<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>5</volume><submitter>Ali T</submitter><pubmed_abstract>The pathological hallmarks of Alzheimer's disease (AD) include amyloid beta (Aβ) 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 μg/g, intraperitoneally, 4 hr) at 3 and 40 days post-intracerebroventricular injection of Aβ1-42 significantly ameliorated Aβ1-42-induced memory impairment in mice. These results revealed that osmotin reverses Aβ1-42 injection-induced synaptic deficits, Aβ accumulation and BACE-1 expression. Treatment with osmotin also alleviated the Aβ1-42-induced hyperphosphorylation of the tau protein at se</pubmed_abstract><journal>Scientific reports</journal><pagination>11708</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4484370</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Osmotin attenuates amyloid beta-induced memory impairment, tau phosphorylation and neurodegeneration in the mouse hippocampus.</pubmed_title><pmcid>PMC4484370</pmcid><pubmed_authors>Shah SA</pubmed_authors><pubmed_authors>Ali T</pubmed_authors><pubmed_authors>Kim MO</pubmed_authors><pubmed_authors>Lee HY</pubmed_authors><pubmed_authors>Yoon GH</pubmed_authors></additional><is_claimable>false</is_claimable><name>Osmotin attenuates amyloid beta-induced memory impairment, tau phosphorylation and neurodegeneration in the mouse hippocampus.</name><description>The pathological hallmarks of Alzheimer's disease (AD) include amyloid beta (Aβ) 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 μg/g, intraperitoneally, 4 hr) at 3 and 40 days post-intracerebroventricular injection of Aβ1-42 significantly ameliorated Aβ1-42-induced memory impairment in mice. These results revealed that osmotin reverses Aβ1-42 injection-induced synaptic deficits, Aβ accumulation and BACE-1 expression. Treatment with osmotin also alleviated the Aβ1-42-induced hyperphosphorylation of the tau protein at se</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Jun</publication><modification>2025-04-26T06:13:33.244Z</modification><creation>2019-03-27T01:54:10Z</creation></dates><accession>S-EPMC4484370</accession><cross_references><pubmed>26118757</pubmed><doi>10.1038/srep11708</doi></cross_references></HashMap>