Imaging the evolution and pathophysiology of Alzheimer disease
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Technologies for imaging the pathophysiology of Alzheimer disease (AD) now permit studies of the relationships between the two major proteins deposited in this disease - amyloid-β (Aβ) and tau - and their effects on measures of neurodegeneration and cognition in humans. Deposition of Aβ in the medial parietal cortex appears to be the first stage in the development of AD, although tau aggregates in the medial temporal lobe (MTL) precede Aβ deposition in cognitively healthy older people. Whether aggregation of tau in the MTL is the first stage in AD or a fairly benign phenomenon that may be transformed and spread in the presence of Aβ is a major unresolved question. Despite a strong link between Aβ and tau, the relationship between Aβ and neurodegeneration is weak; rather, it is tau that is associated with brain atrophy and hypometabolism, which, in turn, are related to cognition. Although there is support for an interaction between Aβ and tau resulting in neurodegeneration that leads to dementia, the unknown nature of this interaction, the strikingly different patterns of brain Aβ and tau deposition and the appearance of neurodegeneration in the absence of Aβ and tau are challenges to this model that ultimately must be explained.
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These and other studies strongly support the concept of AD as an amyloid-provoked or facilitated tauopathy, although there is also evidence that both pathologies act in synergy.
“These and other studies 13,24,133,134 strongly support the concept of AD as being an amyloid-provoked, or facilitated, tauopathy, although there is also evidence that both pathologies act in synergy 135 .”
From The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics (2022) · cites this paper as [13]
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- Authors
- Jagust, W.
- Affiliations
- Lawrence Berkeley National Laboratory (US)
- Corresponding author
- Jagust, William
- ORCID
- Jagust, William
- Venue
- Nature Reviews Neuroscience
- Published
- 2018-09-28
- Volume
- 19
- Issue
- 11
- Pages
- 687-700
- ISSN
- 1471-003X (ISSN-L)
- 1471-0048
- PMC
- PMC7032048
- OpenAlex
- W2894357926
- Cited by
- 604
- References
- 213
- Citations by year
- 2026: 73 · 2025: 85 · 2024: 89 · 2023: 94 · 2022: 76 · 2021: 85 · 2020: 58 · 2019: 40 · 2018: 2
- FWCI
- 7.13
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R01AG045611, R01AG062542, P01AG019724, R01AG034570)
- 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 › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid-beta, tau protein, neurodegeneration, brain atrophy, hypometabolism, medial parietal cortex, medial temporal lobe, cognitive decline, dementia, disease progression
- MeSH terms
- Aging, Alzheimer Disease, Brain, Humans, Amyloid beta-Peptides, tau Proteins, Disease Progression, Multimodal Imaging
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