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Co‐localization of β‐peptide and phosphorylated tau in astrocytes in a patient with corticobasal degeneration
Author(s) -
Wakabayashi Koichi,
Mori Fumiaki,
Hasegawa Masato,
Kusumi Tomomi,
Yoshimura Ihoko,
Takahashi Hitoshi,
Kaneko Sunao
Publication year - 2006
Publication title -
neuropathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 61
eISSN - 1440-1789
pISSN - 0919-6544
DOI - 10.1111/j.1440-1789.2006.00635.x
Subject(s) - corticobasal degeneration , subiculum , entorhinal cortex , senile plaques , pathology , gliosis , neuroscience , cerebral cortex , cytoplasm , cortex (anatomy) , tau protein , tauopathy , chemistry , biology , atrophy , hippocampus , microbiology and biotechnology , alzheimer's disease , medicine , neurodegeneration , progressive supranuclear palsy , dentate gyrus , disease
The co‐localization of amyloid β (Aβ) and phosphorylated tau in astrocytes in a patient with corticobasal degeneration is described. At autopsy, the present case exhibited neuropathological findings compatible with those of corticobasal degeneration, including atrophy of the frontal and temporal lobes, neuronal loss and gliosis in the cortical and subcortical regions, and presence of cortical ballooned neurons and astrocytic plaques. Moreover, many senile plaques were found in the cerebral cortex. There were also clusters of Aβ‐positive granules associated with astrocytic cytoplasm and processes in the subiculum and entorhinal cortex. In the entorhinal cortex, the Aβ‐positive granules were occasionally co‐localized with phosphorylated tau‐positive fibrillary structures in the astrocytic cytoplasm. To our knowledge, this is the first demonstration of co‐localization of Aβ and phosphorylated tau in astrocytes. This phenomenon implies that phagocytosis of Aβ coincides with production of phosphorylated tau in the same reactive astrocytes.