Autosomal dominant and sporadic late onset Alzheimer's disease share a common in vivo pathophysiology
Open accessAbstract
The extent to which the pathophysiology of autosomal dominant Alzheimer's disease corresponds to the pathophysiology of ‘sporadic’ late onset Alzheimer's disease is unknown, thus limiting the extrapolation of study findings and clinical trial results in autosomal dominant Alzheimer's disease to late onset Alzheimer's disease. We compared brain MRI and amyloid PET data, as well as CSF concentrations of amyloid-β42, amyloid-β40, tau and tau phosphorylated at position 181, in 292 carriers of pathogenic variants for Alzheimer's disease from the Dominantly Inherited Alzheimer Network, with corresponding data from 559 participants from the Alzheimer’s Disease Neuroimaging Initiative. Imaging data and CSF samples were reprocessed as appropriate to guarantee uniform pipelines and assays. Data analyses yielded rates of change before and after symptomatic onset of Alzheimer's disease, allowing the alignment of the ∼30-year age difference between the cohorts on a clinically meaningful anchor point, namely the participant age at symptomatic onset. Biomarker profiles were similar for both autosomal dominant Alzheimer's disease and late onset Alzheimer's disease. Both groups demonstrated accelerated rates of decline in cognitive performance and in regional brain volume loss after symptomatic onset. Although amyloid burden accumulation as determined by PET was greater after symptomatic onset in autosomal dominant Alzheimer's disease than in late onset Alzheimer's disease participants, CSF assays of amyloid-β42, amyloid-β40, tau and p-tau181 were largely overlapping in both groups. Rates of change in cognitive performance and hippocampal volume loss after symptomatic onset were more aggressive for autosomal dominant Alzheimer's disease participants. These findings suggest a similar pathophysiology of autosomal dominant Alzheimer's disease and late onset Alzheimer's disease, supporting a shared pathobiological construct.
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Accumulation of Aβ is a hallmark pathological feature in both autosomal dominant AD and sporadic late-onset AD patients.
“The accumulation of Aβ is a hallmark pathological feature in both extensively studied autosomal dominant AD and sporadic late-onset AD patients.110”
From Recent advances in Alzheimer's disease: Mechanisms, clinical trials and new drug development strategies. (2024) · cites this paper as [110]
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Self-citationAisen, P. S. S., Zhou, J., Irizarry, M. C., Kramer, L. D., Swanson, C. J., Dhadda, S., Rabe, M. P., Krause, S., Li, D. J., Raman, R., et al. (2020) · Alzheimer s & Dementia · doi:10.1002/alz.044511 · Cited by 24 · see citing works
Self-citationRoher, A. E., Maarouf, C. L., & Kokjohn, T. A. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-150757 · Cited by 21 · see citing works
Phenotypic Similarities Between Late-Onset Autosomal Dominant and Sporadic Alzheimer Disease
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Self-citationDifferent rates of cognitive decline in autosomal dominant and late‐onset Alzheimer disease
Buckles, V., Xiong, C., Bateman, R. J., Hassenstab, J. J., Allegri, R., Berman, S. B., Chhatwal, J. P., Danek, A., Fagan, A. M., Ghetti, B. F., et al. (2021) · Alzheimer s & Dementia · doi:10.1002/alz.12505 · Cited by 7 · see citing works
Self-citationAssessing the Reliability of Reported Medical History in Older Adults
Day, G. S., Long, A., & Morris, J. C. (2020) · Journal of Alzheimer s Disease · doi:10.3233/jad-200842 · Cited by 5 · see citing works
Self-citation
Flagged first, then by citations
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Zhang, J., Zhang, Y., Wang, J., Xia, Y., Zhang, J., & Chen, L. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01911-3 · Cited by 1,138 · see citing works
Cerebrospinal fluid proteomics define the natural history of autosomal dominant Alzheimer’s disease
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Self-citation
- Authors
- Morris, J. C., Weiner, M., Xiong, C., Beckett, L., Coble, D., Saito, N., Aisen, P. S., Allegri, R., Benzinger, T. L. S., Berman, S. B., Cairns, N. J., Carrillo, M. C., Chui, H. C., Chhatwal, J. P., Cruchaga, C., Fagan, A. M., Farlow, M., Fox, N. C., Ghetti, B., Goate, A. M., Gordon, B. A., Graff-Radford, N., Day, G. S., Hassenstab, J., Ikeuchi, T., Jack, C. R., Jagust, W. J., Jucker, M., Levin, J., Massoumzadeh, P., Masters, C. L., Martins, R., McDade, E., Mori, H., Noble, J. M., Petersen, R. C., Ringman, J. M., Salloway, S., Saykin, A. J., Schofield, P. R., Shaw, L. M., Toga, A. W., Trojanowski, J. Q., Vöglein, J., Weninger, S., Bateman, R. J., & Buckles, V. D.
- Affiliations
- Washington University in St. Louis (US)
- University of California, San Francisco (US)
- University of California, Davis (US)
- University of Southern California (US)
- Fundación para la Lucha contra las Enfermedades Neurológicas de la Infancia (AR)
- University of Pittsburgh (US)
- University of Exeter (GB)
- Alzheimer’s Association , Chicago, IL , USA
- Massachusetts General Hospital (US)
- Indiana University School of Medicine (US)
- UK Dementia Research Institute (GB)
- Indiana University Indianapolis (US)
- Icahn School of Medicine at Mount Sinai (US)
- Department of Neurology, Mayo Clinic , Jacksonville, FL , USA
- Mayo Clinic in Florida (US)
- Brain Research Institute, Niigata University (JP)
- Mayo Clinic (US)
- University of California, Berkeley (US)
- German Center for Neurodegenerative Diseases (DE)
- Munich Cluster for Systems Neurology (DE)
- The University of Melbourne (AU)
- Edith Cowan University (AU)
- Osaka City University (JP)
- Columbia University Irving Medical Center (US)
- Brown University (US)
- UNSW Sydney (AU)
- University of Pennsylvania (US)
- FBRI , Cambridge, MA , USA
- Corresponding author
- Morris, John C
- ORCID
- Morris, John C
- Weiner, Michael
- Xiong, Chengjie
- Beckett, Laurel
- Coble, Dean
- Saito, Naomi
- Allegri, Ricardo
- Benzinger, Tammie L S
- Berman, Sarah B
- Chui, Helena C
- Chhatwal, Jasmeer P
- Cruchaga, Carlos
- Fagan, Anne M
- Farlow, Martin
- Fox, Nick C
- Ghetti, Bernardino
- Goate, Alison M
- Gordon, Brian A
- Day, Gregory S
- Hassenstab, Jason
- Ikeuchi, Takeshi
- Jack, Clifford R
- Jagust, William J
- Jucker, Mathias
- Levin, Johannes
- Massoumzadeh, Parinaz
- Masters, Colin L
- Martins, Ralph
- McDade, Eric
- Mori, Hiroshi
- Noble, James M
- Petersen, Ronald C
- Ringman, John M
- Salloway, Stephen
- Saykin, Andrew J
- Schofield, Peter R
- Shaw, Leslie M
- Toga, Arthur W
- Trojanowski, John Q
- Vöglein, Jonathan
- Weninger, Stacie
- Bateman, Randall J
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2022-05-17
- Volume
- 145
- Issue
- 10
- Pages
- 3594-3607
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC9989348
- OpenAlex
- W4280526065
- Cited by
- 68
- References
- 83
- Citations by year
- 2026: 17 · 2025: 16 · 2024: 19 · 2023: 15 · 2022: 1
- FWCI
- 7.89
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Brain (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Open access LMU (Ludwid Maxmilian's Universitat Munchen) (submittedVersion)
- IUScholarWorks (Indiana University) (submittedVersion)
- Funders
- Alzheimer’s Association (DIAN_ADNI-16-434364)
- Dominantly Inherited Alzheimer Network (U19AG032438)
- National Institute on Aging
- German Center for Neurodegenerative Diseases
- Institute for Neurological Research
- Japan Agency for Medical Research and Development (NP21dk0207049)
- NIHR
- UCL/UCLH
- Biomedical Research Centre
- Dementias Platform UK (MR/L023784/1, MR/009076/1)
- NIH
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- autosomal dominant Alzheimer's disease, late-onset Alzheimer's disease, pathophysiology, amyloid PET, amyloid-beta 42, Aβ40, tau protein, p-tau181, cerebrospinal fluid biomarkers, brain MRI, hippocampal atrophy, cognitive decline, Alzheimer's Disease Neuroimaging Initiative, genetic carriers
- MeSH terms
- Alzheimer Disease, Amyloidosis, Humans, Magnetic Resonance Imaging, Biomarkers, Amyloid beta-Peptides
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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