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[Vol.38 No.2 contents]
Japanese/English
Full Text of this Articlein Japanese PDF (1533K) |
| ArticleTitle | Neuropathology of FTLD |
| Language | J |
| AuthorList | Ryohei Watanabe1)2), Tetsuaki Arai2) |
| Affiliation |
1)Department of Psychiatry, Tokyo Medical University Ibaraki Medical Center 2)Department of Psychiatry, University of Tsukuba |
| Publication | Japanese Journal of Neuropsychology: 38 (2), 96-108, 2022 |
| Received | |
| Accepted | |
| Abstract | Ataxin-2 (ATXN2) has recently been highlighted as a disease modifier of TDP-43 proteinopathy, but its characteristics in human brain tissue remain largely unknown. We analyzed the detailed cytoplasmic localization and expression levels of ATXN2 in brain samples from controls and frontotemporal lobar degeneration with TDP-43 (FTLD-TDP) cases. ATXN2 localized mainly to ribosomes in the neuronal cytoplasm, indicating a function in the translation process. In patient brains, ATXN2 expression was significantly lower than in controls, and ATXN2 also colocalized with phosphorylated TDP-43-positive inclusion bodies. These results suggest that ATXN2 may be involved in the pathological process of FTLD-TDP. |
| Keywords | frontotemporal dementia, frontotemporal lobar degeneration, RNA-binding protein, TDP-43, ataxin-2 |
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