Comorbid neuropathological diagnoses in early versus late-onset Alzheimer's disease
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Abstract
Co-pathologies play an important role in the expression of the Alzheimer’s disease clinical phenotype and may influence treatment efficacy. Early-onset Alzheimer’s disease, defined as manifesting before age 65, is viewed as a relatively pure form of Alzheimer’s disease with a more homogeneous neuropathological substrate. We sought to compare the frequency of common neuropathological diagnoses in a consecutive autopsy series of 96 patients with early-onset Alzheimer’s disease (median age of onset = 55 years, 44 females) and 48 with late-onset Alzheimer’s disease (median age of onset = 73 years, 14 females). The UCSF Neurodegenerative Disease Brain Bank database was reviewed to identify patients with a primary pathological diagnosis of Alzheimer’s disease. Prevalence and stage of Lewy body disease, limbic age-related TDP-43 encephalopathy (LATE), argyrophilic grain disease, hippocampal sclerosis, cerebral amyloid angiopathy, and vascular brain injury were compared between the two cohorts. We found at least one non-Alzheimer’s disease pathological diagnosis in 98% of patients with early-onset Alzheimer’s disease (versus 100% of late onset), and the number of comorbid diagnoses per patient was lower in early-onset than in late-onset Alzheimer’s disease (median = 2 versus 3, Mann-Whitney Z = 3.00, P = 0.002). Lewy body disease and cerebral amyloid angiopathy were common in both early and late onset Alzheimer’s disease (cerebral amyloid angiopathy: 86% versus 79%, Fisher exact P = 0.33; Lewy body disease: 49% versus 42%, P = 0.48, respectively), although amygdala-predominant Lewy body disease was more common in early than late onset Alzheimer’s disease (22% versus 6%, P = 0.02). In contrast, LATE (35% versus 8%, P < 0.001), hippocampal sclerosis (15% versus 3%, P = 0.02), argyrophilic grain disease (58% versus 41%, P = 0.052), and vascular brain injury (65% versus 39%, P = 0.004) were more common in late than in early onset Alzheimer’s disease, respectively. The number of co-pathologies predicted worse cognitive performance at the time of death on Mini-Mental State Examination [1.4 points/pathology (95% confidence interval, CI −2.5 to −0.2) and Clinical Dementia Rating-Sum of Boxes (1.15 point/pathology, 95% CI 0.45 to 1.84)], across early and late onset cohorts. The effect of sex on the number of co-pathologies was not significant (P = 0.17). Prevalence of at least one APOE ε4 allele was similar across the two cohorts (52% and 54%) and was associated with a greater number of co-pathologies (+0.40, 95% CI 0.01 to 0.79, P = 0.047), independent of age of symptom onset, sex, and disease duration. Females showed higher density of neurofibrillary tangles compared to males, controlling for age of onset, APOE ε4, and disease duration. Our findings suggest that non-Alzheimer’s disease pathological diagnoses play an important role in the clinical phenotype of early onset Alzheimer’s disease with potentially significant implications for clinical practice and clinical trials design.
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Although clinicians typically attempt to predict the single most likely proteinopathy that underlies an individual's dementia syndrome, a substantial proportion of patients have two or more proteinopathies identified at autopsy.
“Although clinicians typically attempt to predict the single most likely proteinopathy that underlies an individual's dementia syndrome, a substantial proportion of patients have two or more proteinopathies identified at autopsy.28”
From Advances and controversies in frontotemporal dementia: diagnosis, biomarkers, and therapeutic considerations (2022) · cites this paper as [28]
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Self-citationCortical hypometabolism reflects local atrophy and tau pathology in symptomatic Alzheimer’s disease
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- Authors
- Spina, S., La Joie, R., Petersen, C., Nolan, A. L., Cuevas, D., Cosme, C., Hepker, M., Hwang, J.-H., Miller, Z. A., Huang, E. J., Karydas, A. M., Grant, H., Boxer, A. L., Gorno-Tempini, M. L., Rosen, H. J., Kramer, J. H., Miller, B. L., Seeley, W. W., Rabinovici, G. D., & Grinberg, L. T.
- Affiliations
- University of California, San Francisco (US)
- Department of Neurology, Memory and Aging Center, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94158, USA
- Corresponding author
- Spina, Salvatore
- ORCID
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2021-03-09
- Volume
- 144
- Issue
- 7
- Pages
- 2186-2198
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC8502474
- OpenAlex
- W3135857182
- Cited by
- 278
- References
- 78
- Citations by year
- 2026: 53 · 2025: 67 · 2024: 65 · 2023: 41 · 2022: 39 · 2021: 13
- FWCI
- 28.31
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Brain (publishedVersion)
- medRxiv (acceptedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institute for Health (P30-AG062422)
- Alzheimer’s Disease Research Center (P01-AG019724, K99 AG065501, R01 AG045611, AG045333, K08-AG052648, K08-NS114170, K24AG053435, U01 AG057195, U54 NS100717)
- NIH
- 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 › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- Alzheimer's disease, early-onset Alzheimer's disease, late-onset Alzheimer's disease, Lewy body disease, argyrophilic grain disease, hippocampal sclerosis, cerebral amyloid angiopathy, vascular brain injury
- MeSH terms
- Aged, Alzheimer Disease, Brain Diseases, Female, Humans, Male, Middle Aged, Comorbidity, Age of Onset
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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