Lauren Walker (United Kingdom)
Newacstle University
Translational and Clinical Research Institute
Dr. Lauren Walker is an Alzheimer's Research UK fellow at the Translational and Clinical Research Institute at Newcastle University. Her research focusses on neurodegenerative diseases that affect the ageing brain, with a particular interest on the impact of multiple pathologies in the clinical and pathological phenotypes of Lewy body diseases. Her studies have mainly focussed on histological evaluation of human post-mortem tissue and uses high-throughput automated quantitative neuropathological assessment from extensively clinically characterised cases, with the aim of teasing out distinct subtypes of neurodegenerative diseases. Current research aims are to incorporate in vivo studies to investigate when the onset of pathology may have an impact on the clinical and neuropathological outcomes of mixed dementia.

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INVESTIGATING THE PREVALENCE AND SEVERITY OF CEREBRAL AMYLOID ANGIOPATHY IN LEWY BODY DISEASE.

Session Name
0840 - CONGOPHILIC AMYLOID ANGIOPATHY (CAA), VASCULAR DEMENTIA, VASCULAR DAMAGE IN DEMENTIA, BLOOD-BRAIN BARRIER, ARIA (ID 48)
Session Type
SYMPOSIUM
Date
Thu, 17.03.2022
Session Time
05:15 PM - 07:15 PM
Room
ONSITE: 112
Lecture Time
05:45 PM - 06:00 PM
Presenter

Abstract

Aims

Dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD), collectively known as Lewy body diseases (LBDs) are neuropathologically characterised by the presence of alpha-synuclein. However, it is common for DLB and PDD to also exhibit pathology more commonly 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 and PDD, and if this differs from AD.

Methods

CAA type, severity, and topographical distribution was assessed in human post-mortem tissue from 103 AD cases, 34 DLB cases, and 13 PDD cases. The cortical brain regions assessed included frontal, temporal, parietal, and occipital cortices.

Results

Type 1 CAA was observed in AD and DLB cases (32% and 14% respectively), whilst it was absent in PDD. The occipital lobe was the region most affected by CAA in all cases assessed, however this was closely followed by the frontal cortex (AD 87% of cases, DLB 63%, whilst only 22% of PDD cases were affected by CAA).

Conclusions

Topographical patterns 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 presence of type 1 CAA in DLB and absence in PDD are related to the onset of cognitive symptoms and is a distinguishing factor between LBDs.

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