Alzheimer disease
Alzheimer disease
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DOI:
10.1016/b978-0-12-802395-2.00023-7
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发表时间:
2018-01-01
期刊:
影响因子:
2.3
通讯作者:
Duyckaerts, Charles
中科院分区:
文献类型:
--
作者:
Calderon-Garciduenas, Ana Laura;Duyckaerts, Charles
Alzheimer disease neuropathology is characterized by the extracellular accumulation of A beta peptide and intracellular aggregation of hyperphosphorylated tau. With the progression of the disease, macroscopic atrophy affects the entorhinal area and hippocampus, amygdala, and associative regions of the neocortex. The locus coeruleus is depigmented. The deposition of A beta is first made of diffuse deposits. Amyloid focal deposits constitute the core of the senile plaque which also comprises a corona of tau-positive neurites. A beta deposits are found successively in the neocortex, the hippocampus, the striatum, the mesencephalon, and finally the cerebellum together with the pontine nuclei (Thal phases). Tau pathology affects in a stereotyped order some specific nuclei of the brainstem, the entorhinal area, the hippocampus, and the neocortex - first the associative areas and secondarily the primary cortices (Braak stages). Loss of synapses is observed in association with tau and A beta pathology; neuronal loss occurs in the most affected areas. Granulovacuolar degeneration and perisomatic granules are also linked to Alzheimer disease pathology. The physiopathology of Alzheimer disease remains unknown. Familial cases suggest that A beta\ deposition is the initial step, but tau pathology appears early in the course and seems to be better correlated with the symptoms.