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Causes

The brain deficit of the elderly or the old is not so much dependent on the continued loss of brain cells (neurons) or the reduced blood supply as the decrease or lack of neurotransmitters: that is, those chemicals that neurons use at the synapses to exchange messages.
According to a rather accredited theory, in the brain of the Alzheimer patient there is a reduced production of acetylcholine, which is one of the molecules without which the signal is not transmitted. We also understood the great importance of two enzymes: one is that which synthesizes acetylcholine (it is called choline acetyltransferase and appears to be deficient in the brains of patients suffering from Alzheimer's disease), the other is that which destroys it (cholinesterase) . As will be seen later about the possibilities of treating dementia, some remedies proposed against Alzheimer's disease aim precisely at inhibition - that is to block - of cholinesterase.
Another hypothesis on the causes of the disease concerns the lack of the so-called "nerve growth factor" (the acronym NGF comes from the English Nerve Growth Factor), discovered by Rita Levi Montalcini. As NGF stimulates the formation of new synapses, if the brain does not produce enough of it, no new connections are formed between the neurons and this leads to an inevitable mental deterioration.
Furthermore: in recent years, experimental data have revealed in the patients with Alzheimer's disease the existence of particular "biochemical" cellular alterations. Such as the increase in the concentration of calcium inside the brain cell; this, favoring the production of free radicals (and therefore an oxidative stress), eventually causes membrane lesions and cell death.
It is still unclear why brain cells are preserved intact in people who age well, while they degenerate and die in those suffering from Alzheimer's disease. Studies conducted on brains of more than one hundred have actually confirmed the presence of well-developed neurons. Also in laboratory animals (rats) a correlation between intellectual activity and resistance of neurons to aging has been observed: by comparing the performance of two groups of rats, of which only one was stimulated with games and forced to exercise, it was since the brains of the strained animals contained 25% more synapses than rats kept in an "inert" environment. Active brain cells, those that release neurotransmitters, stimulate the production of neurotrophic factors such as NGF, ie proteins that facilitate the formation of synapses and their resistance to aging.
Physical activity also seems to increase the concentration of neurotrophic factors in the brain. Therefore, if adequate social and intellectual stimulation can delay the appearance of cognitive defects typical of dementia, a life poor in social contacts can instead accelerate the onset of such symptoms.
A recent Swedish study showed that living alone, and feeling more isolated, would greatly increase the risk of developing Alzheimer's dementia in people over 75. A figure of some importance, if we consider that after 70 years the frequency of the disease doubles every 5 years. The risk would also increase among those who are not satisfied with the daily exchanges with their children. The disease would affect less among those who maintain social, cultural and creative activities of various kinds.
(source: Pharmacy thirty-three)
 

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