Cited by 262Alzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Dysregulation of the mTOR Pathway Mediates Impairment of Synaptic Plasticity in a Mouse Model of Alzheimer's Disease

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Ma, Tao, Hoeffer, Charles A., Capetillo-Zarate, Estibaliz, Yu, Fangmin, Wong, Helen, Lin, Michael T., Tampellini, Davide, Klann, Eric, Blitzer, Robert D., Gouras, Gunnar K.·2010·PLoS ONE

DOI 10.1371/journal.pone.0012845PMC PMC2942840

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Abstract

BACKGROUND: The mammalian target of rapamycin (mTOR) is an evolutionarily conserved Ser/Thr protein kinase that plays a pivotal role in multiple fundamental biological processes, including synaptic plasticity. We explored the relationship between the mTOR pathway and β-amyloid (Aβ)-induced synaptic dysfunction, which is considered to be critical in the pathogenesis of Alzheimer's disease (AD). METHODOLOGY/PRINCIPAL FINDINGS: We provide evidence that inhibition of mTOR signaling correlates with impairment in synaptic plasticity in hippocampal slices from an AD mouse model and in wild-type slices exposed to exogenous Aβ1-42. Importantly, by up-regulating mTOR signaling, glycogen synthase kinase 3 (GSK3) inhibitors rescued LTP in the AD mouse model, and genetic deletion of FK506-binding protein 12 (FKBP12) prevented Aβ-induced impairment in long-term potentiation (LTP). In addition, confocal microscopy demonstrated co-localization of intraneuronal Aβ42 with mTOR. CONCLUSIONS/SIGNIFICANCE: These data support the notion that the mTOR pathway modulates Aβ-related synaptic dysfunction in AD.

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Authors: Ma, T., Hoeffer, C. A., Capetillo-Zarate, E., Yu, F., Wong, H., Lin, M. T., Tampellini, D., Klann, E., Blitzer, R. D., & Gouras, G. K.
Affiliations: Weill Cornell Medicine (US)
New York University (US)
Icahn School of Medicine at Mount Sinai (US)
Corresponding author: Gouras, Gunnar K.
ORCID: Ma, Tao
Hoeffer, Charles A.
Wong, Helen
Tampellini, Davide
Klann, Eric
Blitzer, Robert D.
Gouras, Gunnar K.
Venue: PLoS ONE
Publisher: Public Library of Science (PLoS)
Published: 2010-09-20
Volume: 5
Issue: 9
Pages: e12845
ISSN: 1932-6203 (ISSN-L)
DOI: 10.1371/journal.pone.0012845
PMC: PMC2942840
OpenAlex: W2071279551
Cited by: 262
References: 52
Citations by year: 2026: 9 · 2025: 12 · 2024: 7 · 2023: 13 · 2022: 13 · 2021: 20 · 2020: 26 · 2019: 10 · 2018: 11 · 2017: 14 · 2016: 18 · 2015: 17 · 2014: 30 · 2013: 23 · 2012: 22
FWCI: 13.22
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (unspecified)
Locations: PLoS ONE (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Communities in ADDI (University of the Basque Country) (submittedVersion, cc-by)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Figshare (submittedVersion, cc-by)
Hispana (submittedVersion, cc-by)
Lund University Publications (Lund University) (submittedVersion)
Funders: National Institutes of Health (N S03400 7, AG‐09464, AG28174)
National Institute on Aging (R01AG027140, AG09464, R01AG020729, K02AG028174, AG28174, AG027140, P01AG009464)
National Institute of General Medical Sciences (R01GM054508, GM-054508)
National Institute of Neurological Disorders and Stroke (R37NS034007, R01NS034007, R29NS034007, NS-034007)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: mTOR signaling, Alzheimer's disease, synaptic plasticity, amyloid-beta, amyloid-beta 42, long-term potentiation, glycogen synthase kinase-3, GSK-3 inhibitors, FKBP12, hippocampus, synaptic dysfunction, intraneuronal amyloid-beta
MeSH terms: Alzheimer Disease, Animals, Disease Models, Animal, Hippocampus, Humans, Mice, Inbred C57BL, Neuronal Plasticity, Peptide Fragments, Synapses, Signal Transduction, Amyloid beta-Peptides, Long-Term Potentiation, Mice, TOR Serine-Threonine Kinases

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Dysregulation of the mTOR Pathway Mediates Impairment of Synaptic Plasticity in a Mouse Model of Alzheimer's Disease

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