Tau deletion promotes brain insulin resistance
Open accessAbstract
The molecular pathways underlying tau pathology–induced synaptic/cognitive deficits and neurodegeneration are poorly understood. One prevalent hypothesis is that hyperphosphorylation, misfolding, and fibrillization of tau impair synaptic plasticity and cause degeneration. However, tau pathology may also result in the loss of specific physiological tau functions, which are largely unknown but could contribute to neuronal dysfunction. In the present study, we uncovered a novel function of tau in its ability to regulate brain insulin signaling. We found that tau deletion leads to an impaired hippocampal response to insulin, caused by altered IRS-1 and PTEN (phosphatase and tensin homologue on chromosome 10) activities. Our data also demonstrate that tau knockout mice exhibit an impaired hypothalamic anorexigenic effect of insulin that is associated with energy metabolism alterations. Consistently, we found that tau haplotypes are associated with glycemic traits in humans. The present data have far-reaching clinical implications and raise the hypothesis that pathophysiological tau loss-of-function favors brain insulin resistance, which is instrumental for cognitive and metabolic impairments in Alzheimer’s disease patients.
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Additional physiological functions for tau include regulation of iron export and insulin signaling.
“Additional physiological functions for tau include regulation of iron export and insulin signaling [139, 140].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [140]
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Tau and neuroinflammation: what impact for Alzheimer's disease and tauopathies?
Laurent, C., Buée, L., & Blum, D. (2018) · Biomedical Journal · doi:10.1016/j.bj.2018.01.003 · Cited by 348 · see citing works
Self-citationDendritic Tau in Alzheimer’s Disease
Ittner, A., & Ittner, L. M. (2018) · Neuron · doi:10.1016/j.neuron.2018.06.003 · Cited by 278 · see citing works
Alzheimer's disease and type 2 diabetes: a critical assessment of the shared pathological traits
Chatterjee, S., & Mudher, A. (2018) · Frontiers in Neuroscience · doi:10.3389/fnins.2018.00383 · Cited by 270 · see citing works
Tau: Enabler of diverse brain disorders and target of rapidly evolving therapeutic strategies
Chang, C.-W., Shao, E., & Mucke, L. (2021) · Science · doi:10.1126/science.abb8255 · Cited by 263 · see citing works
Vercruysse, P., Vieau, D., Blum, D., Petersén, Å., & Dupuis, L. (2018) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2018.00002 · Cited by 172 · see citing works
Self-citationNovak, P., Schmidt, R., Kontsekova, E., Kovacech, B., Smolek, T., Katina, S., Fialova, L., Prcina, M., Parrak, V., Dal-Bianco, P., et al. (2018) · Alzheimer's Research & Therapy · doi:10.1186/s13195-018-0436-1 · Cited by 147 · see citing works
Ten Years of Tau-Targeted Immunotherapy: The Path Walked and the Roads Ahead
Novak, P., Kontsekova, E., Zilka, N., & Novak, M. (2018) · Frontiers in Neuroscience · doi:10.3389/fnins.2018.00798 · Cited by 87 · see citing works
“Reducing healthy tau protein was found to have detrimental effects (Marciniak et al., 2017), and (presumably) diluting the effect of the antibody between healthy (irrelevant) and pathological tau forms could reduce the overall efficacy of the treatment.”
BackgroundSun, H., Gao, X., Niu, J., Chen, P., He, S., Xu, S., & Ge, J. (2024) · eneuro · doi:10.1523/eneuro.0310-24.2024 · Cited by 12 · see citing works
- Authors
- Marciniak, E., Leboucher, A., Caron, E., Ahmed, T., Tailleux, A., Dumont, J., Issad, T., Gerhardt, E., Pagesy, P., Vileno, M., Bournonville, C., Hamdane, M., Bantubungi, K., Lancel, S., Demeyer, D., Eddarkaoui, S., Vallez, E., Vieau, D., Humez, S., Faivre, E., Grenier-Boley, B., Outeiro, T. F., Staels, B., Amouyel, P., Balschun, D., Buee, L., & Blum, D.
- Affiliations
- Inserm (FR)
- Université de Lille, Institut National de la Santé et de la Recherche Medicale (INSERM), CHU Lille, UMR-S 1172 JPArc, Lille, France 1
- Hamad bin Khalifa University (QA)
- Centre National de la Recherche Scientifique (FR)
- Universitätsmedizin Göttingen (DE)
- INSERM U1016, CNRS UMR8104, Université Paris Descartes Sorbonne Paris Cité, Institut Cochin, Paris, France 6
- LabEx DISTALZ (Development of Innovative Strategies for a Transdisciplinary approach to ALZheimer’s disease), Lille, France 2
- KU Leuven (BE)
- Corresponding author
- Blum, David
- ORCID
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2017-06-26
- Volume
- 214
- Issue
- 8
- Pages
- 2257-2269
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC5551570
- OpenAlex
- W2695553179
- Cited by
- 205
- References
- 87
- Citations by year
- 2026: 6 · 2025: 15 · 2024: 24 · 2023: 26 · 2022: 25 · 2021: 21 · 2020: 24 · 2019: 26 · 2018: 33 · 2017: 5
- FWCI
- 17.80
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by)
- Figshare (submittedVersion, cc-by)
- LillOA (Université de Lille (University Of Lille)) (submittedVersion, other-oa)
- Newcastle University ePrints (Newcastle Univesity) (cc-by)
- Funders
- France Alzheimer
- Fondation de France
- FHU VasCog
- ANR
- Fondation pour la Recherche Médicale
- LECMA
- Alzheimer Forschung Initiative
- Fondation Plan Alzheimer
- INSERM
- CNRS
- Université Lille 2
- Lille Métropole Communauté Urbaine
- Région Nord/Pas-de-Calais
- FEDER
- DN2M
- FUI MEDIALZ
- CHRU and Région Haut de France
- Lille 2 University
- Hauts de France
- DFG
- FWO (G0D76.14, G0587.14)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- tau protein, brain insulin resistance, insulin signaling, IRS-1, PTEN, hippocampus, hypothalamus, energy metabolism, glycemic traits, Alzheimer's disease
- MeSH terms
- Animals, Brain, Haplotypes, Hippocampus, Humans, Insulin, Insulin Resistance, Male, Mice, Inbred C57BL, tau Proteins, Mice, Knockout, Mice, Cognitive Dysfunction
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