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Voir également : La maladie d'Alzheimer (Diagnostic, Bilan, Traitement)
Voir également : Prévention de la maladie d'Alzheimer


Researchers at the Johns Hopkins Alzheimer's Disease Research Center tested 210 people with the disease over time to see how rapidly they lost cognitive ability. Some showed rapid mental deterioration, while others declined more slowly. Then the researchers reviewed everyone's medical records to see who had been taking NSAIDs. They found that as NSAID use increased, the rate of mental deterioration decreased.(Rich, J.B., et al. "Nonsteroidal Anti-Inflammatory Drugs in Alzheimer's Disease," Neurology (1995) 45:51)

Finally, as part of the 38-year Baltimore Longitudinal Study of Aging, researchers from the National Institute on Aging assessed NSAID use in 1,828 elderly people, 110 of whom developed Alzheimer's from 1980 to 1995. Every two years, all subjects filled out extensive food and drug surveys, and were given a battery of cognition and memory tests. People who took NSAIDs more than occasionally for at least two years were 30% to 60% less likely to develop Alzheimer's disease. As duration of NSAID use increased, Alzheimer's risk decreased. All NSAIDs other than aspirin significantly reduced risk. Aspirin did not reach statistical significance, but there was a trend toward lower risk with increased duration of more-than-occasional aspirin use (Stephenson, J. "More Evidence Links NSAIDs, Estrogen with Reduced Alzheimer's Risk," Journal of the American Medical Association (May 8, 1996) 275:1389)


Antioxidants: Nutrients That Can Slow Alzheimer's
People need oxygen to live, but oxygen also has a downside. In the body, some oxygen molecules become so highly chemically reactive that they disrupt other body processes. These troublemaker molecules are called free radicals, and many scientists believe that the damage they inflict (oxidative damage) is at the root of both cancer and heart disease. (Smoking and a high-fat diet greatly increase the number of free radicals in the blood.)

Free radicals also contribute to the development of Alzheimer's disease. The destructive action of free radicals fits neatly with two other risk factors for Alzheimer's: one form of the gene for apolipoprotein E (APOE) and beta-amyloid. The APOE gene controls synthesis of apolipoprotein, which transports cholesterol in the blood. People with two copies of the APOE4 variety of this gene have higher concentrations of low-density lipoprotein (LDL, so-called "bad cholesterol" because it increases risk of heart attack). High LDL levels have also been linked to Alzheimer's risk.

In addition, high LDL levels also seem to favor deposition of beta-amyloid, the major component of the senile plaques characteristic of Alzheimer's. Beta-amyloid appears to react with the cells that line blood vessels in the brain to produce excessive quantities of free radicals, which damage brain tissue even more. Brain tissue is highly susceptible to free radical damage because, unlike many other tissues, it does not contain significant amounts of protective antioxidant compounds. [1] Fortunately, certain nutrients -- antioxidants -- can prevent the oxidative damage free radicals cause. Antioxidant nutrients include:
  • Vitamin A
  • Vitamin C
  • Vitamin E
  • The mineral selenium
  • The carotenoids, among them beta-carotene
  • These nutrients are abundant in plant foods, and many studies show that as fruit and vegetable consumption increases, risk of cancer decreases. A few studies have investigated the effects of antioxidants on Alzheimer's disease. Results to date have been intriguing:
    Czech researchers gave the antioxidant drug selegiline to 173 people with mild to moderate Alzheimer's disease. After six months, their memory improved significantly.
    In another study, selegiline enhanced the benefits of tacrine (Cognex), one of the two drugs currently approved for Alzheimer's treatment. [2]

  • 1 Lancet, 349:1189, 4-26-97
  • 2 Kawas, C., et al. "Treating Alzheimer's Disease: Today and Tomorow," Patient Care (Nov. 15, 1996) pp. 62-83


    In a 1996 study, German researchers recruited 156 people with either Alzheimer's disease or multi-infarct dementia, and gave half of them a placebo, and half a standardized ginkgo extract (120 mg twice a day). After 24 weeks, compared with the placebo group, those taking ginkgo showed significant improvement in cognitive function, as measured by a variety of standardized tests. About 6% of the ginkgo users reported minor side effects: allergic skin reactions, headache, and stomach upset. [2]

    In a report released in 1994, Commission E, the German equivalent of the Food and Drug Administration, endorsed ginkgo for early-stage dementias.


    Compared with men, women are at greater risk of developing Alzheimer's disease. But recent studies show that they also have a treatment option unavailable to most men -- the female sex hormone estrogen, which helps prevent, delay, and treat Alzheimer's disease.

    Several studies show that women who take estrogen after menopause have an unexpectedly low incidence of Alzheimer's disease. Among women with Alzheimer's, those taking estrogen suffer less severe symptoms and slower mental deterioration. In addition, animal studies show that estrogen improves blood circulation through the brain, and stimulates nerve cell growth in areas of the brain affected by Alzheimer's.

    These findings are summarized in a report published in the July 1996 Journal of the American Geriatric Society by Stanley Birge, M.D., a geriatrician at the Washington University School of Medicine in St. Louis. Birge calls these estrogen findings "terribly exciting" and potentially "among the most promising recent discoveries about treating Alzheimer's."

    Estrogen boosts the production of acetylcholine, a key chemical (neurotransmitter) involved in the transmission of nerve impulses across the tiny gaps between nerve cells (synapses). Estrogen also impedes the deposition of beta-amyloid, the protein involved in the characteristic plaques of Alzheimer's disease. In addition, estrogen improves blood flow through the brain, and enhances verbal abilities of postmenopausal women who take hormone replacement therapy. Estrogen also helps maintain the integrity of the hippocampus, a structure in the brain involved in memory. [1]

    Several lines of evidence show that estrogen helps prevent and treat Alzheimer's disease:
  • Several epidemiological studies show that taking estrogen reduces women's risk of Alzheimer's disease. [2] Notably, New York City researchers investigated Alzheimer's risk among 1,124 elderly women. During the follow-up period, the disease developed in 14.9% of them. Among women who had never used estrogen, the figure was 16.3%, while only 5.8% of estrogen users developed Alzheimer's. Among estrogen users, risk decreased with hormone use longer than one year. [3]
  • In a 30-week study of 318 women with mild to moderate Alzheimer's disease, all participants took Cognex (tacrine), one of only two drugs currently approved to treat the disease, and some also took estrogen replacement therapy. Compared with those on tacrine only, the women taking tacrine plus estrogen fared better on a number of cognitive measures. [4]
  • In an eight-week study of 12 Tacoma, Washington, women with mild to moderate Alzheimer's, all the women received skin patches -- half that released estrogen into the blood, and half that contained a placebo. "The estrogen had a rapid effect," said Sanjay Asthana, M.D., who presented the results at a meeting of the Society for Neuroscience. "Within a week, the women on estrogen showed improvement." By the end of the study, the estrogen users' cognitive test scores had almost doubled. The more estrogen the women absorbed, the greater their mental improvement. [5]
  • Finally, as part of the 38-year Baltimore Longitudinal Study of Aging, researchers from the National Institute on Aging assessed 16 year's worth of medical records for 514 postmenopausal women. They found that compared with women who had never taken estrogen, those who had were 54% less likely to develop Alzheimer's disease. [6]
  • In addition to helping prevent and treat Alzheimer's disease, a great deal of research shows that the sex hormone also helps prevent heart disease, women's leading cause of death, and osteoporosis, bone-thinning that can lead to serious fractures.
    "But for all its benefits, estrogen also carries some risks. It may increase breast cancer slightly, although studies remain inconclusive. Estrogen is known to increase uterine cancer risk if a woman takes it without another sex hormone, progesterone. [7]"

  • 1 Kawas, C., et al. "Treating Alzheimer's Disease: Today and Tomorrow," Patient Care Nov. 15, 1996, 62-83
  • 2 Paganini-Hill, A., et al. " Estrogen Deficiency and Risk of Alzheimer's Disease," American Journal of Epidemiology (1994) 140:256
  • 3 Tang, M.X., et al. "Effect of Estrogen During Menopause on Risk and Age at Onset of Alzheimer's Disease," Lancet (1996) 348:429
  • 4 Schneider, L.S., et al. "Effects of Estrogen Replacement Therapy on Response to Tacrine in Patients with Alzheimer's Disease," Neurology (1996) 46:1580
  • 5 The New York Times, Nov. 21, 1996 6 Stephenson, J. "More Evidence Links NSAID, Estrogen Use with Reduced Alzheimer's Risk," Journal of the American Medical Association (May 8, 1996) 275:1389
  • 7 Bush, T. et al. "Hormone Replacement Therapy and Risk of Breast Cancer," Journal of the American Medical Association (June 9, 1999) 281:2140


    Ampakines are a new class of drugs that improve memory. According to researcher Gary Lynch of the University of California-Irvine, who has studied ampakines since 1991, they increase activity in the brain's cortex.

    Lynch and Gary Rogers, head of drug development at Cortex Pharmaceuticals in Southern California, have developed an ampakine drug, Ampalex, that increases levels of a specific neurotransmitter in the brain, AMPA-glutamate. In a recent 16-day animal study, animals not taking Ampalex scored 50% on a variety of memory tests, while those taking the drug scored 85%.

    In humans, Ampalex has been tested in Germany and Sweden on 54 people, age 21 to 73, with normal brain function. Compared with those not taking the drug, those using Amaplex scored twice as well on short-term memory tests.

    Calcium-channel blockers

    As nerve cells die, they lose the ability to regulate the flow of calcium across their cell membranes. Some researchers speculate that calcium channel blockers -- drugs that affect this mineral's flow in and out of cells -- may prolong nerve cell life.

    Nerve growth factor

    This hormone stimulates the growth of the nerve cells that release acetylcholine, the neurotransmitter that declines in people with Alzheimer's disease. Some researchers believe that by introducing nerve growth factor or a similar compound into the brains of people with early Alzheimer's, they may be able to slow or reverse cognitive deterioration. Unfortunately, nerve growth factor does not cross the blood-brain barrier, so the hormone cannot be given orally or by injection.


    Ce feuillet vous est offert à titre d'information seulement. La Société Alzheimer ne souscritpas nécessairement à l'utilisation de la Propentofylline.
    Qu'est-ce que la propentofylline ?
    La Propentofylline (HWA 285) est un médicament en processus de fabrication par Hoechst Marion Roussel Canada Inc. Ce médicament est présentement mis à l'essai dans le traitement des symptômes de la maladie d'Alzheimer et la démence vasculaire.

    De quelle façon ce produit aidera-t-il au traitement de la maladie d'Alzheimer ?
    La maladie d'Alzheimer est causée par un dommage progressif et sélectif aux cellules du cerveau, menant éventuellement à la mort des cellules nerveuses. On croit que la propentofylline peut diminuer certains des processus qui causent la mort des cellules et améliorer le fonctionnement des cellules nerveuses dans le cerveau des personnes atteintes de la maladie d'Alzheimer.

    De quelle façon ce produit aidera-t-il au traitement de la démence vasculaire ?
    La démence vasculaire est le résultat de multiples accidents vasculaires cérébraux, légers ou aigüs, qui peuvent être causés par une variété de conditions. Ces accidents compromettent le flot sanguin au cerveau. Il est possible que les individus subissent des «minis-accidents» ce qui peut causer la détérioration des cellules nerveuses. On croit que la propentofylline améliore le flot sanguin et le métabolisme énergétique dans le cerveau ce qui pourrait interrompre certains des facteurs qui causent la détérioration des cellules du cerveau. On espère que la propentofylline améliorera le fonctionnement des cellules nerveuses du cerveau des personnes atteintes de démence vasculaire.

    Y-a-t-il des effets secondaires connus ?
    Dans le cas de la propentofylline, les effets secondaires les plus fréquents sont des maux de tête, des étourdissements, des nausées, la perte d'appétit et des rougeurs.

    À quelle échelle ces essais cliniques sont-ils tentés ?
    Au Canada, 463 individus atteints de la maladie d'Alzheimer et/ou de démence vasculaire ont été recrutés pour une étude de 12 mois. Le recrutement pour cette étude est terminé.

    En quoi consiste les essais cliniques ?
    Cette étude durera 12 mois et tous les participants recevront de la propentofylline. Les patients et leurs aidants doivent revoir le médecin de l’étude tous les trois mois durant l’année.
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