Alzheimer’s disease: reality or an artificial construction?
Another significant element is that the brain of people considered as normal on a cognitive level conceals neuropathological signs perceived as characteristic of dementia. “The older people become, the more their brain is affected by such signs”, Martial Van der Linden explains. “Beyond 85 years old, there is about the same number of amyloid plaques in the brain of dementia sufferers as in the brain of people who aren’t.” In addition, Swedish researchers have shown that the areas of the brain affected by so-called normal aging are the same as those affected in the case of dementia. Assuming the complex nature of cerebral agingFurthermore, Martial Van der Linden points out that the brain of the large majority of people diagnosed with Alzheimer's disease shows signs of suffering from various types of vascular injuries. Therefore, some authors suggest that amyloid cascade or the phosphorylation of tau protein (neurofibrillary tangles) aren’t causal factors of Alzheimer’s disease, but an adaptive mechanism or a protective response of the brain to injuries that various mechanisms would have generated. “Consequently, we should beware of seeking to eliminate amyloid plaques or neurofibrillary tangles, as it may potentially accelerate the neurodegenerative process”, underlines Martial Van der Linden. Even if clinical trials have begun, such drugs with a curative vocation (or just with a deleterious effect…) aren’t available in clinical practice, because research fails to make progress. Opponents to the biomedical approach to cerebral and cognitive aging would exclaim that it is completely logical. As for symptomatic drugs – cholinesterase inhibitors and memantine -, they have no real efficacy as regards autonomy and quality of life in people diagnosed with Alzheimer’s and they don’t improve the cognitive functioning of individuals diagnosed with Mild Cognitive Impairment. (3) Buchman, A.S. et al. (2012). Total daily physical activity and the risk of AD and cognitive decline in older adults. Neurology, 78, 1323-1329. |
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