ArticleBrain pathology (Zurich, Switzerland)2022
Variability in the type and layer distribution of cortical Aβ pathology in familial Alzheimer's disease.
Article in Brain pathology (Zurich, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Clinical and pathologic correlations of machine learning quantification of Aβ deposits across 3 brain regions of decedents with Alzheimer disease.Journal of neuropathology and experimental neurology · 2026Article
- Synapse vulnerability and resilience across the clinical spectrum of dementias.Nature reviews. Neurology · 2025Review
- Layer-Specific Colocalization of Microglia with Amyloid Plaques in the Middle Temporal Gyrus Predicts Cognitive Decline in Alzheimer's Disease.Aging and disease · 2025Article
- Chemical imaging delineates Aβ plaque polymorphism across the Alzheimer's disease spectrum.Nature communications · 2025Article
- Article
- Innovations in Alzheimer's disease diagnostic technologies: clinical prospects of novel biomarkers, multimodal integration, and non-invasive detection.Frontiers in neurology · 2025Review
- Spatial and single-nucleus transcriptomic analysis of genetic and sporadic forms of Alzheimer's disease.Nature genetics · 2024Article
- Novel insights into presenilin 1 mutation associated with a distinctive dementia phenotype and cotton wool plaques.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Article
- Amyloid-β peptide signature associated with cerebral amyloid angiopathy in familial Alzheimer's disease with APPdup and Down syndrome.Acta neuropathologica · 2024Article
- The presenilin 1 mutation P436S causes familial Alzheimer's disease with elevated Aβ43 and atypical clinical manifestations.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Thiophene-Based Ligands for Specific Assignment of Distinct Aβ Pathologies in Alzheimer's Disease.ACS chemical neuroscience · 2024Article
- Spatial Neurolipidomics at the Single Amyloid-β Plaque Level in Postmortem Human Alzheimer's Disease Brain.ACS chemical neuroscience · 2024Article
- Clinical considerations in early-onset cerebral amyloid angiopathy.Brain : a journal of neurology · 2023Review
- Observational
- Presenilin-1 (PSEN1) Mutations: Clinical Phenotypes beyond Alzheimer's Disease.International journal of molecular sciences · 2023Review
- High affinity of β-amyloid proteins to cerebral capillaries: implications in chronic lead exposure-induced neurotoxicity in rats.Fluids and barriers of the CNS · 2023Article
- Expanding the spectrum of amyloid-β plaque pathology: the Down syndrome associated 'bird-nest plaque'.Acta neuropathologica · 2022Article
- 11C-PiB PET can underestimate brain amyloid-β burden when cotton wool plaques are numerous.Brain : a journal of neurology · 2022Article
- Variability in the type and layer distribution of cortical Aβ pathology in familial Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2022Article
- Sex and ethnicity in early-onset Alzheimer's disease biomarkers and global function.Alzheimer's & dementia (Amsterdam, Netherlands)Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Familial Alzheimer's disease (FAD) is caused by autosomal dominant mutations in the PSEN1, PSEN2 or APP genes, giving rise to considerable clinical and pathological heterogeneity in FAD. Here we investigate variability in clinical data and the type and distribution of Aβ pathologies throughout the cortical layers of different FAD mutation cases. Brain tissue from 20 FAD cases [PSEN1 pre-codon 200 (n = 10), PSEN1 post-codon 200 (n = 6), APP (n = 4)] were investigated. Frontal cortex sections were stained immunohistochemically for Aβ, and Nissl to define the cortical layers. The frequency of different amyloid-beta plaque types was graded for each cortical layer and the severity of cerebral amyloid angiopathy (CAA) was determined in cortical and leptomeningeal blood vessels. Comparisons were made between FAD mutations and APOE4 status, with associations between pathology, clinical and genetic data investigated. In this cohort, possession of an APOE4 allele was associated with increased disease duration but not with age at onset, after adjusting for mutation sub-group and sex. We found Aβ pathology to be heterogeneous between cases although Aβ load was highest in cortical layer 3 for all mutation groups and a higher Aβ load was associated with APOE4. The PSEN1 post-codon 200 group had a higher Aβ load in lower cortical layers, with a small number of this group having increased cotton wool plaque pathology in lower layers. Cotton wool plaque frequency was positively associated with the severity of CAA in the whole cohort and in the PSEN1 post-codon 200 group. Carriers of the same PSEN1 mutation can have differing patterns of Aβ deposition, potentially because of differences in risk factors. Our results highlight possible influences of APOE4 genotype, and PSEN1 mutation type on Aβ deposition, which may have effects on the clinical heterogeneity of FAD.
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