Mild to moderate Alzheimer dementia with insufficient neuropathological changes
Open accessAbstract
Recently, ~16% of participants in an anti-Aβ passive immunotherapy trial for mild-to-moderate Alzheimer disease (AD) had a negative baseline amyloid positron emission tomography (PET) scan. Whether they have AD or are AD clinical phenocopies remains unknown. We examined the 2005-2013 National Alzheimer's Coordinating Center autopsy database and found that ~14% of autopsied subjects clinically diagnosed with mild-to-moderate probable AD have no or sparse neuritic plaques, which would expectedly yield a negative amyloid PET scan. More than half of these "Aβ-negative" subjects have low neurofibrillary tangle Braak stages. These findings support the implementation of a positive amyloid biomarker as an inclusion criterion in future anti-Aβ drug trials.
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The multidomain amnestic dementia phenotype is not specific; it can be the product of other diseases as well as AD.
“Thus, the multidomain amnestic dementia phenotype is not specific; it can be the product of other diseases as well as AD [51].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [51]
The Discussion (page not provided) reports clinical phenocopies of probable AD with insufficient plaques and tangles, supporting the point that an AD-like dementia presentation is not specific to AD pathology. It says their pathological substrate remains elusive, however, and does not establish that other identified diseases produced the phenotype or specifically characterize it as multidomain amnestic. (LLM, conf=0.84)
Experimental — accuracy not yet measuredAD neuropathologic change is documented in approximately 80% of cases with a traditional clinical diagnosis of "AD dementia".
“AD neuropathologic change is documented in approximately 80% of cases with a traditional clinical diagnosis of “AD dementia” (see Fig. 5 for an example of clinical misdiagnosis of “AD dementia”) [50–52,162,185,209–211].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [51]
The Discussion (page unavailable) reports that 22 of 161 (about 14%) people clinically diagnosed with mild-to-moderate probable AD had no or only sparse neuritic plaques, consistent with substantial plaque pathology in roughly 86%. But this was a selected autopsy sample that excluded people with a primary non-AD diagnosis; the paper does not establish that approximately 80% of all traditionally diagnosed “AD dementia” cases have AD neuropathologic change. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe prototypical multidomain amnestic dementia phenotype historically used to define probable AD does not 'rule in' AD pathologic change at autopsy.
“It is now well established that the prototypical multidomain amnestic dementia phenotype historically used to define probable AD [1] does not “rule in” AD pathologic change (which implies change from normal) at autopsy [50–52]”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [51]
The absence of the prototypical multidomain amnestic dementia syndrome does not 'rule out' AD pathologic change.
“and the absence of the syndrome does not “rule out” AD pathologic change.”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [51]
The Discussion examines people who had a clinical diagnosis of probable AD and found that some lacked sufficient AD pathology. That addresses whether the syndrome establishes AD pathology, not whether its absence rules pathology out. Searches for the absence of the syndrome and for AD pathology in cognitively normal people found no passage addressing the claim. (LLM, conf=0.74)
Experimental — accuracy not yet measured
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- Authors
- Serrano‐Pozo, A., Qian, J., Monsell, S. E., Blacker, D., Gómez‐Isla, T., Betensky, R. A., Growdon, J. H., Johnson, K. A., Frosch, M. P., Sperling, R. A., & Hyman, B. T.
- Affiliations
- University of Iowa Hospitals and Clinics (US)
- University of Massachusetts Amherst (US)
- University of Washington (US)
- Harvard University (US)
- Massachusetts General Hospital (US)
- Brigham and Women's Hospital (US)
- Corresponding author
- Hyman, Bradley T.
- ORCID
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2014-04
- Volume
- 75
- Issue
- 4
- Pages
- 597-601
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- PMC
- PMC4016558
- OpenAlex
- W2171032841
- Cited by
- 120
- References
- 23
- Citations by year
- 2026: 3 · 2025: 15 · 2024: 10 · 2023: 10 · 2022: 14 · 2021: 9 · 2020: 11 · 2019: 9 · 2018: 6 · 2017: 9 · 2016: 11 · 2015: 10 · 2014: 3
- FWCI
- 8.40
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (P50 AG0001534, U01AG016976, P50AG005134, P30AG062421)
- 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 PET, neuritic plaques, neurofibrillary tangles, Braak stages, neuropathology, trial inclusion criteria
- MeSH terms
- Aged, Aged, 80 and over, Algorithms, Alzheimer Disease, Apolipoproteins E, Autopsy, Brain, Female, Humans, Male, Mental Status Schedule, Middle Aged, Retrospective Studies, Cohort Studies, Disease Progression
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