Osmotin attenuates amyloid beta-induced memory impairment, tau phosphorylation and neurodegeneration in the mouse hippocampus
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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 serine 413 through the regulation of the aberrant phosphorylation of p-PI3K, p-Akt (serine 473) and p-GSK3β (serine 9). Moreover, our western blots and immunohistochemical results indicated that osmotin prevented Aβ1-42-induced apoptosis and neurodegeneration in the Aβ1-42-treated mice. Furthermore, osmotin attenuated Aβ1-42-induced neurotoxicity in vitro.To our knowledge, this study is the first to investigate the neuroprotective effect of a novel osmotin against Aβ1-42-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.
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Osmotin has neuroprotective effects by preventing memory impairment and neuroinflammation induced by amyloid or LPS injections.
“Other studies have demonstrated its neuroprotective effects by preventing memory impairment and neuroinflammation induced by either amyloid or LPS injections [128,129].”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [128]
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- Authors
- Ali, T., Yoon, G. H., Shah, S. A., Lee, H. Y., & Kim, M. O.
- Affiliations
- Gyeongsang National University (KR)
- Corresponding author
- Kim, Myeong Ok
- Venue
- Scientific Reports
- Published
- 2015-06-29
- Volume
- 5
- Issue
- 1
- Pages
- 11708-11708
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC4484370
- OpenAlex
- W748543715
- Cited by
- 146
- References
- 61
- Citations by year
- 2026: 2 · 2025: 9 · 2024: 12 · 2023: 14 · 2022: 9 · 2021: 18 · 2020: 25 · 2019: 14 · 2018: 15 · 2017: 13 · 2016: 14 · 2015: 1
- FWCI
- 10.55
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Research Foundation
- National Research Foundation of Korea (2012-0009521)
- Commercializations Promotion Agency for R and D Outcomes
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- osmotin, amyloid-beta 42, Alzheimer's disease, neuroprotection, memory impairment, tau hyperphosphorylation, BACE1, PI3K/Akt/GSK-3β signaling, apoptosis, neurodegeneration, hippocampus, tobacco, plant proteins, neurotoxicity
- MeSH terms
- Glycogen Synthase Kinase 3 beta, Animals, Behavior, Animal, Hippocampus, Male, Memory Disorders, Mice, Inbred C57BL, Neurotoxins, Phosphorylation, Plant Proteins, Synapses, Signal Transduction, Amyloid beta-Peptides, Aspartic Acid Endopeptidases, tau Proteins, Apoptosis, Neurodegenerative Diseases, Phosphatidylinositol 3-Kinases, Glycogen Synthase Kinase 3, Proto-Oncogene Proteins c-akt
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