ArticleActa neuropathologica communications2024
Prevalence, distribution, and severity of cerebral amyloid angiopathy differ between Lewy body diseases and Alzheimer's disease.
Article in Acta neuropathologica communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Longitudinal effects of cerebrovascular reactivity and cerebral pulsatility in cognitively intact older adults with APOE4: links with cognition.GeroScience · 2026Article
- Cognitive decline in Dutch-type hereditary and sporadic cerebral amyloid angiopathy: a 5-year follow-up study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Retinal Microvascular Dysfunction Reflects Vascular and Alzheimer's-Related Pathology in Dementia With Lewy Bodies.CNS neuroscience & therapeutics · 2026Article
- Where do PDD and DLB SYNdromes fit in neuronal alpha-SYNuclein biological frameworks?Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Spatially resolved transcriptomic profiling identifies distinct signatures in parenchymal and vascular microenvironments in Alzheimer's Disease with Cerebral Amyloid Angiopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Pathological insights into cerebral amyloid angiopathy underlying intracerebral haemorrhage: population-based autopsy study.Acta neuropathologica · 2026Article
- Deciphering the role of APOE in cerebral amyloid angiopathy: from genetic insights to therapeutic horizons.Annals of medicine · 2025Review
- Post-Translational Modifications Distinguish Amyloid-β Isoforms in Cerebral Amyloid Angiopathy and Alzheimer's Disease.Journal of neurochemistry · 2025Article
- Article
- Herpesvirus initiation of dementias and autoimmune diseases.Journal of neurovirology · 2025Review
- Implications and opportunities regarding biological frameworks in overt and prodromal dementia with Lewy bodies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Dementia with Lewy bodies and Parkinson disease dementia - the same or different and is it important?Nature reviews. Neurology · 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
- Cerebral microbleeds: prevalence and relationship to clinical features in cognitive impairment with lewy body disease.BMC neurology · 2025Article
- Impact of 6-OHDA injection and microtrauma in the ratHistology and histopathology · 2025Article
- Multivariate Analyses with Two-Step Dimension Reduction for an Association Study BetweenBioengineering (Basel, Switzerland) · 2025Article
- Cerebral amyloid angiopathy: a narrative review.Frontiers in aging neuroscience · 2025Review
- Innovations in Alzheimer's disease diagnostic technologies: clinical prospects of novel biomarkers, multimodal integration, and non-invasive detection.Frontiers in neurology · 2025Review
- Anti-Amyloid Imaging Abnormality in the Era of Anti-Amyloid Beta Monoclonal Antibodies: Recent Updates for the Radiologist.Journal of the Korean Society of Radiology · 2025Review
- Key motor and non-motor features in early dementia with Lewy bodies.Frontiers in neurology · 2025Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Dementia with Lewy bodies (DLB), Parkinson's disease dementia (PDD), and Parkinson's disease (PD) collectively known as Lewy body diseases (LBDs) are neuropathologically characterised by α-synuclein deposits (Lewy bodies and Lewy neurites). However, LBDs also exhibit pathology associated with Alzheimer's disease (AD) (i.e. hyperphosphorylated tau and amyloid β (Aβ). Aβ can be deposited in the walls of blood vessels in the brains of individuals with AD, termed cerebral amyloid angiopathy (CAA). The aim of this study was to investigate the type and distribution of CAA in DLB, PDD, and PD and determine if this differs from AD. CAA type, severity, and topographical distribution was assessed in 94 AD, 30 DLB, 17 PDD, and 11 PD cases, and APOE genotype evaluated in a subset of cases where available. 96.3% AD cases, 70% DLB cases and 82.4% PDD cases exhibited CAA (type 1 or type 2). However only 45.5% PD cases had CAA. Type 1 CAA accounted for 37.2% of AD cases, 10% of DLB cases, and 5.9% of PDD cases, and was not observed in PD cases. There was a hierarchical topographical distribution in regions affected by CAA where AD and DLB displayed the same distribution pattern that differed from PDD and PD. APOE ε4 was associated with severity of CAA in AD cases. Topographical patterns and severity of CAA in DLB more closely resembled AD rather than PDD, and as type 1 CAA is associated with clinical dementia in AD, further investigations are warranted into whether the increased presence of type 1 CAA in DLB compared to PDD are related to the onset of cognitive symptoms and is a distinguishing factor between LBDs. Possible alignment of the the topographical distribution of CAA and microbleeds in DLB warrants further investigation. CAA in DLB more closely resembles AD rather than PDD or PD, and should be taken into consideration when stratifying patients for clinical trials or designing disease modifying therapies.
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