Degenerative terminals of the perforant pathway are human alpha-synuclein-immunoreactive in the hippocampus of patients with diffuse Lewy body disease.
We investigated the hippocampal pathology in diffuse Lewy body disease (DLBD) using alpha-synuclein immunohistochemistry. Ubiquitin-positive intrahippocampal structures caused by the degeneration of terminal axons of the perforant pathway were observed to be alpha-synuclein immunoreactive. These alpha-synuclein-positive degenerative terminals contained granulo-filamentous or vesiculo-tubular components similar to those of Lewy bodies (LB) immunoelectron microscopically, suggesting that alpha-synuclein may abnormally aggregate into filamentous or membranous cytoskeletal components including neurofilaments and synaptic vesicles in DLBD. A 'dying back' degenerating process due to a blockage of axonal transport may explain why the degenerative terminals and LB share similar alpha-synuclein-positive components, but the origin cells of the perforant pathway contain only a few LB.
Iseki
E
E
Department of Psychiatry, Yokohama City University School of Medicine, Yokohama, Japan.
Marui
W
W
Kosaka
K
K
Akiyama
H
H
Ueda
K
K
Iwatsubo
T
T
D000368:Aged; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D006801:Humans; D007150:Immunohistochemistry; D016631:Lewy Bodies / Q000648:ultrastructure; D016253:Microscopy, Immunoelectron; D008875:Middle Aged; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D010300:Parkinson Disease / Q000473:pathology*; D019580:Perforant Pathway / Q000473:pathology*; D010750:Phosphoproteins / Q000378:metabolism; D017729:Presynaptic Terminals / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D051843:Synucleins; D013702:Temporal Lobe / Q000473:pathology; D014452:Ubiquitins / Q000378:metabolism; D051844:alpha-Synuclein
D009419:Nerve Tissue Proteins; D010750:Phosphoproteins; C497604:SNCA protein, human; D051843:Synucleins; D014452:Ubiquitins; D051844:alpha-Synuclein