Disclaimer: The information provided in this Technical Bulletin is strictly educational. It may not be used to promote USANA productsnor is it intended as medical advice. For diagnosis and treatment of medical disorders, consult your health care professional. When thereare references to third party websites, addresses and/or phone numbers, USANA, Inc. makes no claim, actual or implied, regarding thecontent or validity of the information obtained from these outside sources. This Technical Bulletin may be copied and freely distributedonly if all text remains intact and unchanged. Alzheimer’s General Description
• Alzheimer’s disease is a progressive neurodegenerative disorder which primarily
affects brain structures involved in memory processes and motor skills. Alzheimer’sdisease is the most common form of dementia, which generally refers to a progressivedecline in mental function, memory and acquired intellectual skills. 1
• Pathologically, the brain is reduced in size (atrophy), especially in the frontal occcipital
and temporal regions. Histologically, it is characterized by thickening, conglutination,and distortion of the intracellular neurofibrils (neurofibrillary tangles) and by plaquescomposed of granular or filamentous masses, found predominately in the nerve cells ofthe cerebral cortex, amygdala, and hippocampus. 1
• Major clinical criteria for the clinical diagnosis of probable Alzheimer's include: 1)
deficits in two or more areas of cognition, 2) progressive worsening of memory, 3)absence of other medical or psychological disorders that could account for memoryimpairment and 4) clear consciousness despite memory impairment.
• The exact cause of Alzheimer’s is unknown. The etiology is complex and may involve
several genes and possible environmental factors.2
• Chronic exposure to aluminum has been suggested as a possible causative agent in
Alzheimer’s. However, clinical evidence for this link is inconclusive.3
• Oxidative stress may play a role in the pathogenesis of neuron degeneration and death
in Alzheimer’s 4,5 An increase in free radical production has been demonstrated inAlzheimer’s disease brain tissue.
• In particular, iron has been shown to be a significant component of senile plaques in
Alzheimer’s disease6 and may contribute to the disease process by initiating lipidperoxidation, leading to membrane damage and ultimately cell death.7
• Alzheimer's disease is obviously related to age, - that is, the older you get the more
likely you are to develop Alzheimer's disease or dementia. For instance, the prevalenceof dementia is roughly 3% for individuals aged 65 to 74, whereas it is 18.7% forindividuals between the ages of 75 and 84 and nearly 50% for those over age 85. In
1997, USANA, Inc. All rights reserved. Page 1 of 3
addition, there is evidence to suggest that genetic factors may play a part in someforms of AD.
• Clinical manifestations of mental deterioration, memory loss, confusion, and
disorientation may begin in late mid-life (>45 years old). Death usually results in about5 to 10 years after diagnosis. Prevention and Management
• Nutritional support is important in the treatment of Alzheimer’s.2
• In patients with moderately severe impairment from Alzheimer's disease, treatment
with alpha-tocopherol (vitamin E) or selegiline slows the progression of disease.8
• There is an association between Alzheimer’s and low serum cobalamin (vitamin B12)
• Deficiency of choline, an important component of membrane phospholipids and the
neurotransmitter acetylcholine, may play a role in the etiology of Alzheimer’s10
Abstracts Sano M et al. A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer's disease. N Engl J Med 1997 Apr 24;336(17):1216-22. BACKGROUND: There is evidence that medications or vitamins that increase the levels of brain catecholamines and protect against oxidative damage may reduce the neuronal damage and slow the progression of Alzheimer's disease. METHODS: We conducted a double-blind, placebo-controlled, randomized, multicenter trial in patients with Alzheimer's disease of moderate severity. A total of 341 patients received the selective monoamine oxidase inhibitor selegiline (10 mg a day), alpha-tocopherol (vitamin E, 2000 IU a day), both selegiline and alpha-tocopherol, or placebo for two years. The primary outcome was the time to the occurrence of any of the following: death, institutionalization, loss of the ability to perform basic activities of daily living, or severe dementia (defined as a Clinical Dementia Rating of 3). RESULTS: Despite random assignment, the baseline score on the Mini-Mental State Examination was higher in the placebo group than in the other three groups, and this variable was highly predictive of the primary outcome (P<0.001). In the unadjusted analyses, there was no statistically significant difference in the outcomes among the four groups. In analyses that included the base-line score on the Mini-Mental State Examination as a covariate, there were significant delays in the time to the primary outcome for the patients treated with selegiline (median time, 655 days; P=0.012), alpha-tocopherol (670 days, P=0.001) or combination therapy (585 days, P=0.049), as compared with the placebo group (440 days) CONCLUSIONS: In patients with moderately severe impairment from Alzheimer's disease, treatment with selegiline or alpha-tocopherol slows the progression of disease. References
1 Kandel, ER, Schwartz, JH, Jessel, TM. Principles of Neural Science, 3rd Edition. Elsevier: New York, 1991. 2 Folstein M. Nutrition and Alzheimer’s disease. Nutr Rev 1997 55(Part 1): 23-5. 3 Armstrong, RA, Winsper, SJ, Blair, JA. Aluminium and Alzheimer’s disease: review of possible pathogenic mechanisms. Dementia 1996 7(1): 1-9. 4 Markesbery, WR. Oxidative stress hypothesis in Alzheimer’s disease. Free Radic Biol Med 1997 23(1):134-47. 5 Butterfield, DA. Beta-amyloid-associated free radical oxidative stress and neurotoxicity: implications for Alzheimer’s disease. Chem Res Toxicol 1997 10(5): 495-506.
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6 Connor JR. Proteins of iron regulation in the brain in Alzheimer’s disease. In Lauffer RB (ed)m Iron andhuman disease. CRC Press, Ann Arbor, MI, 1992, pp. 365-393. 7 Halliwell, B. Reactive oxygen species in living systems: source, biochemistry, and role of human disease. Am J Med 91(suppl 3c): 14s-22s. 8 Sano M, Ernesto C, Thomas RG, Klauber MR, et al. A controlled trial of selegiline, alpha-tocopherol,or both as treatment for Alzheimer's disease. The Alzheimer's Disease Cooperative Study. N Engl J Med1997 336(17):1216-229 McCaddon A, Regland B, Fear CF. Trypsin inhibition: a potential cause of cobalamin deficiencycommon to the pathogenesis of Alzheimer-type dementiaand AIDS dementia complex? Med Hypotheses1995 45(2): 200-4. 10 Canty DJ, Zeisel SH. Lecithin and choline in human health and disease. Nutr Rev 1994 52(10): 327-39.
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