Network Tau spreading is vulnerable to the expression gradients of APOE and glutamatergic-related genes
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A key hallmark of Alzheimer’s disease (AD) pathology is the intracellular accumulation of tau protein in the form of neurofibrillary tangles across large-scale networks of the human brain cortex. Currently, it is still unclear how tau accumulates within specific cortical systems and whether in situ genetic traits play a role in this circuit-based propagation progression. In this study, using two independent cohorts of cognitively normal older participants, we reveal the brain network foundation of tau spreading and its association with using high-resolution transcriptomic genetic data. We observed that specific connectomic and genetic gradients exist along the tau spreading network. In particular, we identified 577 genes whose expression is associated with the spatial spreading of tau. Within this set of genes, APOE and glutamatergic synaptic genes, such as SLC1A2 , play a central role. Thus, our study characterizes neurogenetic topological vulnerabilities in distinctive brain circuits of tau spreading and suggests that drug development strategies targeting the gradient expression of this set of genes should be explored to help reduce or prevent pathological tau accumulation.
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Loss or dysfunction of SLC1A2 has been implicated in multiple neurodegenerative and neuropsychiatric disorders, including AD where it is closely associated with cognitive decline.
“Loss or dysfunction of SLC1A2 has been implicated in multiple neurodegenerative and neuropsychiatric disorders, including AD where it is closely associated with cognitive decline [126–131].”
From Tau Ablation Rewires Brain Cell Programs in Health and Restores Function in Disease (2026) · cites this paper as [130]
The Discussion (page unavailable) links SLC1A2 to tau pathology in Alzheimer’s disease and reports that lower expression in astrocytes and neurons was associated with worse cognitive performance. It does not address SLC1A2 loss or dysfunction across multiple neurodegenerative and neuropsychiatric disorders, so that broader part of the claim is unsupported by this source. (LLM, conf=0.85)
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- Authors
- Montal, V., Diez, I., Kim, C.-M., Orwig, W., Bueichekú, E., Gutiérrez-Zúñiga, R., Bejanin, A., Pegueroles, J., Dols-Icardo, O., Vannini, P., El-Fakhri, G., Johnson, K. A., Sperling, R. A., Fortea, J., & Sepulcre, J.
- Affiliations
- Gordon Center for Medical Imaging, Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
- Harvard University (US)
- Universitat Autònoma de Barcelona (ES)
- Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autonoma de Barcelona, Barcelona 08041, Spain.
- Brigham and Women's Hospital (US)
- Corresponding author
- Sepulcre, Jorge
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2022-07-27
- Volume
- 14
- Issue
- 655
- Pages
- eabn7273-eabn7273
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC9942690
- OpenAlex
- W4288068424
- Cited by
- 52
- References
- 57
- Citations by year
- 2026: 13 · 2025: 7 · 2024: 17 · 2023: 13 · 2022: 2
- FWCI
- 6.03
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- TECNALIA Publications (Fundación TECNALIA Research & Innovation) (submittedVersion, public-domain)
- Funders
- National Institutes of Health (7p41eb022544-08)
- National Institute on Aging (R01AG061083, R01AG061811, R01AG046396, R01AG027435, R01AG061445, P01AG036694)
- National Institute of Biomedical Imaging and Bioengineering (P41-EB022544)
- 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 propagation, Alzheimer's disease, neurofibrillary tangles, brain network topology, apolipoprotein E, GLT-1, gene expression gradients, connectomics, cortical circuits
- MeSH terms
- Alzheimer Disease, Apolipoproteins E, Brain, Humans, Neurofibrillary Tangles, tau Proteins
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