Nec-1 alleviates cognitive impairment with reduction of A and tau abnormalities in APP/PS1 miceopen access
- Authors
- Yang, Seung-Hoon; Lee, Dongkeun Kenneth; Shin, Jisu; Lee, Sejin; Baek, Seungyeop; Kim, Jiyoon; Jung, Hoyong; Hah, Jung-Mi; Kim, YoungSoo
- Issue Date
- Jan-2017
- Publisher
- WILEY
- Keywords
- Alzheimer' s disease; A aggregation; cognitive deficit; necrostatin-1; tau hyperphosphorylation
- Citation
- EMBO MOLECULAR MEDICINE, v.9, no.1, pp.61 - 77
- Indexed
- SCIE
SCOPUS
- Journal Title
- EMBO MOLECULAR MEDICINE
- Volume
- 9
- Number
- 1
- Start Page
- 61
- End Page
- 77
- URI
- https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/10587
- DOI
- 10.15252/emmm.201606566
- ISSN
- 1757-4676
- 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- (A) and hyperphosphorylation of tau. Here, we found that an anti-necroptotic molecule necrostatin-1 (Nec-1) directly targets A 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 A oligomers, plaques and hyperphosphorylated tau without affecting production of A, 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.
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