Affiliations: [a] Department of Psychiatry and Neurobiology, Kanazawa University Graduate School of Medicine, Kanazawa, Japan | [b] National Sanatorium Hokuriku Hospital, Nobusue, Jouhana-machi, Toyama, Japan | [c] Department of Psychiatry, Takaoka Municipal Hospital, Takaoka, Japan
Correspondence:
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Correspondind author: Department of Psychiatry and Neurobiology, Kanazawa University Graduate School of Medicine, 13-1, Takara-machi, Kanazawa, Ishikawa-ken, 920-8641, Japan. Tel.: +81 76 265 2000; Fax: +81 76 234 4254; E-mail: [email protected].
Abstract: The relationships between astrocytic apoptosis and both senile plaques and neurofibrillary tangles (NFT) in gray matter lesions were examined quantitatively in Alzheimer's disease (AD) brains. Seven cortical regions were examined in seven AD brains by terminal dUTP nick end-labeling and immunolabeling with antibodies to glial fibrillary acidic protein, phosphorylated tau protein (AT180), apoptosis-related proteins (caspase-3, bcl-2, and CD95), and beta amyloid protein. Senile plaques showed the lowest density in the cornu ammonis. The density of apoptotic astrocytes was significantly correlated with the density of uncored and cored senile plaques. Neuronal caspase-3 and CD95 expression levels were too low to allow statistical assessment, but Bcl-2 was expressed strongly in the astrocytes and neurons with and without NFT. The correlation of the density of apoptotic astrocytes with apoptotic neurons and NFT was not statistically significant. The density of Bcl2-positive neurons correlated significantly with those of NFT and cored senile plaques, but Bcl2-positive astrocyte density showed no correlation with density of senile plaques or apoptotic astrocytes. These observations suggest that senile plaques may be a cause of astrocytic apoptosis in the gray matter, and that Bcl-2 protein is associated with NFT formation.
