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ALZEIMER'S
General Description
Alzheimers
disease is a progressive neurodegenerative disorder which primarily affects
brain structures involved in memory processes and motor skills. Alzheimers
disease is the most common form of dementia, which generally refers to a
progressive decline 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 plaques composed of granular or filamentous
masses, found predominately in the nerve cells of the 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 memory impairment and 4) clear consciousness despite memory
impairment.
Causes
The
exact cause of Alzheimers 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 Alzheimers. However, clinical evidence for this link is inconclusive.3
Oxidative stress may play a role in the pathogenesis of neuron degeneration
and death in Alzheimers 4,5 An increase in free radical production has been
demonstrated in Alzheimers disease brain tissue.
In particular, iron has been shown to be a significant component of senile
plaques in Alzheimers disease6 and may contribute to the disease process
by initiating lipid peroxidation, leading to membrane damage and ultimately
cell death.7
At Risk
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 prevalence of dementia is roughly 3% for individuals aged 65 to 74,
whereas it is 18.7% for individuals between the ages of 75 and 84 and nearly
50% for those over age 85. In addition, there is evidence to suggest that
genetic factors may play a part in some forms 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 about 5 to 10 years after diagnosis.
Prevention and Management
Nutrition influences:
Nutritional
support is important in the treatment of Alzheimers.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 Alzheimers and low serum cobalamin (vitamin
B12) levels.9
Deficiency of choline, an important component of membrane phospholipids
and the neurotransmitter acetylcholine, may play a role in the etiology
of Alzheimers10
Healthier Lifestyles Product Recommendations
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 Alzheimers disease. Nutr Rev 1997 55(Part 1):
23-5.
3 Armstrong, RA, Winsper, SJ, Blair, JA. Aluminium and Alzheimers disease:
review of possible pathogenic mechanisms. Dementia 1996 7(1): 1-9.
4 Markesbery, WR. Oxidative stress hypothesis in Alzheimers disease. Free
Radic Biol Med 1997 23(1):134-47.
5 Butterfield, DA. Beta-amyloid-associated free radical oxidative stress
and neurotoxicity: implications for Alzheimers disease. Chem Res Toxicol
1997 10(5): 495-506.
6 Connor JR. Proteins of iron regulation in the brain in Alzheimers disease.
In Lauffer RB (ed)m Iron and human 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 Med 1997 336(17):1216-22
9 McCaddon A, Regland B, Fear CF. Trypsin inhibition: a potential cause
of cobalamin deficiency common to the pathogenesis of Alzheimer-type dementiaand
AIDS dementia complex? Med Hypotheses 1995 45(2): 200-4.
10 Canty DJ, Zeisel SH. Lecithin and choline in human health and disease.
Nutr Rev 1994 52(10): 327-39.
Information provided by Usana Health Sciences (www.usana.com)