Synaptic Tau Seeding Precedes Tau Pathology in Human Alzheimer’s Disease Brain
Open accessAbstract
Alzheimer’s disease (AD) is defined by the presence of intraneuronal neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau aggregates and extracellular amyloid-beta plaques. The presence and spread of tau pathology through the brain is classified by Braak stages and thought to correlate to the progression of AD. Several in vitro and in vivo studies have examined tau pathology moving from one neuron to the next, suggesting a “prion-like” spread of tau aggregates may be an underlying cause of Braak tau staging in AD. Using the HEK293 TauRD-P301S-CFP/YFP expressing biosensor cells as a highly sensitive and specific tool to identify the presence of seed competent aggregated tau in brain lysate – ie., tau aggregates that are capable of recruiting and misfolding monomeric tau – , we detected substantial tau seeding levels in the entorhinal cortex from human cases with only very rare NFTs, suggesting that soluble tau aggregates can exist prior to the development of overt tau pathology. We next looked at tau seeding levels in human brains of varying Braak stages along six regions of the Braak Tau Pathway. Tau seeding levels were detected not only in the brain regions impacted by pathology, but also in the subsequent non-pathology containing region along the Braak pathway. These data imply that pathogenic tau aggregates precede overt tau pathology in a manner that is consistent with transneuronal spread of tau aggregates. We then detected tau seeding in frontal white matter tracts and the optic nerve, two brain regions comprised of axons that contain little to no neuronal cell bodies, implying that tau aggregates can indeed traverse along axons. Finally, we isolated cytosolic and synaptosome fractions along the Braak Tau Pathway from brains of varying Braak stages. Phosphorylated and seed competent tau was significantly enriched in the synaptic fraction of brain regions that did not have extensive cellular tau pathology, further suggesting that aggregated tau seeds move through the human brain along synaptically connected neurons. Together, these data provide further evidence that the spread of tau aggregates through the human brain along synaptically connected networks results in the pathogenesis of human AD.
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Seeding precedes tau pathogenesis and can even occur in brain regions where tau pathology does not usually present.
“Several studies have shown that seeding precedes tau pathogenesis and can even occur in brain regions where tau pathology does not usually present (DeVos et al., 2018; Kaufman et al., 2018; Stopschinski et al., 2021).”
From Network analysis identifies strain-dependent response to tau and tau seeding-associated genes (2023) · cites this paper as DeVos et al., 2018
Prion-like seeding and spreading may represent a mechanism whereby tau pathology propagates from the entorhinal cortex to the neocortex in AD.
“Thus, prion-like seeding and spreading may represent a mechanism whereby tau pathology propagates from the entorhinal cortex to the neocortex in AD”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as DeVos et al., 2018
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- Authors
- DeVos, S. L., Corjuc, B. T., Oakley, D. H., Nobuhara, C. K., Bannon, R. N., Chase, A., Commins, C., Gonzalez, J. A., Dooley, P. M., Frosch, M. P., & Hyman, B. T.
- Affiliations
- Harvard University (US)
- Corresponding author
- Hyman, Bradley T.
- ORCID
- Venue
- Frontiers in Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2018-04-24
- Volume
- 12
- Pages
- 267-267
- ISSN
- 1662-453X (ISSN-L)
- PMC
- PMC5928393
- OpenAlex
- W2800998714
- Cited by
- 285
- References
- 63
- Citations by year
- 2026: 13 · 2025: 28 · 2024: 47 · 2023: 41 · 2022: 34 · 2021: 50 · 2020: 36 · 2019: 23 · 2018: 11 · 2013: 1
- FWCI
- 20.63
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (AG000222, AG026249)
- BrightFocus Foundation
- 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
- Alzheimer's disease, tau seeding, tau pathology, neurofibrillary tangles, Braak staging, prion-like spread, transneuronal spread, entorhinal cortex, optic nerve, synaptosomes, tau phosphorylation, P301S tau, human brain
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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