Cited by 230Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsAging and Gerontology Research

Beta‐amyloid deposition and the aging brain

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Rodrigue, Karen M., Kennedy, Kristen M., Park, Denise C.·2009·Neuropsychology Review

Abstract

A central issue in cognitive neuroscience of aging research is pinpointing precise neural mechanisms that determine cognitive outcome in late adulthood as well as identifying early markers of less successful cognitive aging. One promising biomarker is beta amyloid (Abeta) deposition. Several new radiotracers have been developed that bind to fibrillar Abeta providing sensitive estimates of amyloid deposition in various brain regions. Abeta imaging has been primarily used to study patients with Alzheimer's Disease (AD) and individuals with Mild Cognitive Impairment (MCI); however, there is now building data on Abeta deposition in healthy controls that suggest at least 20% and perhaps as much as a third of healthy older adults show significant deposition. Considerable evidence suggests amyloid deposition precedes declines in cognition and may be the initiator in a cascade of events that indirectly leads to age-related cognitive decline. We review studies of Abeta deposition imaging in AD, MCI, and normal adults, its cognitive consequences, and the role of genetic risk and cognitive reserve.

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  • AD is not driven by a single pathological process but by complex interactions among neurons and glial cells-including astrocytes, microglia, and oligodendrocytes-that contribute to synaptic dysfunction, neuroinflammation, white matter injury, and neuronal loss.

    “AD is not driven by a single pathological process but rather by complex interactions among neurons and glial cells—including astrocytes, microglia, and oligodendrocytes—that contribute to synaptic dysfunction, neuroinflammation, white matter injury, and neuronal loss.”

    From Diffusion MRI reveals amyloid plaque–associated cellular signatures through spatial transcriptomic integration (2026) · cites this paper as [3]

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  1. Ichise M Plett S Joshi A Stern Y van Heertum R Lowe V 2008 Quantitative comparison of three novel 18F-labeled ligands for PET imaging of brain amyloid-β plaques in Alzheimer’s disease Journal of Nuclear Medicine 49 214
  2. Raz N Kennedy KM 2009 A systems approach to age-related change: Neuroanatomical changes, their modifiers, and cognitive correlates Jagust W D’Esposito M Imaging the aging brain Ch 4 43 70 Oxford UP NYC
  3. Skovronsky D Coleman RE Frey K Garg P Ichise M Lowe V 2008 Results of multi-center clinical trials comparing four 18F PET amyloid-imaging agents: preclinical to clinical correlations Journal of Nuclear Medicine Meeting Abstracts 49 1 34P

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Authors
Rodrigue, K. M., Kennedy, K. M., & Park, D. C.
Affiliations
The University of Texas at Dallas (US)
Corresponding author
Park, Denise C.
Venue
Neuropsychology Review
Published
2009-11-12
Volume
19
Issue
4
Pages
436-450
ISSN
  • 1040-7308 (ISSN-L)
  • 1573-6660
OpenAlex
W2065971926
Cited by
230
References
86
Citations by year
2026: 11 · 2025: 19 · 2024: 16 · 2023: 20 · 2022: 31 · 2021: 23 · 2020: 21 · 2019: 15 · 2018: 6 · 2017: 9 · 2016: 9 · 2015: 8 · 2014: 10 · 2013: 10 · 2012: 9
FWCI
0.92
Type
journal article
Language
en
Open access
Locations
  • Neuropsychology Review (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Institute on Aging (RF1AG006265, R01AG006265, R37AG006265, AG-006265-23)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Social Sciences › Psychology › Neuropsychology and Physiological Psychology › Aging and Gerontology Research
Keywords
amyloid-beta deposition, cognitive aging, amyloid imaging, Alzheimer's disease, mild cognitive impairment, healthy older adults, radioactive tracers, genetic risk, cognitive reserve, age-related cognitive decline, biomarkers
MeSH terms
Aging, Brain, Cognition Disorders, Humans, Models, Neurological, Amyloid beta-Peptides, Genetic Predisposition to Disease, Plaque, Amyloid

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