Journal article
Spread of pathological tau proteins through communicating neurons in human Alzheimer's disease
Nature communications, Vol.11(1), pp.2612-2612
05/26/2020
DOI: 10.1038/s41467-020-15701-2
PMCID: PMC7251068
PMID: 32457389
Abstract
Tau is a hallmark pathology of Alzheimer's disease, and animal models have suggested that tau spreads from cell to cell through neuronal connections, facilitated by β-amyloid (Aβ). We test this hypothesis in humans using an epidemic spreading model (ESM) to simulate tau spread, and compare these simulations to observed patterns measured using tau-PET in 312 individuals along Alzheimer's disease continuum. Up to 70% of the variance in the overall spatial pattern of tau can be explained by our model. Surprisingly, the ESM predicts the spatial patterns of tau irrespective of whether brain Aβ is present, but regions with greater Aβ burden show greater tau than predicted by connectivity patterns, suggesting a role of Aβ in accelerating tau spread. Altogether, our results provide evidence in humans that tau spreads through neuronal communication pathways even in normal aging, and that this process is accelerated by the presence of brain Aβ.
Details
- Title: Subtitle
- Spread of pathological tau proteins through communicating neurons in human Alzheimer's disease
- Creators
- Jacob W Vogel - Montreal Neurological Institute and HospitalYasser Iturria-Medina - Montreal Neurological Institute, McGill University, Montréal, QC, CanadaOlof T Strandberg - Clinical Memory Research Unit, Lund University, Lund, SwedenRuben Smith - Memory Clinic, Skåne University Hospital, Lund, SwedenElizabeth Levitis - Montreal Neurological Institute, McGill University, Montréal, QC, CanadaAlan C Evans - Montreal Neurological Institute, McGill University, Montréal, QC, CanadaOskar Hansson - Memory Clinic, Skåne University Hospital, Lund, Sweden. oskar.hansson@med.lu.seAlzheimer’s Disease Neuroimaging InitiativeSwedish BioFinder Study
- Contributors
- HyungSub Shim (Contributor) - University of Iowa, Neurology
- Resource Type
- Journal article
- Publication Details
- Nature communications, Vol.11(1), pp.2612-2612
- DOI
- 10.1038/s41467-020-15701-2
- PMID
- 32457389
- PMCID
- PMC7251068
- NLM abbreviation
- Nat Commun
- ISSN
- 2041-1723
- eISSN
- 2041-1723
- Grant note
- P30 AG066462 / NIA NIH HHS P30 AG062715 / NIA NIH HHS CIHR U01 AG024904 / NIA NIH HHS
- Language
- English
- Date published
- 05/26/2020
- Academic Unit
- Neurology; Psychiatry
- Record Identifier
- 9984302204702771
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