65 0

Nec-1 alleviates cognitive impairment with reduction of Aβ and tau abnormalities in APP/PS1 mice

Title
Nec-1 alleviates cognitive impairment with reduction of Aβ and tau abnormalities in APP/PS1 mice
Author
하정미
Keywords
Alzheimer's disease; A aggregation; cognitive deficit; necrostatin-1; tau hyperphosphorylation; BETA-AMYLOID PEPTIDE; ALZHEIMERS-DISEASE; A-BETA; CELL-DEATH; CROSS-LINKING; MOUSE MODEL; HYPOTHETICAL MODEL; DYNAMIC BIOMARKERS; DIFFUSE PLAQUES; BRAIN ATROPHY
Issue Date
2017-01
Publisher
WILEY-BLACKWELL
Citation
EMBO MOLECULAR MEDICINE, v. 9, No. 1, Page. 61-77
Abstract
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by cognitive symptoms of learning and memory deficits. Such cognitive impairments are attributed to brain atrophy resulting from progressive neuronal and synaptic loss; therefore, alleviation of neural cell death is as an important target of treatment as other classical hallmarks of AD, such as aggregation of amyloid‐β (Aβ) and hyperphosphorylation of tau. Here, we found that an anti‐necroptotic molecule necrostatin‐1 (Nec‐1) directly targets Aβ and tau proteins, alleviates brain cell death and ameliorates cognitive impairment in AD models. In the cortex and hippocampus of APP/PS1 double‐transgenic mice, Nec‐1 treatment reduced the levels of Aβ oligomers, plaques and hyperphosphorylated tau without affecting production of Aβ, while it altered the levels of apoptotic marker proteins. Our results showing multiple beneficial modes of action of Nec‐1 against AD provide evidence that Nec‐1 may serve an important role in the development of preventive approach for AD.
URI
http://embomolmed.embopress.org/content/early/2016/11/16/emmm.201606566https://repository.hanyang.ac.kr/handle/20.500.11754/71647
ISSN
1757-4676; 1757-4684
DOI
10.15252/emmm.201606566
Appears in Collections:
COLLEGE OF PHARMACY[E](약학대학) > PHARMACY(약학과) > Articles
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE