ArticleActa neuropathologica2018
Patterns and severity of vascular amyloid in Alzheimer's disease associated with duplications and missense mutations in APP gene, Down syndrome and sporadic Alzheimer's disease.
Article in Acta neuropathologica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Plasma amyloid and tau as dementia biomarkers in Down syndrome: Systematic review and meta-analyses.Developmental neurobiology · 2019Pooled it
- APOE and genetic risk variants influence Alzheimer's disease onset in carriers of an extra copy of APP, with and without Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Multiomics and proteomic insights into Alzheimer's disease biology in Down syndrome.Expert review of neurotherapeutics · 2026Review
- Frequency of mixed neuropathologies in individuals with down syndrome with and without Alzheimer's dementia.Acta neuropathologica · 2026Article
- Lifestyle intervention and cognitive outcomes in Down syndrome: a horizon 21 European Down syndrome consortium scoping review.Journal of neurodevelopmental disorders · 2026Article
- Use of anti-amyloid-β monoclonal antibodies in persons with Down syndrome Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Review
- Reviewing the possible connection between cerebral amyloid angiopathy and blood-brain barrier integrity in Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Developments in MRI radiomics research for vascular cognitive impairment.Insights into imaging · 2025Review
- Genetically determined Alzheimer's disease research advances: The Down Syndrome & Autosomal Dominant Alzheimer's Disease 2024 Conference.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Apolipoprotein E abundance is elevated in the brains of individuals with Down syndrome-Alzheimer's disease.Acta neuropathologica · 2025Article
- Microglial activation states and their implications for Alzheimer's Disease.The journal of prevention of Alzheimer's disease · 2025Review
- What Can We Learn About Alzheimer's Disease from People with Down Syndrome?Current topics in behavioral neurosciences · 2025Review
- On the Therapeutic Use of Monoclonal Antibodies Against Amyloid Plaques in Older Adults with Down Syndrome: A Narrative Review and Perspective.Brain sciences · 2024Review
- Amyloid-β peptide signature associated with cerebral amyloid angiopathy in familial Alzheimer's disease with APPdup and Down syndrome.Acta neuropathologica · 2024Article
- Cryo-EM structures of amyloid-β and tau filaments in Down syndrome.Nature structural & molecular biology · 2024Article
- Amyloid Precursor Protein: A Regulatory Hub in Alzheimer's Disease.Aging and disease · 2024Review
- Molecular neuroimaging in dominantly inherited versus sporadic early-onset Alzheimer's disease.Brain communications · 2024Article
- Exploring semantic verbal fluency patterns and their relationship to age and Alzheimer's disease in adults with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Clinical considerations in early-onset cerebral amyloid angiopathy.Brain : a journal of neurology · 2023Review
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 3 countries.
Funding
Abstract
In this study, we have compared the severity of amyloid plaque formation and cerebral amyloid angiopathy (CAA), and the subtype pattern of CAA pathology itself, between APP genetic causes of AD (APPdup, APP mutations), older individuals with Down syndrome (DS) showing the pathology of Alzheimer's disease (AD) and individuals with sporadic (early and late onset) AD (sEOAD and sLOAD, respectively). The aim of this was to elucidate important group differences and to provide mechanistic insights related to clinical and neuropathological phenotypes. Since lipid and cholesterol metabolism is implicated in AD as well as vascular disease, we additionally aimed to explore the role of APOE genotype in CAA severity and subtypes. Plaque formation was greater in DS and missense APP mutations than in APPdup, sEOAD and sLOAD cases. Conversely, CAA was more severe in APPdup and missense APP mutations, and in DS, compared to sEOAD and sLOAD. When stratified by CAA subtype from 1 to 4, there were no differences in plaque scores between the groups, though in patients with APPdup, APP mutations and sEOAD, types 2 and 3 CAA were more common than type 1. Conversely, in DS, sLOAD and controls, type 1 CAA was more common than types 2 and 3. APOE ε4 allele frequency was greater in sEOAD and sLOAD compared to APPdup, missense APP mutations, DS and controls, and varied between each of the CAA phenotypes with APOE ε4 homozygosity being more commonly associated with type 3 CAA than types 1 and 2 CAA in sLOAD and sEOAD. The differing patterns in CAA within individuals of each group could be a reflection of variations in the efficiency of perivascular drainage, this being less effective in types 2 and 3 CAA leading to a greater burden of CAA in parenchymal arteries and capillaries. Alternatively, as suggested by immunostaining using carboxy-terminal specific antibodies, it may relate to the relative tissue burdens of the two major forms of Aβ, with higher levels of Aβ
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.