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Aging 

Alzheimer's disease is a slow degenerating process, that takes several decades to develop.

Therefore, aging is the window that reveals Alzheimer's disease, but this is not the cause (see Exp Gerontol), stricto sensus,  of the disease.

Normal aging

Pathway of neurofibrillary degeneration visualized by the presence of pathological tau proteins in the different brain areas. This degenerating process starts int the transentorhinal cortex, then the entorhinal cortex, followed by the hippocampus. At the biochemical level,this process is systematically observed in non-demented and demented patients aged over 75 years. This tau pathology is linked to aging. It shows the vulnerability of the hippocampal area to a tau pathology. But tau pathology is no directly expressed as a function of aging, demonstrating that it is a pathology that appears lately, but not resulting from aging.In the following figures, it is shown that this process can be amplified by amyloid or APP dysfunction, to produce Alzheimer's disease.

ALZHEIMER: INFRACLINICAL

Alzheimer pathology starts by a dysfunction of APP, either as a loss of function, or a gain of toxic function, through the production of amyloid. Dysfunction of APP is likely an ubiquitous event, since this protein is in all cells of all living animals.This dysfunction is represened as "APP*", meaning that we do not choose if it is due to APP, APP carboxyterminal fragments or Abeta.APP* weighs first on the most fragile brain area, which is always the entorhinal and hippocampal formations, that are always affected in old age.APP* will intensify tau pathology of these regions, that in turn will provoke an extension of tau pathology in other brain areas, like a chian reaction.

ALZHEIMER'S DISEASE

There is a dynamic of the spreading of tau pathology, which depends on numerous factors. Some of them are risk factors, that accelerate the disease; others are neuroprotectants.

.Cofactors, risk factors

16/02/05
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