Novel osmotin inhibits SREBP2 via the AdipoR1/AMPK/SIRT1 pathway to improve Alzheimer’s disease neuropathological deficits

Shah, S A; Yoon, G H; Chung, S S; Abid, M N; Kim, T H; Lee, H Y; Kim, M O

doi:10.1038/mp.2016.23

Cited by 206Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

Novel osmotin inhibits SREBP2 via the AdipoR1/AMPK/SIRT1 pathway to improve Alzheimer’s disease neuropathological deficits

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Shah, S A, Yoon, G H, Chung, S S, Abid, M N, Kim, T H, Lee, H Y, Kim, M O·2017·Molecular Psychiatry

DOI 10.1038/mp.2016.23PMC PMC5322276

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Abstract

Extensive evidence has indicated that a high rate of cholesterol biogenesis and abnormal neuronal energy metabolism play key roles in Alzheimer’s disease (AD) pathogenesis. Here, for we believe the first time, we used osmotin, a plant protein homolog of mammalian adiponectin, to determine its therapeutic efficacy in different AD models. Our results reveal that osmotin treatment modulated adiponectin receptor 1 (AdipoR1), significantly induced AMP-activated protein kinase (AMPK)/Sirtuin 1 (SIRT1) activation and reduced SREBP2 (sterol regulatory element-binding protein 2) expression in both in vitro and in vivo AD models and in Adipo −/− mice. Via the AdipoR1/AMPK/SIRT1/SREBP2 signaling pathway, osmotin significantly diminished amyloidogenic Aβ production, abundance and aggregation, accompanied by improved pre- and post-synaptic dysfunction, cognitive impairment, memory deficits and, most importantly, reversed the suppression of long-term potentiation in AD mice. Interestingly, AdipoR1, AMPK and SIRT1 silencing not only abolished osmotin capability but also further enhanced AD pathology by increasing SREBP2, amyloid precursor protein (APP) and β-secretase (BACE1) expression and the levels of toxic Aβ production. However, the opposite was true for SREBP2 when silenced using small interfering RNA in APPswe/ind-transfected SH-SY5Y cells. Similarly, osmotin treatment also enhanced the non-amyloidogenic pathway by activating the α-secretase gene that is, ADAM10 , in an AMPK/SIRT1-dependent manner. These results suggest that osmotin or osmotin-based therapeutic agents might be potential candidates for AD treatment.

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Osmotin improves neuropathological deficits of Alzheimer's through an AdipoR1-AMPK-dependent mechanism in in vitro and in vivo models.
“It was further shown to improve the neuropathological deficits of Alzheimer’s, through an AdipoR1-AMPK-dependent mechanism, in in vitro and in vivo models of the disease [130,131]”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [130]

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Authors: Shah, S. A., Yoon, G. H., Chung, S. S., Abid, M. N., Kim, T. H., Lee, H. Y., & Kim, M. O.
Affiliations: Gyeongsang National University (KR)
Yonsei University (KR)
Corresponding author: Kim, M O
ORCID: Chung, S S
Kim, T H
Lee, H Y
Kim, M O
Venue: Molecular Psychiatry
Publisher: Springer Science and Business Media LLC
Published: 2016-03-22
Volume: 22
Issue: 3
Pages: 407-416
ISSN: 1359-4184 (ISSN-L)
1476-5578
DOI: 10.1038/mp.2016.23
PMC: PMC5322276
OpenAlex: W2332304720
Cited by: 206
References: 35
Citations by year: 2026: 8 · 2025: 19 · 2024: 28 · 2023: 24 · 2022: 17 · 2021: 27 · 2020: 20 · 2019: 19 · 2018: 14 · 2017: 21 · 2016: 9
FWCI: 16.91
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0 (tdm)
Locations: Molecular Psychiatry (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion, cc-by-nc-sa)
PubMed (publishedVersion)
YUHSpace (Yonsei University Medical Library) (submittedVersion, cc-by-nc-nd)
Funders: National Research Foundation
Ministry of Science, ICT and Future Planning (2012-0009521)
National Research Foundation of Korea (2012-0009521)
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: osmotin, Alzheimer's disease, SREBP2, AdipoR1, AMPK, SIRT1, amyloid-beta, amyloid precursor protein, BACE1, ADAM10, long-term potentiation, synaptic dysfunction, cognitive impairment, cholesterol biosynthesis, neuronal energy metabolism
MeSH terms: Alzheimer Disease, Animals, Disease Models, Animal, Humans, Memory Disorders, Mice, Transgenic, Phosphorylation, Plant Proteins, Signal Transduction, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Long-Term Potentiation, Mice, Sterol Regulatory Element Binding Protein 2, Amyloid Precursor Protein Secretases, Receptors, Adiponectin, AMP-Activated Protein Kinases, Sirtuin 1

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Novel osmotin inhibits SREBP2 via the AdipoR1/AMPK/SIRT1 pathway to improve Alzheimer’s disease neuropathological deficits

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