4.5 Article

Immunolocalization of Tom1 in relation to protein degradation systems in Alzheimer's disease

Journal

JOURNAL OF THE NEUROLOGICAL SCIENCES
Volume 365, Issue -, Pages 101-107

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.jns.2016.03.035

Keywords

Tom1 (target of Myb1); Tollip; Myosin IV; Ubiquitin; Autophagy; Alzheimer's disease; Dystrophic neurites; Perisomatic granules

Funding

  1. Health and Labor Sciences Research Grant for Research on Intractable Diseases from the Ministry of Health, Labor and Welfare of Japan
  2. Ministry of Education, Culture, Sports, Science and Technology, Japan [126461304, 6K09665]
  3. Research Committee for Ataxic Disease, Ministry of Health, Labour and Welfare, Japan
  4. Grants-in-Aid for Scientific Research [26461264, 26461304] Funding Source: KAKEN

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Alzheimer's disease (AD) is an age-related neurodegenerative disorder. Its pathological hallmarks are senile plaques (SPs), which contain extracellular deposits of amyloid beta (A beta) protein fibrils and dystrophic neurites (DNs), and neurofibrillary tangles (NFTs) containing hyperphosphorylated tau. Impairment of protein degradation systems, including the ubiquitin-proteasome and the autophagy-lysosome systems, has been proposed as one of the causes of the accumulation of these aberrant proteins in AD brains. Tom1 (target of Myb1) was originally identified by the induction of its expression by the v-Myb oncogene and is a part of two major protein-degradation systems. The present study was conducted by immunohistochemical and immunofluorescent stainings to show that Tom1 was localized in DNs, perisomatic granules (PSGs), and NFTs in AD brains. Moreover, in DNs, Tom1 colocalized with ubiquitin, lysosomal proteins, and Tom1-related proteins (Tollip and myosin VI), which act in both protein-degradation systems via Tom1. These results indicate that Tom1 plays important roles in protein-degradation systems in AD pathogenesis. (C) 2016 Elsevier B.V. All rights reserved.

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