Neurological manifestations of autosomal dominant familial Alzheimer’s disease: a comparison of the published literature with the Dominantly Inherited Alzheimer Network observational study (DIAN-OBS)
Open accessAbstract
Background Autosomal dominant familial Alzheimer's disease (ADAD) is a rare disorder with non-amnestic neurological symptoms in some clinical presentations. We aimed to compile and compare data from symptomatic participants in the Dominantly Inherited Alzheimer Network observational study (DIAN-OBS) with those reported in the literature to estimate the prevalences of non-amnestic neurological symptoms in participants with ADAD.Methods We prospectively collected data from the DIAN-OBS database, which recruited participants from study centres in the USA, Europe, and Australia, between Feb 29, 2008, and July 1, 2014. We also did a systematic review of publications to extract individual-level clinical data for symptomatic participants with ADAD. We used data for age of onset (from first report of cognitive decline), disease course from onset to death, and the presence of 13 neurological findings that have been reported in association with ADAD. Using multivariable linear regression, we investigated the prevalences of various non-amnestic neurological symptoms and the contributions of age of onset and specific mutation type on symptoms.Findings The DIAN-OBS dataset included 107 individuals with detailed clinical data (forming the DIAN-OBS cohort). Our systematic review yielded 188 publications reporting on 1228 symptomatic individuals, with detailed neurological examination descriptions available for 753 individuals (forming the published data cohort). The most prevalent non-amnestic cognitive manifestations in participants in the DIAN-OBS cohort were those typical of mild to moderate Alzheimer's disease, including visual agnosia (55·1%, 95% CI 45·7-64·6), aphasia (57·9%, 48·6-67·3), and behavioural changes (61·7%, 51·5-70·0). Non-amnestic cognitive manifestations were less prevalent in the published data cohort (eg, visual agnosia [5·6%, 3·9-7·2], aphasia [23·0%, 20·0-26·0], and behavioural changes [31·7%, 28·4-35·1]). Prevalence of non-cognitive neurological manifestations in the DIAN-OBS cohort was low, including myoclonus and spasticity (9·3%, 95% CI 3·8-15·0), and seizures (2·8%, 0·5-5·9) and moderate for parkinsonism (11·2%, 5·3-17·1). By constrast, prevalence was higher in the published data cohort for myoclonus and spasticity (19·4%, 16·6-22·2 and 15·0%, 12·5-17·6, respectively), parkinsonism (12·5%, 10·1-15·0), and seizures (20·3%, 17·4-23·2). In an analysis of the published data cohort, ischaemic stroke was more prevalent at older ages of onset of symptoms of ADAD (odds ratio 1·09 per 1 year increase in age of onset, 95% CI 1·04-1·14, p=0·0003); and motor symptoms were more common at younger age of onset (myoclonus 0·93, 0·90-0·97, p=0·0007; seizures 0·95, 0·92-0·98, p=0·0018; corticobulbar deficits 0·91, 0·86-0·96, p=0·0012; and cerebellar ataxia 0·82, 0·74-0·91, p=0·0002). In the DIAN-OBS cohort, non-cognitive symptoms were more common at more severe stages of disease.Interpretation The non-cognitive clinical manifestations of Alzheimer's disease seem to affect a small proportion of participants with mild to moderate ADAD, and are probably influenced by disease severity, environmental, and genetic factors. When evaluating patients with potential ADAD, clinicians should note that cognitive symptoms typical of sporadic Alzheimer's disease are the most consistent finding, with some patients manifesting non-cognitive neurological symptoms. Future work is needed to determine the environmental and genetic factors that cause these neurological symptoms.Funding National Institutes of Health and German Center for Neurodegenerative Diseases.
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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 [38]
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A Review of ApoE4 Interference Targeting Mitophagy Molecular Pathways for Alzheimer's Disease
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Self-citationDiagnosis and Management of Seizures in Neurodegenerative Diseases
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Self-citationNight Watch on the Titanic: Detecting Early Signs of Epileptogenesis in Alzheimer Disease
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Presenilin-1 Mutations Are a Cause of Primary Lateral Sclerosis-Like Syndrome
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Self-citationVisuomotor integration deficits are common to familial and sporadic preclinical Alzheimer’s disease
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Self-citationMolecular neuroimaging in dominantly inherited versus sporadic early-onset Alzheimer’s disease
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Self-citation15 years of longitudinal genetic, clinical, cognitive, imaging, and biochemical measures in DIAN
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Self-citationDoes the Right Focal Variant of Alzheimer’s Disease Really Exist? A Literature Analysis
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Lessons from genetic studies in Alzheimer disease
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Self-citationA Pathogenic Variant p.Phe177Val in PSEN1 Causes Early-Onset Alzheimer’s Disease in a Chinese Family
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HMGB1-mediated neuroinflammation: molecular mechanisms and emerging therapeutic approaches
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Self-citationImaging Clinical Subtypes and Associated Brain Networks in Alzheimer’s Disease
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What contribution can genetics make to predict the risk of Alzheimer's disease?
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Artificial Intelligence based Modern Approaches to Diagnose Alzheimer s
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Az Alzheimer-kór heterogenitása
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Self-citationPosterior Cortical Atrophy Due to Alzheimer Disease in a Person With Down Syndrome
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Parkinsonism in genetic and sporadic Alzheimer's disease
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Sex differences in sleep fragmentation in 5xFAD mice
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Refractory epilepsy in PSEN 1 mutation (I83T)
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- Authors
- Tang, M., Ryman, D. C., McDade, E., Jasielec, M. S., Buckles, V. D., Cairns, N. J., Fagan, A. M., Goate, A., Marcus, D. S., Xiong, C., Allegri, R. F., Chhatwal, J. P., Danek, A., Farlow, M. R., Fox, N. C., Ghetti, B., Graff-Radford, N. R., Laske, C., Martins, R. N., Masters, C. L., Mayeux, R. P., Ringman, J. M., Rossor, M. N., Salloway, S. P., Schofield, P. R., Morris, J. C., & Bateman, R. J.
- Affiliations
- Washington University in St. Louis (US)
- Brigham and Women's Hospital (US)
- German Center for Neurodegenerative Diseases (DE)
- Indiana University School of Medicine (US)
- UCL Queen Square Institute of Neurology (GB)
- Edith Cowan University (AU)
- Mental Health Research Institute (AU)
- Columbia University Irving Medical Center (US)
- University of Southern California (US)
- Brown University (US)
- UNSW Sydney (AU)
- Corresponding author
- Bateman, Randall J
- ORCID
- Tang, Mengxuan
- Ryman, Davis C
- McDade, Eric
- Fagan, Anne M
- Goate, Alison
- Marcus, Daniel S
- Xiong, Chengjie
- Allegri, Ricardo F
- Chhatwal, Jasmeer P
- Danek, Adrian
- Farlow, Martin R
- Fox, Nick C
- Ghetti, Bernardino
- Martins, Ralph N
- Masters, Colin L
- Mayeux, Richard P
- Ringman, John M
- Rossor, Martin N
- Salloway, Stephen P
- Schofield, Peter R
- Morris, John C
- Bateman, Randall J
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2016-12
- Volume
- 15
- Issue
- 13
- Pages
- 1317-1325
- ISSN
- 1474-4422 (ISSN-L)
- PMC
- PMC5116769
- OpenAlex
- W2535940399
- Cited by
- 121
- References
- 31
- Citations by year
- 2026: 10 · 2025: 13 · 2024: 13 · 2023: 9 · 2022: 11 · 2021: 16 · 2020: 20 · 2019: 15 · 2018: 7 · 2017: 5 · 2016: 2
- FWCI
- 7.72
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Lancet Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion, cc-by-nc-nd)
- UNSWorks (University of New South Wales, Sydney, Australia) (submittedVersion, cc-by-nc-nd)
- Minerva Access (University of Melbourne) (submittedVersion, cc-by-nc-nd)
- Edith Cowan University Research Online (Edith Cowan University) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- DZNE Pub (submittedVersion)
- Conicet (submittedVersion, cc-by-nc-sa)
- Funders
- Alzheimer's Association
- Glenn Foundation for Medical Research
- Eli Lilly and Company
- GlaxoSmithKline
- Sanofi
- Biogen
- BrightFocus Foundation
- Washington University in St. Louis
- Cure Alzheimer's Fund
- TauRx Pharmaceuticals
- National Institute for Health and Care Research (NF-SI-0512-10033, NF-SI-0513-10134, MR/009076/1, MR/L023784/1)
- Eisai
- Deutsches Zentrum für Neurodegenerative Erkrankungen (UF1AG032438)
- Foundation for Biomedical Research and Innovation
- Servier
- Dementias Platform UK (MR/L023784/1, MR/009076/1)
- National Institutes of Health
- Genentech
- Novartis Pharma
- Medical Research Council (MR/L023784/1, MR/L023784/2, UF1AG032438, MR/009076/1)
- National Institute on Aging (K23AG049087, UF1AG032438, K23AG046363, P50AG005142, U19AG032438, U01AG032438, U24AG021886)
- 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
- visual agnosia, aphasia, behavior change, myoclonus, spasticity, seizures, age of onset, presenilin mutations, APP mutations, clinical course, prevalence, cognitive decline, clinical phenotype variability, preclinical Alzheimer's disease
- MeSH terms
- Alzheimer Disease, Humans
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