The relevance of beta-amyloid on markers of Alzheimer’s disease in clinically normal individuals and factors that influence these associations
Open accessAbstract
Aberrant accumulation of beta-amyloid (Aβ) is thought to be an early event in a biological cascade that eventually leads to Alzheimer's disease (AD). Along these lines, many clinically normal (CN) older individuals have evidence of beta-amyloid (Aβ) accumulation, which may be indicative of preclinical AD. However, relationships between Aβ and "downstream" AD markers are often inconsistent across studies. These inconsistencies may be due to the presence of other age-related processes that also influence AD markers, as well as additional risk factors that interact with Aβ to influence downstream changes. For instance, it is possible that the effect of Aβ is modified by neurodegeneration, genetics, sex-differences and cognitive reserve. Thus, a multivariate approach to determining risk of AD within CN participants may be more appropriate than reliance on Aβ status alone. An understanding of how additional risk factors interact with Aβ to influence an individual's trajectory towards AD is essential for characterizing preclinical AD and has implications for prevention trials.
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The correlation between hallmark lesions and the presence and severity of disease is modest.
“the correlation between hallmark lesions and the presence and severity of disease is modest”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [104]
The Cognition section (page not provided) describes a subtle association between beta-amyloid and cross-sectional cognitive performance in clinically normal individuals. That supports a modest association in this specific setting, but not the broader claim about hallmark lesions collectively correlating with the presence and severity of disease. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIt is well established that the pathological burden of diverse lesions and proteinopathies can be substantial in people who are living independently and are clinically asymptomatic.
“it is well established that the pathological burden of diverse lesions and proteinopathies can be substantial in people who are living independently and are clinically asymptomatic [103–107].”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [104]
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- Authors
- Mormino, E. C.
- Affiliations
- Harvard University (US)
- Corresponding author
- Mormino, Elizabeth C.
- Venue
- Neuropsychology Review
- Published
- 2014-08-10
- Volume
- 24
- Issue
- 3
- Pages
- 300-312
- ISSN
- 1040-7308 (ISSN-L)
- 1573-6660
- PMC
- PMC4313873
- OpenAlex
- W2023331656
- Cited by
- 44
- References
- 146
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 4 · 2023: 2 · 2022: 4 · 2021: 2 · 2020: 1 · 2019: 4 · 2018: 3 · 2017: 4 · 2016: 5 · 2015: 8 · 2013: 1
- FWCI
- 0.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neuropsychology Review (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Mayo Clinic
- National Institutes of Health
- National Institute on Aging (F32AG044054, P01AG036694)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Cancer-related cognitive impairment studies
- Keywords
- amyloid-beta, Alzheimer's disease, preclinical Alzheimer's disease, neurodegeneration, genetic risk factors, sex differences, cognitive reserve, risk factors, prevention trials
- MeSH terms
- Age Factors, Alzheimer Disease, Atrophy, Brain, Cognition, Female, Humans, Male, Memory Disorders, Risk Factors, Sex Factors, Biomarkers, Amyloid beta-Peptides
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