Abstract
Parkinson’s disease dementia (PDD) and dementia with Lewy bodies (DLB) are relentlessly progressive neurodegenerative disorders that are likely to represent two ends of a disease spectrum. It is well established that both are characterised pathologically by widespread cortical Lewy body deposition. However, until recently, the pathophysiological mechanisms leading to neuronal damage were not known. It was also not understood why some cells are particularly vulnerable in PDD/DLB, nor why some individuals show more aggressive and rapid dementia than others. Recent studies using animal and cell models as well as human post-mortem analyses have provided important insights into these questions. Here, we review recent developments in the pathophysiology in PDD/DLB. Specifically, we examine the role of pathological proteins other than α-synuclein, consider particular morphological and physiological features that confer vulnerabilities on some neurons rather than others, and finally examine genetic factors that may explain some of the heterogeneity between individuals with PDD/DLB.
Funder
Alzheimer's Society
Medical Research Council
Alzheimer's UK
Brain Research Trust
National Institute for Health Research
Amgen
European Commission
Parkinson's UK
Wellcome Trust
Engineering and Physical Sciences Research Council
Movement Disorders Society
Economic and Social Research Council
Academy of Medical Sciences
GE Healthcare
Wolfson Foundation
Horizon 2020
Subject
General Pharmacology, Toxicology and Pharmaceutics,General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine
Cited by
34 articles.
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