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Mild cognitive impairment due to Alzheimer disease in the community
Open accessAbstract
Objective: The newly proposed National Institute on Aging–Alzheimer's Association (NIA‐AA) criteria for mild cognitive impairment (MCI) due to Alzheimer disease (AD) suggest a combination of clinical features and biomarker measures, but their performance in the community is not known. Methods: The Mayo Clinic Study of Aging (MCSA) is a population‐based longitudinal study of nondemented subjects in Olmsted County, Minnesota. A sample of 154 MCI subjects from the MCSA was compared to a sample of 58 amnestic MCI subjects from the Alzheimer's Disease Neuroimaging Initiative 1 (ADNI‐1) to assess the applicability of the criteria in both settings and to assess their outcomes. Results: Fourteen percent of MCSA and 16% of ADNI‐1 of subjects were biomarker negative. In addition, 14% of MCSA and 12% of ADNI‐1 subjects had evidence for amyloid deposition only, whereas 43% of MCSA and 55% of ADNI‐1 subjects had evidence for amyloid deposition plus neurodegeneration (magnetic resonance imaging atrophy, fluorodeoxyglucose positron emission tomography hypometabolism, or both). However, a considerable number of subjects had biomarkers inconsistent with the proposed AD model; for example, 29% of MCSA subjects and 17% of ADNI‐1 subjects had evidence for neurodegeneration without amyloid deposition. These subjects may not be on an AD pathway. Neurodegeneration appears to be a key factor in predicting progression relative to amyloid deposition alone. Interpretation: The NIA‐AA criteria apply to most MCI subjects in both the community and clinical trials settings; however, a sizeable proportion of subjects had conflicting biomarkers, which may be very important and need to be explored. Ann Neurol 2013;74:199–208
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“The rate of cognitive decline is significantly greater for cognitively impaired and CU individuals who have abnormalities in both an amyloid biomarker and a second biomarker type (which could be CSF T-tau or P-tau, atrophy, or hypometabolism) in comparison to individuals who have neither or only one of these biomarker abnormalities [30–35,39,40,42–45].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [39]
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“However, the combination of an abnormal MRI, CSF T-tau, or FDG PET study with an abnormal amyloid biomarker provides much more powerful prediction of future cognitive decline [30–35,39,40,42–45] than an abnormal amyloid study alone.”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [39]
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“studies assessing biomarkers for Alzheimer's disease with PET scans have reported that about half of people with MCI have Alzheimer's-related brain changes.230,231”
From 2023 Alzheimer's disease facts and figures (2023) · cites this paper as [230]
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“Meanwhile, studies assessing biomarkers for Alzheimer's disease with PET scans have reported that about half of people with MCI have Alzheimer's‐related brain changes.”
From 2024 Alzheimer's disease facts and figures (2024) · cites this paper as [246]
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“MCI with negative biomarkers versus 1 or more AD pathology biomarkers (ie, AD pattern in CSF, high amyloid load in amyloid PET) or biomarkers of neurodegeneration (eg, AD pattern on structural MRI or fluorodeoxyglucose [FDG]-PET; high CSF tau and phospho-tau levels) has a 2 to 3 relative risk of progression to dementia (8% vs 17%-22% per year 33 ).”
From The Alzheimer’s Disease Clinical Spectrum (2019) · cites this paper as [33]
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Self-citationAlbert, M. S., DeKosky, S. T., Dickson, D., Dubois, B., Feldman, H. H., Fox, N. C., Gamst, A., Holtzman, D. M., Jagust, W. J., Petersen, R. C., et al. (2011) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.03.008 · Cited by 10,152
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Fischl, B. R., & Dale, A. M. (2000) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.200033797 · Cited by 5,995
Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade
Jack, C. R., Knopman, D. S., Jagust, W. J., Shaw, L. M., Aisen, P. S., Weiner, M. W., Petersen, R. C., & Trojanowski, J. Q. (2010) · The Lancet Neurology · doi:10.1016/s1474-4422(09)70299-6 · Cited by 4,806
Self-citationJack, C. R., Knopman, D. S., Jagust, W. J., Petersen, R. C., Weiner, M. W., Aisen, P. S., Shaw, L. M., Vemuri, P., Wiste, H. J., Weigand, S. D., et al. (2013) · The Lancet Neurology · doi:10.1016/s1474-4422(12)70291-0 · Cited by 4,396
Self-citationKaplan, E., Goodglass, H., Weıntraub, S., & Segal, O. (2001) · Medical Entomology and Zoology · Cited by 4,378
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NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease
Jack, C. R., Bennett, D. A., Blennow, K., Carrillo, M. C., Dunn, B., Haeberlein, S. B., Holtzman, D. M., Jagust, W., Jessen, F., Karlawish, J., et al. (2018) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2018.02.018 · Cited by 10,537
Self-citation2023 Alzheimer's disease facts and figures
(2023) · Alzheimer's & Dementia · doi:10.1002/alz.13016 · Cited by 3,212
Knopman, D. S., Amieva, H., Petersen, R. C., Chételat, G., Holtzman, D. M., Hyman, B. T., Nixon, R. A., & Jones, D. T. (2021) · Nature Reviews Disease Primers · doi:10.1038/s41572-021-00269-y · Cited by 2,606
Self-citation2024 Alzheimer's disease facts and figures
(2024) · Alzheimer's & Dementia · doi:10.1002/alz.13809 · Cited by 2,536
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Metadata
- Authors
- Petersen, R. C., Aisen, P., Boeve, B. F., Geda, Y. E., Ivnik, R. J., Knopman, D. S., Mielke, M., Pankratz, V. S., Roberts, R., Rocca, W. A., Weigand, S., Weiner, M., Wiste, H., & Jack, C. R.
- Affiliations
- Mayo Clinic (US)
- University of California San Diego (US)
- University of California, San Francisco (US)
- Corresponding author
- Petersen, Ronald C.
- ORCID
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2013-08
- Volume
- 74
- Issue
- 2
- Pages
- 199-208
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- PMC
- PMC3804562
- OpenAlex
- W1559001474
- Cited by
- 265
- References
- 51
- Citations by year
- 2026: 11 · 2025: 11 · 2024: 15 · 2023: 13 · 2022: 16 · 2021: 21 · 2020: 18 · 2019: 31 · 2018: 25 · 2017: 26 · 2016: 28 · 2015: 25 · 2014: 18 · 2013: 7
- FWCI
- 18.42
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health (5u01ag024904-10)
- Canadian Institutes of Health Research
- National Institute on Aging (U01-AG-024904, R01AG034676, P30AG010129, U01AG006786, K01AG030514, R01AG011378, R01AG041851, P50AG016574)
- 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
- Health Sciences › Medicine › Oncology › Cancer-related cognitive impairment studies
- Keywords
- mild cognitive impairment, Alzheimer's disease, NIA-AA criteria, amyloid deposition, neurodegeneration, biomarkers, amyloid PET, FDG-PET hypometabolism, brain atrophy, conversion to dementia, Mayo Clinic Study of Aging, non-demented elderly
- MeSH terms
- Aged, Aged, 80 and over, Aging, Alzheimer Disease, Amyloid, Female, Humans, Male, Neuropsychological Tests, Random Allocation, Residence Characteristics, Biomarkers, Cognitive Dysfunction
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