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2015 ; 5
(ä): 11708
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Osmotin attenuates amyloid beta-induced memory impairment, tau phosphorylation
and neurodegeneration in the mouse hippocampus
#MMPMID26118757
Ali T
; Yoon GH
; Shah SA
; Lee HY
; Kim MO
Sci Rep
2015[Jun]; 5
(ä): 11708
PMID26118757
show ga
The pathological hallmarks of Alzheimer's disease (AD) include amyloid beta (A?)
accumulation, neurofibrillary tangle formation, synaptic dysfunction and neuronal
loss. In this study, we investigated the neuroprotection of novel osmotin, a
plant protein extracted from Nicotiana tabacum that has been considered to be a
homolog of mammalian adiponectin. Here, we observed that treatment with osmotin
(15 ?g/g, intraperitoneally, 4 hr) at 3 and 40 days post-intracerebroventricular
injection of A?1-42 significantly ameliorated A?1-42-induced memory impairment in
mice. These results revealed that osmotin reverses A?1-42 injection-induced
synaptic deficits, A? accumulation and BACE-1 expression. Treatment with osmotin
also alleviated the A?1-42-induced hyperphosphorylation of the tau protein at
serine 413 through the regulation of the aberrant phosphorylation of p-PI3K,
p-Akt (serine 473) and p-GSK3? (serine 9). Moreover, our western blots and
immunohistochemical results indicated that osmotin prevented A?1-42-induced
apoptosis and neurodegeneration in the A?1-42-treated mice. Furthermore, osmotin
attenuated A?1-42-induced neurotoxicity in vitro.To our knowledge, this study is
the first to investigate the neuroprotective effect of a novel osmotin against
A?1-42-induced neurotoxicity. Our results demonstrated that this ubiquitous plant
protein could potentially serve as a novel, promising, and accessible
neuroprotective agent against progressive neurodegenerative diseases such as AD.