Alzheimer Disease

and apparented disorders
Alzheimer disease is a common disease (nearly one million patients in France) that impairs cognition.

The cognitive deficit is related to lesions which can be seen at microscopical examination.Two types of lesions have been identified: those that are related to the deposit of Aβ peptide in the extracellular space and those that are constituted by the accumulation of tau protein in neurons. Both Aβ peptide and tau protein are normally produced in the brain. Why they become insoluble and accumulate is not known. The Aβ peptide is part of a larger protein which crosses the cell membrane (the amyloid precursor protein or APP). Tau protein interact with microtubules that are part of the "skeleton" of the cell. The two types of lesions are linked but in a way that remains badly understood. For more information, you may look at the video (in French): "Mécanismes et secrets de la maladie d'Alzheimer : le cerveau à la loupe".

Fondation Vaincre Alzheimer logo

Senile plaque

In the senile plaque, the core, made of an Aβ deposit (shown here in brown), is surrounded by neurites, containing tau protein

Neurofibrillary tangle

Tau protein may accumulate in the cell body of the neuron where it constitutes a "neurofibrillary tangle" (here in green). It may also accumulate in axons that surround the core of the senile plaque, or in dendrites (the "neuropil threads").

The lesions progress in a stereotyped way in the brain: tau protein accumulation is initially found in the hippocampus (a brain area that is essential to the acquisition of new memories). It secondarily affects cortical regions that are involved in langage, voluntary movements, visual recognition, etc... Aβ peptide, by contrast, deposits first in these cortical regions, before involving the hippocampus and subcortical nuclei.