Alzheimer Anatomical Pathology

The brain of the patient with Alzheimer's disease has two types of injuries:

The senile plaques (or amyloid plaques)

This is extracellular lesions of Alzheimer's disease. These plates are the accumulation of peptide and abnormal nerve of 42 amino acids, peptide Aβ42, the most amyloidogenic amyloïde.Ce beta-peptide, normally of 40 amino acids, comes from a bad cleavage of the protein APP (amyloid protein precursor). This would participate in the massive entry of calcium into the neuron and activate microglia (inflammation), resulting in the inevitable death of the neuron by necrosis or apoptosis. These plates are mainly located in the neocortex and the hippocampus.

The neurofibrillary degeneration

These cell injury secondary to the accumulation of tau protein (protein association with microtubules that are part of the cytoskeleton) hyperphosphorylée responsible for the formation of filaments matched. When the tau protein is hyperphosphorylée it will comply with a pair of helical filaments, and then aggregate to form fibrillary neurodegeneration. The substances needed for the proper functioning of the neuron can no longer be sent to cell body and the neuron will die.

The cortical atrophy

In patients with Alzheimer's disease, the brain can lose 8 to 10% of its weight every ten years, while in healthy subjects this loss is only 2%. The cortical atrophy accompanied by an expansion of brain ventricles and cortical paths and a neuronal loss particularly affecting the cholinergic system (basal nucleus of Meynert, septum, entorhinal cortex, amygdala and hippocampus).