Autosomal-dominant Alzheimer's disease: a review and proposal for the prevention of Alzheimer's disease
Open accessAbstract
Autosomal-dominant Alzheimer's disease has provided significant understanding of the pathophysiology of Alzheimer's disease. The present review summarizes clinical, pathological, imaging, biochemical, and molecular studies of autosomal-dominant Alzheimer's disease, highlighting the similarities and differences between the dominantly inherited form of Alzheimer's disease and the more common sporadic form of Alzheimer's disease. Current developments in autosomal-dominant Alzheimer's disease are presented, including the international Dominantly Inherited Alzheimer Network and this network's initiative for clinical trials. Clinical trials in autosomal-dominant Alzheimer's disease may test the amyloid hypothesis, determine the timing of treatment, and lead the way to Alzheimer's disease prevention.
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Colombia has the largest and most homogeneous family group known to have an early-onset (~35 years of age) form of FAD caused by the autosomal dominant and fully penetrant E280A mutation in PSEN1.
“Interestingly, Colombia has the largest and most homogeneous family group known to have an early‐onset (~35 years of age) form of FAD [54, 59] caused by the autosomal dominant and fully penetrant E280A mutation in PSEN1 [60, 61], which generally produces a more aggressive course of pathology than SAD [55, 56].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [59]
The Clinical presentation of ADAD section says PSEN1-related symptoms typically begin between ages 30 and 50, and the Introduction describes dominantly inherited AD with near-certain disease development in mutation carriers. The paper does not identify a Colombian family as the largest or most homogeneous, give an onset of approximately 35 years for that family, or name the E280A mutation. (LLM, conf=0.85)
Experimental — accuracy not yet measuredA small subset of Alzheimer's disease cases is caused by autosomal-dominant AD mutations in PSEN1, PSEN2, and APP, leading to early-onset AD with amyloid plaques and neurofibrillary tangles.
“While most cases are sporadic (SAD), a small subset is caused by autosomal-dominant AD (ADAD) mutations in presenilin 1 (PSEN1), presenilin 2 (PSEN2), and amyloid precursor protein (APP), leading to early-onset AD with hallmark amyloid plaques and neurofibrillary tangles (Bateman et al., 2011; Bird, 2008; Selkoe and Hardy, 2016).”
From Isogenic human stem cell models reveal mutation-dependent protective mechanisms of APOE3 Christchurch (2026) · cites this paper as Bateman et al., 2011
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 [36]
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- Authors
- Bateman, R. J., Aisen, P. S., De Strooper, B., Fox, N. C., Lemere, C. A., Ringman, J. M., Salloway, S., Sperling, R. A., Windisch, M., & Xiong, C.
- Affiliations
- Washington University in St. Louis (US)
- University of California San Diego (US)
- UCL Queen Square Institute of Neurology (GB)
- Brigham and Women's Hospital (US)
- University of California, Los Angeles (US)
- Brown University (US)
- Corresponding author
- Bateman, Randall J
- ORCID
- Venue
- Alzheimer's Research & Therapy
- Published
- 2010
- Volume
- 3
- Issue
- 1
- Pages
- 1
- ISSN
- 1758-9193 (ISSN-L)
- PMC
- PMC3109410
- OpenAlex
- W2116964904
- Cited by
- 573
- References
- 93
- Citations by year
- 2026: 26 · 2025: 54 · 2024: 49 · 2023: 34 · 2022: 37 · 2021: 63 · 2020: 50 · 2019: 34 · 2018: 36 · 2017: 27 · 2016: 19 · 2015: 30 · 2014: 20 · 2013: 45 · 2012: 29
- FWCI
- 19.89
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Alzheimer s Research & Therapy (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion, other-oa)
- Pure Amsterdam UMC (submittedVersion, other-oa)
- Lirias (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Funders
- National Institute for Health and Care Research (NF-SI-0508-10123)
- Vlaamse regering
- National Institutes of Health
- Medical Research Council
- National Institute on Aging (U19AG010483, U01AG032438)
- National Institute of Neurological Disorders and Stroke (R01NS136122)
- 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, Alzheimer's disease prevention, amyloid hypothesis, sporadic Alzheimer's disease, clinical trials, pathophysiology, amyloid imaging, treatment timing
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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