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Characterization of the novel protein P9TLDR (temporal lobe down-regulated) with a brain-site-specific gene expression modality in Alzheimer's disease brain

Authors
Yokota, TomokoAkatsu, HiroyasuMiyauchi, TakashiHeese, Klaus
Issue Date
Dec-2012
Publisher
Elsevier B.V.
Keywords
Alzheimer' s disease; Amyloid; Brain; Mapt; Neurotoxicity; Neurodegeneration; Tau
Citation
FEBS LETTERS, v.586, no.24, pp.4357 - 4361
Indexed
SCIE
SCOPUS
Journal Title
FEBS LETTERS
Volume
586
Number
24
Start Page
4357
End Page
4361
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/164087
DOI
10.1016/j.febslet.2012.10.050
ISSN
0014-5793
Abstract
Alzheimer's disease (AD) is an aging-related neurodegenerative disorder characterized by irreversible loss of higher cognitive functions. The disease is characterized by the presence of amyloid plaques and neurofibrillary tangles (NFT). In the current study we isolated from an intra-cerebral brain-site-specific (AD temporal lobe vs. AD occipital lobe) polymerase chain reaction (PCR)-select cDNA suppression subtractive hybridization (PCR-cDNA-SSH) expression analysis the novel gene P9TLDR, potentially a microtubule-associated protein involved in neuronal migration, with an altered expression pattern: down-regulated in the temporal lobe cortex of early stage AD brains. In an in vitro AD-related cell model, amyloid-beta peptide (A beta)-treated neurons, reduced P9TLDR expression correlated with increased tau protein phosphorylation. In conclusion, interference with the P9TLDR signalling pathways might be a therapeutic strategy for the treatment of AD.
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Heese, Klaus
GRADUATE SCHOOL OF BIOMEDICAL SCIENCE AND ENGINEERING (DEPARTMENT OF BIOMEDICAL SCIENCE)
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