mTORC2 (Rictor) in Alzheimer’s Disease and Reversal of Amyloid-β Expression-Induced Insulin Resistance and Toxicity in Rat Primary Cortical Neurons
Open accessAbstract
Mammalian target of rapamycin complex 1 (mTORC1), a nutrient sensor and central controller of cell growth and proliferation, is altered in various models of Alzheimer's disease (AD). Even less studied or understood in AD is mammalian target of rapamycin complex 2 (mTORC2) that influences cellular metabolism, in part through the regulations of Akt/PKB and SGK. Dysregulation of insulin/PI3K/Akt signaling is another important feature of AD pathogenesis. We found that both total mTORC1 and C2 protein levels and individual C1 and C2 enzymatic activities were decreased in human AD brain samples. In two rodent AD models, mTORC1 and C2 activities were also decreased. In a neuronal culture model of AD characterized by accumulation of cellular amyloid-β (Aβ)42, mTORC1 activity was reduced. Autophagic vesicles and markers were correspondingly increased and new protein synthesis was inhibited, consistent with mTORC1 hypofunction. Interestingly, mTORC2 activity in neural culture seemed resistant to the effects of intracellular amyloid. In various cell lines, Aβ expression provoked insulin resistance, characterized by inhibition of stimulated Akt phosphorylation, and an increase in negative mTORC1 regular, p-AMPK, itself a nutrient sensor. Rapamycin decreased phospho-mTOR and to lesser degree p-Rictor. This further suppression of mTORC1 activity protected cells from Aβ-induced toxicity and insulin resistance. More striking, Rictor over-expression fully reversed the Aβ-effects on primary neuronal cultures. Finally, using in vitro assay, Rictor protein addition completely overcame oligomeric Aβ-induced inhibition of the PDK-Akt activation step. We conclude that striking a new balance by restoring mTORC2 abundance and/or inhibition of mTORC1 has therapeutic potential in AD.
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RICTOR activation is protective against Aβ toxicity.
“RICTOR activation is protective against Aβ toxicity, 54 suggesting a compensatory increase due to the early onset of amyloid pathology in DS.”
The increase in RICTOR activation in CA3/CA4 may be a compensatory increase due to the early onset of amyloid pathology in DS.
“RICTOR activation is protective against Aβ toxicity, 54 suggesting a compensatory increase due to the early onset of amyloid pathology in DS.”
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de la Monte, S. M. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-240069 · Cited by 24 · see citing works
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Insight into the Regulation of NDRG1 Expression
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mTORC2: A neglected player in aging regulation
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Dysregulated mTOR networks in experimental sporadic Alzheimer’s disease
de la Monte, S. M., & Tong, M. (2024) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2024.1432359 · Cited by 6 · see citing works
de la Monte, S. M., & Sutherland, G. T. (2025) · ASN NEURO · doi:10.1080/17590914.2025.2573965 · Cited by 5 · see citing works
Hou, Z., Yang, X., Jiang, L., Song, L., Li, Y., Li, D., Che, Y., Zhang, X., Sun, Z., Shang, H., et al. (2023) · Aging · doi:10.18632/aging.204912 · Cited by 3 · see citing works
Signaling pathways in the treatment of Alzheimer’s disease with acupuncture: a narrative review
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Role of branched chain amino acid metabolism on aging
Wang, Z., Yu, S., Du, X., Yan, X., & Xin, Y. (2025) · Biogerontology · doi:10.1007/s10522-025-10309-9 · Cited by 2 · see citing works
Transcriptomic analysis of ipsilateral spinal cord in rats after bone fracturePreprint
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Rictor/mTORC2 signaling pathway mediates Benzo[a]pyrene-induced renal injury
Han, J.-Q., Qu, Y., Zhu, Y., Qi, Y., Liu, T.-F., Li, Y.-M., Zhang, Y.-J., Tan, J., Han, H., & Ma, X. (2025) · Scientific Reports · doi:10.1038/s41598-025-29025-y · Cited by 1 · see citing works
Exploring cannabinoid modulation on autophagy mechanisms in Alzheimer’s disease: a review
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Mitophagy Impairments as Culprit of Alzheimer’s Disease
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“50,53,54 The convergence between ST-and proteomics-based upstream regulator analysis supports the biologicalrelevance of the identified networks.”
Mammalian target of rapamycin complexes
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Self-citationMammalian target of rapamycin complexes
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The Pharmacology and Dual Role of Proteostasis in Amyloidoses
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Neurosteroid-Mediated Neuroprotection via mTORC1/AMPK/BDNF Signaling Pathway in Alzheimer’s Disease
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The role of mTORC2 in the in vitro neurotoxicity of Parkinsonian mimetics 6-OHDA and MPP+
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- Authors
- Lee, H.-K., Kwon, B., Lemere, C. A., de la Monte, S., Itamura, K., Ha, A. Y., & Querfurth, H. W.
- Affiliations
- Department of Neurology, Rhode Island Hospital and Brown University Warren Alpert Medical School, Providence, RI, USA
- Brown University (US)
- Brigham and Women's Hospital (US)
- Department of Pathology, Rhode Island Hospital and Brown University Warren Alpert Medical School, Providence, RI, USA
- Corresponding author
- Querfurth, Henry W.
- Venue
- Journal of Alzheimer's Disease
- Publisher
- SAGE Publications
- Published
- 2017-02-03
- Volume
- 56
- Issue
- 3
- Pages
- 1015-1036
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- PMC
- PMC5577393
- OpenAlex
- W2567266077
- Cited by
- 57
- References
- 111
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 9 · 2023: 7 · 2022: 7 · 2021: 4 · 2020: 6 · 2019: 6 · 2018: 2 · 2017: 1
- FWCI
- 2.42
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- McLean Hospital
- Bennett Foundation
- National Institutes of Health
- National Institute on Alcohol Abuse and Alcoholism (R37AA011431)
- National Institute on Aging (R44AG049510, R41AG044871)
- National Institute of Neurological Disorders and Stroke (R01NS136122)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- mTORC2, Rictor
- MeSH terms
- Mechanistic Target of Rapamycin Complex 1, Mechanistic Target of Rapamycin Complex 2, Aged, Aged, 80 and over, Alzheimer Disease, Animals, Autophagy, Cell Survival, Cells, Cultured, Cerebral Cortex, Female, Humans, Insulin Resistance, Male, Mice, Transgenic, Middle Aged, Neurons, Peptide Fragments, Amyloid beta-Peptides, Rats, Sprague-Dawley, Proto-Oncogene Proteins c-akt
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