152. Johansson,M.,et.al., Pharmacokinetic studies of cholinesterase inhibitors.
Acta Neurol Scand, 1993, 149: 22-25.
153. Caltagirone,C.,et.al., Oral administration of chronic physostigmine does not improve cognitive or mnesic performances in alzheimer's presenile
dementia. Int J Neurosci,1982,16: 247-249.
154. Jenike,M.A., et.al., Oral physostigmine as treatment for primary degenerative dementia: a double-blind, placebo-controlled inpatient trial.
J Geriatr Psychiatry, 1990, 3: 13-16.
155. Stern,Y., et.al., Long-term administration of oral physostigmine in alzheimer's disease.
Neurology, 1988, 38: 1837-1841.
156. Mohs,R.C.,et.al., Clinical studies of the cholinergic deficit in alzheimer's disease.
J Am Geriatr Soc, 1985, 33: 749-757.
157. Schwartz,A.S., et.al., Physostigmine effects in alzheimer's disease: realtionship to dementia severity.
Life Sci, 1986, 38: 1021-1028.
158. Levy,A., et.al., Transdermal physostigmine in the treatment of alzheimer's disease.
Alzheimer Dis Assoc Disord, 1994, 8: 15-21.
159. Gustafson,L., Physostigmine and tetrahydroaminoacridine treatment of alzheimer's disease.
Acta Neurol Scand, 1993, 149: 39-41.
160. Stoppe,G.,et.al., Prescribing practice with cognition enhancers in outpatient care: are there differences regarding types of
dementia?--Results of a representitive survey in Saxony,Germany. Pharmacopsychiatry, 1996, 29: 150-155.
161. Flicker,L., et.al., Piracetam for dementia or cognitive impairment.
Cochrane Database Syst Rev,2001, 2: CD001011.
162. Pierlovisi-Lavaivre,M.,et.al., The significance of quantified EEG in alzheimer's disease. Changes induced by piracetam.
Neurophysiol Clin, 1991,21: 411-423.
163. Pauszek,M.E., Propanolol for treatment of agitation in senile dementia.
Indiana Med, 1991, 84: 16-17.
164. Weiler,P.G., et.al., Propanolol for the control of disruptive behavior in senile dementia.
J Geriatr Psychiatry Neurol, 1988, 1: 226-230.
165. Shankle,W.R.,et.al., Low-dose propanolol reduces aggression and agitation resembling that associated with orbitofrontal dysfunction in elderly
demented patients. Alzheimer Dis Assoc Disord, 1995, 9: 233-237.
166. Rother,M.,et.al., Propentofylline in the treatment of alzheimer's disease and vascular dementia: a review of phase 3 trials.
Dement Geriatr Cogn Disord, 1998, 9: 36-43.
167. Mielke,R., et.al., Propentofylline enhances cerebral metabolic response to auditory memory stimulation in alzheimers.
J Neurol Sci, 1998, 154: 76-82.
168. Marcusson,J., et.al., A 12 month, randomized,placebo-controlled trial of propentofylline in patients with dementia according to DSM III-R.
Dement Geriatr Cogn Disord, 1997, 8: 320-328.
169. Bachynsky,J., et.al., Propentofylline treatment for alzheimer disease and vascular dementia: an economic evaluation based on functional abilities.
Alzheimer Dis Assoc Disord, 2000, 2: 102-111.
170. Mielke,R., et.al., Propentofylline in the treatment of vascular dementia and alzheimer-type dementia: overview of phase 1and phase 2 clinical trials.
Alzheimer Dis Assoc Disord, 1998, 12:Suppl, S29-S35.
171. McRae,A., et.al., Propentofylline depresses amyloid and alzheimer's CSF microglial antigens after ischemia.
Neuroreport, 1994, 5: 1193-1196.
172. Koriyama,Y.,et.al., Evaluation of neurotoxicity of alzheimer's amyloid beta protein in cultured hippocampal cells and its prevention by propentofylline.
Jpn J Pharmacol, 2000, 82: 301-306.
173. Nabeshima,T., Nerve growth factor strategy and preparation of animal model for alzheimer-type senile dementia.
Yakugaku Zaashi, 1995, 115: 499-512.
174. Frenchman,I.B.,et.al., Clinical experience with risperidone,haloperidol,and thioridazine for dementia-associated behavioral disturbances.
Int Psychogeriatr, 1997, 9: 431-435.
175. Claus,A., et.al., Risperidone versus haloperidol in the treatment of chronic schizophrenic inpatients: a multicenter double-blind comparative study.
Acta Psychiatr Scand, 1992, 85: 295-305.
176. Lopez,I., et.al., Risperidone in the treatment of chronic schizophrenia: multicenter study comparative to haloperidol.
Actas Luso Esp Neurol Psiquiatr Cienc Afines, 1996, 24: 165-172.
177. Raheja,R.K., et.al.,Efficacy of risperidone for behavioral disorders in the elderly: a clinical observation.
J Geriatr Psychiatr Neurol, 1995, 8: 159-161.
178. Goldberg,R.J., et.al., Risperidone for dementia-related disturbed behavior in nursing home residents: a clinical experience.
Int Psychogeriatr,1997, 9: 65-68.
179. Barcia,D., et.al., Risperidone in the treatment of psychotic,affective and behavioral symptoms associated to alzheimer's disease.
Actas Esp Psiquiatr, 1999, 27: 185-190.
180. Katz,I.R., et.al., Comparison of risperidone and placebo for psychosisand behavioral disturbances associated with dementia: a randomized,double-blind trial.
J Clin Psychiatry,1999, 60: 107-115.
181. Christensen,H., et.al., Cholinergic blockade as a model of the cognitive deficits in alzheimer's disease.
Brain, 1992, 115: 1681-1699.
182. Rabey,J.M., et.al., Cognitive effects of scopolamine in dementia.
J Neural Transm Gen Sect, 1996, 103: 873-881.
183. Sunderland,T., et.al., Anticholinergic sensitivity in patients with dementia of the alzheimer type and age-matched controls, A dose-response study.
Arch Gen Psychiatry, 1987, 44: 418-426.
184. Krieger,J., Sleep apneas. Rev Med Interne, 1994, 15: 460-470.
185. Pressman,M.R., et.al., Nocturia: A rarely recognized symptom of sleep apnea and other occult sleep disorders.
Arch Intern Med, 1996, 156: 545-550.
186. Hudgel,D.W., Neuropsychiatric manifestations of obstructive sleep apnea: a review.
Int J Psycjiatry Med, 1989, 19: 11-22.
187. Yesavage,J., et.al., Preliminary communication: intellectual deficit and sleep-related respiratory disturbance in the elderly.
Sleep, 1985, 8: 30-33.
188. Kaluza,C.L., et.al., Obstructive sleep apnea: a multisystemic disorder.
J Am Osteopath Assoc, 1995, 95: 420-426.
189. Guilleminault,C., Obstructive sleep apnea syndrome: a review.
Psychiatr Clin North Am,1987, 10: 607-621.
190. Hoch,C.C., et.al., Electroencephalographic sleep in late-life neuropsychiatric disorders.
Int Psychogeriatr, 1989, 1: 51-62.
191. Erkinjuntti,T., et.al., Sleep apnea in multiinfarct dementia and alzheimer's disease.
Sleep, 1987, 10: 419-425.
192. Hoch,C.C., et.al., Sleep-disordered breathing in normal and pathologic aging.
J Clin Psychiatry, 1986, 47: 499-503.
193. Erkinjuntti,T., et.al., Snoring and dementia. Age Ageing, 1987, 16: 305-310.
194. Keenan,P.A., et.al., The effect on memory of chronic prednisone treatment in patients with systemic disease.
Neurology, 1996, 47: 13896-1402.
195. Varney,N.R., et.al., Reversible steroid dementia in patients without steroid psychosis.
Am J Psychiatry, 1984, 141: 369-372.
196. Aisen,P.S., et.al., A randomized controlled trial of prednisone in alzheimer's disease.
Neurology, 2000, 54: 588-593.
197. Chynoweth,R., et.al., Pre-senile dementia responding to steroid therapy.
Brit J Psychiatry, 1969, 115: 703-708.
198. Paulson,G.W., Steroid-sensitive dementia. Am J Psychiatry, 1983, 140: 1031-1033.
199. Griffin,R.L., et.al., An overview of therapeutic touch and its application to patients with alzheimer's disease.
Am J Alzheimer Dis, July-August,1998, 211-215.
200. Gold,M., et.al., Plasma thiamine deficiency asscoiated with alzheimer's disease but not Parkinson's disease.
Metab Brain Dis, 1998, 13: 43-53.
201. Watkins,S.E., et.al., Plasma amino acids in patients with senile dementia and in subjects with Down's syndrome at an age
vulnerable to alzheimer changes. J Ment Defic Res, 1989, 33: 159-166.
202. Blass,J.P., et.al., Thiamine and alzheimer's disease. Arch Neurol, 1988, 45: 833-835.
203. Meador,K., et.al., Preliminary findings of high-dose thiamine in dementia of alzheimer's type.
J Geriatr Psychiatry Neurol, 1993, 6: 222-229.
204. Nolan,K.A., et.al., A trial of thiamine in alzheimer's disease.
Arch Neurol, 1991, 48: 81-83.
205. Sandyk,R., Alzheimer's disease: improvement of visual memory and visuoconstructive performance by treatment with picotesla range magnetic fields.
Int J Neurosci, 1994, 76: 183-225.
206. Sherder,E.J., et.al., Effects of transcutaneous electrical nerve stimulation on memoryand behavior in alzheimer's disease may be
stage-dependent. Biol Psychiatry, 1999, 45: 743-749.
207. Sherder,E.J., et.al., Peripheral nerve stimulation in alzheimer's disease.
Tijdschr Gerontol Geriatr, 1997, 28: 59-68.
208. Lebert,F., et.al., Behavioral effects of trazodone in alzheimer's disease.
J Clin Psychiatry, 1994, 55: 536-538.
209. Sultzer,D.L., et.al., A double-blind comparison of trazodone and haloperidol for treatment of agitation in patients with dementia.
Am J Geriatr Psychiatry, 1997,5: 60-69.
210. Walsh,A.C., Arterial insufficiency of the brain: progression prevented by long-term anticoagulant
therapy in eleven patients. J Am Geriatr Soc, 1969, 17: 93-104.
211. Walsh,A.C., et.al., Senile and presenile dementia: further observations on the benefits of a
dicumarol-psychotherapy regimen. J Am Geriatr Soc, 1972, 20: 127-131.
212. Walsh,A.C., Anticoagulant therapy for dementia: informed consent.
J Neuropsychiatry Clin Neurosci, 1992, 4: 463.
213. Walsh,A.C., Anticoagulant therapy for dementia. J Neuropsychiatry Clin Neurosci, 1995,7: 119.
214. Ratner,J., et.al.,Anticoagulant therapy for senile dementia. 1972, 20: 556-559.
215. Langtry,H.D., et.al., Zolpidem. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic
potential. Drugs, 1990, 40: 291-313.
216. Scharf,M.B., et.al., Dose response effects of zolpidem in normal geriatric subjects.
J Clin Psychiatry, 1991, 52: 77-83.
217. Jackson,C.W., et.al., Zolpidem for the treatment of agitation in elderly demented patients.
J Clin Psychiatry,1996, 57: 372.
218. Shelton,P.S., et.al., Zolpidem for dementia-related insomnia and nightime wandering.
Ann Pharmacother, 1997,31: 319-322.
219. Hoehns,J.D., et.al., Zolpidem: a nonbenzodiazepine hypnotic for treatment of insomnia.
Clin Pharm, 1993, 12: 814-828.
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