Inproceedings: an article in a conference proceedings.
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The frontal cortex may be the site of synaptic and cytoskeleton reorganization in Alzheimer's disease
As executive and attention deficits may be linked to damage of the frontal cortex in the evolution of Alzheimer's disease (AD), we studied in frontal area 9 of 4 AD and 4 control patients, the variations in neuropile intensity of several synaptic and cytoskeletal markers and compared them with beta-amyloid deposits (Zeiss KS400 image analysis system). While the distribution of the presynaptic protein synaptophysin, linking to small synaptic vesicles, was unchanged in AD patients, that of alpha-synuclein, another presynaptic protein and component of Lewy bodies, was significantly increased, as well as that of MAP2, a cytoskeletal protein associated to the somatodendritic part of neurons and to spines. GAP43, a growth-associated protein synthesized in neurons and primarily localized to axons, was on the contrary significantly decreased. These results may indicate an increased remodeling activity in dendrites and spines, as well as a decreased axonal activity and/or connectivity in AD frontal cortex. The latter point was further confirmed by a significant decrease in the staining of non-phosphorylated neurofilament protein with the SMI32 antibody, representing normal cells and dendrites. On the contrary, the SMI31 antibody, reacting with a pathologically phosphorylated epitope in axons, was increased in AD. Phosphorylated protein tau, as detected with the AD2 antibody, was increased as well. In 2 severe AD cases, SMI31 and AD2 stained also a small number of neuronal cell bodies, not reactive in control samples and correlating with neurofibrillary tangles labeled by the Gallyas silver impregnation. The amount of beta-amyloid within senile plaques was significantly higher in AD than in controls, and a correlation was found with the density of AD2, alpha-synuclein and MAP2 staining. These data indicate a clear involvement of the frontal cortex in AD, damaged by beta amyloid deposition and abnormal phosphorylation, but suggest also some attempt to synaptic reorganization.
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