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Cognitive decline may be an inevitable accompaniment of the aging process, although it is minimal on average until individuals reach the eighth decade. [1] However, for a proportion of older people, cognitive decline is accelerated as a result of exposure to toxins such as alcohol, head injury, and dementing processes, especially Alzheimer's Disease (AD). As the aged population increases, particularly in the developed world, there has been a growing interest in research on possible risk factors for accelerated cognitive decline.
In 1986, Calne et al. [2] advanced the hypothesis that AD, Parkinson's disease (PD), and motor neurone disease are due to environmental damage to specific regions of the CNS. This damage remains subclinical for several decades but makes those affected especially prone to the consequences of age-related neuronal attrition. They based the hypothesis on the association found between environmental factors and certain neurodegenerative diseases, for example, methylphenyltetra-hydropyridine and PD, polio virus infection and postpoliomyelitis syndrome, chickling pea ingestion and lathyrism, dietary factors and amyotrophic lateral sclerosis-PD complex of Guam, and boxing and the punch drunk syndrome (dementia pugilistica). In each case, there is a long latency period between exposure to the environmental factor and development of a disorder.
Calne et al. [2] postulated that although the nervous system has a capacity for compensation, this capacity is finite. Neurons lost while an individual is young may go unnoticed when compensation is possible, but advancing age-related neuronal loss is likely to accentuate this earlier cerebral insult. Broe, [3] however, argued that it is unlikely that progressive loss of specific neuronal populations, as in PD, could be attributed to subclinical damage early in life followed by progression due to intrinsic ageing processes.
Abalan [4] and Abalan et al. [5] advanced the hypothesis that malnutrition is a risk factor for AD, either through an …
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