Cited by 610Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

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Imaging the evolution and pathophysiology of Alzheimer disease

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Jagust, William·2018·Nature Reviews Neuroscience

DOI 10.1038/s41583-018-0067-3PMC PMC7032048

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Abstract

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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Authors: Jagust, W.
Affiliations: Lawrence Berkeley National Laboratory (US)
Corresponding author: Jagust, William
ORCID: Jagust, William
Venue: Nature Reviews Neuroscience
Publisher: Springer Science and Business Media LLC
Published: 2018-09-28
Volume: 19
Issue: 11
Pages: 687-700
ISSN: 1471-003X (ISSN-L)
1471-0048
DOI: 10.1038/s41583-018-0067-3
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
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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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