Neuropathologic assessment of participants in two multi‐center longitudinal observational studies: The A lzheimer D isease N euroimaging I nitiative (ADNI) and the D ominantly I nherited A lzheimer N etwork (DIAN)
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It has been hypothesized that the relatively rare autosomal dominant A lzheimer disease (ADAD) may be a useful model of the more frequent, sporadic, late‐onset AD (LOAD). Individuals with ADAD have a predictable age at onset and the biomarker profile of ADAD participants in the preclinical stage may be used to predict disease progression and clinical onset. However, the extent to which the pathogenesis and neuropathology of ADAD overlaps with that of LOAD is equivocal. To address this uncertainty, two multicenter longitudinal observational studies, the A lzheimer D isease N euroimaging I nitiative (ADNI) and the D ominantly I nherited A lzheimer N etwork (DIAN), leveraged the expertise and resources of the existing K night A lzheimer D isease R esearch C enter (ADRC) at W ashington U niversity S chool of M edicine, S t. L ouis, M issouri, USA, to establish a N europathology C ore (NPC). The ADNI/DIAN‐NPC is systematically examining the brains of all participants who come to autopsy at the 59 ADNI sites in the USA and C anada and the 14 DIAN sites in the USA (eight), A ustralia (three), UK (one) and G ermany (two). By 2014, 41 ADNI and 24 DIAN autopsies (involving nine participants and 15 family members) had been performed. The autopsy rate in the ADNI cohort in the most recent year was 93% (total since NPC inception: 70%). In summary, the ADNI/DIAN NPC has implemented a standard protocol for all sites to solicit permission for brain autopsy and to send brain tissue to the NPC for a standardized, uniform and state‐of‐the‐art neuropathologic assessment. The benefit to ADNI and DIAN of the implementation of the NPC is very clear. The NPC provides final “gold standard” neuropathological diagnoses and data against which the antecedent observations and measurements of ADNI and DIAN can be compared.
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Studies indicate that familial and sporadic Alzheimer's disease have very similar pathogenesis, pathophysiology, and progression.
“Studies have indicated that the pathogenesis of familial and sporadic Alzheimer’s disease are very similar and share similar pathophysiology and progression36–39.”
From Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease (2019) · cites this paper as [37]
FAD shows significantly different development of associated neuropathology such as TDP-43 and argyrophilic grain disease compared to sAD; in the ADNI sAD cohort the latter two pathologies occurred in about 20% of subjects, while in the FAD DIAN cohort these pathologies were absent.
“In addition, FAD shows significantly different development of associated neuropathology such as TDP-43 and argyrophilic grain disease compared to sAD; in the ADNI sAD cohort the latter two pathologies occurred in about 20% of subjects, while in the FAD DIAN cohort these pathologies were absent [18].”
From Alzheimer's disease: experimental models and reality (2017) · cites this paper as [18]
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Self-citation
- Authors
- Cairns, N. J., Perrin, R. J., Franklin, E. E., Carter, D., Vincent, B., Xie, M., Bateman, R. J., Benzinger, T., Friedrichsen, K., Brooks, W. S., Halliday, G. M., McLean, C., Ghetti, B., Morris, J. C., Initiative, T. A. D. N., & the Dominantly Inherited Alzheimer Network
- Affiliations
- Washington University in St. Louis (US)
- UNSW Sydney (AU)
- The University of Melbourne (AU)
- Indiana University Indianapolis (US)
- Corresponding author
- Cairns, Nigel J.
- ORCID
- Venue
- Neuropathology
- Publisher
- Wiley
- Published
- 2015-05-12
- Volume
- 35
- Issue
- 4
- Pages
- 390-400
- ISSN
- 0919-6544 (ISSN-L)
- 1440-1789
- PMC
- PMC4521391
- OpenAlex
- W1490623534
- Cited by
- 86
- References
- 28
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 9 · 2023: 9 · 2022: 6 · 2021: 12 · 2020: 8 · 2019: 8 · 2018: 9 · 2017: 4 · 2016: 8 · 2015: 2
- FWCI
- 5.59
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neuropathology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- IUScholarWorks (Indiana University) (submittedVersion)
- PMC
- Funders
- National Institutes of Health (P50 AG05681, P01 AG03991, P01 AG26276, U01 AG032438, U01 AG024904, P30-NS048056)
- ALzheimer's Association
- AstraZeneca AB
- Bristol-Myers Squibb
- Eisai Global Clinical Development
- Elan Corporation plc
- Eli Lilly and Company
- Forest Laboratories
- GlaxoSmithKline
- Institute for the Study of Aging
- Merck and Co. Inc.
- National Institute of Biomedical Imaging and Bioengineering
- Novartis Pharmaceuticals Corporation
- Pfizer Inc.
- Wyeth Research
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- autosomal dominant Alzheimer's disease, late-onset Alzheimer's disease, autopsy, preclinical Alzheimer's disease, biomarkers, brain tissue
- MeSH terms
- Aged, 80 and over, Alzheimer Disease, Autopsy, Brain, Female, Humans, Male, Molecular Sequence Data, Organ Preservation, Tissue Banks, Biomarkers, Neuroimaging
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