Spreading of amyloid, tau, and microvascular pathology in Alzheimer’s disease: Findings from neuropathological and neuroimaging studies.
Open accessAbstract
Primary pathologies including amyloid-β (Aβ) plaques and neurofibrillary tangles (NFT) develop many years before the onset of dementia symptoms in Alzheimer's disease (AD). Age-related small vessel disease (SVD) is common in elderly subjects and may contribute to the clinical syndrome of AD. Each type of pathology shows a specific spatio-temporal sequence of spreading in the brain. Here, we review neuropathological and neuroimaging findings (PET tracers of Aβ and NFT, MRI markers of SVD) to assess whether staging of these primary pathologies is useful to predict clinical symptoms in AD. On the basis of neuropathological data, early stages of Aβ plaque and NFT pathology distribution occur in preclinical AD, but advanced stages with spreading into further brain regions are associated with dementia symptoms. Amyloid PET presumably detects Aβ in advanced neuropathological Aβ stages, and increased global amyloid PET uptake is associated with clinical worsening in non-demented subjects. Tau PET may provide additional predictive value by detecting NFT in the allocortex. There is weak evidence that SVD is related to amyloid or NFT pathology. Global volume of MRI-assessed white matter hyperintensities (WMH) contribute in addition to biomarker levels of Aβ to predict cognitive decline. Regional differences of the effect of WMH on cognition have been demonstrated but are not yet established as a biomarker in AD. In conclusion, biomarkers for amyloid and tau pathology allow a distinction between early and advanced stages of AD, but a subgroup of pathologically identified preclinical AD cases is not identified by the currently available biomarkers.
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The capability to monitor alterations in tissue microstructure caused by Aβ accumulation may provide an important biomarker to monitor disease progression or treatment response.
“The capability to monitor the alterations in tissue microstructure caused by the accumulation of Aβ may provide an important biomarker to monitor disease progression or treatment response (Adlard et al., 2014; Thal et al., 2014).”
From Age-dependent microstructure alterations in 5xFAD mice by high-resolution diffusion tensor imaging (2022) · cites this paper as Thal et al., 2014
The section “Amyloid PET as a predictor of clinical progression to AD dementia” (page unavailable) reports that amyloid PET uptake is associated with faster clinical worsening, supporting the potential value of an Aβ-related biomarker for tracking disease progression. It does not establish that Aβ accumulation causes measurable tissue-microstructure alterations or that monitoring those alterations tracks treatment response. (LLM, conf=0.84)
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- Authors
- Thal, D. R., Attems, J., & Ewers, M.
- Affiliations
- Universität Ulm (DE)
- Newcastle University (GB)
- Institut für Schlaganfall- und Demenzforschung (DE)
- Corresponding author
- Ewers, Michael
- Venue
- Journal of Alzheimer s Disease
- Publisher
- SAGE Publications
- Published
- 2014-10-27
- Volume
- 42
- Issue
- s4
- Pages
- S421-S429
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- OpenAlex
- W2160573346
- Cited by
- 100
- References
- 93
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 11 · 2023: 7 · 2022: 5 · 2021: 7 · 2020: 7 · 2019: 10 · 2018: 14 · 2017: 7 · 2016: 12 · 2015: 7 · 2014: 1
- FWCI
- 6.87
- Type
- journal article
- Language
- en
- Open access
- green
- lirias.kuleuven.be
- Licence
- other-oa
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- Lirias (submittedVersion, other-oa)
- OPen Access Repositorium der Universität Ulm (OPARU) (Ulm University) (submittedVersion)
- Universität Ulm, Kommunikations- und Informationszentrum (kiz)
- Newcastle University ePrints (Newcastle Univesity)
- Funders
- Alzheimer Forschung Initiative (#13803, 10810)
- European Commission
- Novartis Pharma
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, amyloid plaques
- MeSH terms
- Alzheimer Disease, Amyloid, Humans, tau Proteins, Microvessels, Neuroimaging
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