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Spotlight on Research

Roy N. Alcalay, M.D.

Roy N. Alcalay, M.D.

"Why do some people who carry genetic mutations associated with Parkinson’s disease (PD) never develop PD while others do?" asks Roy N. Alcalay, M.D., a postdoctoral fellow at the Center for Parkinson’s Disease and Other Movement Disorders...

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Clinical correlates of pathology in the claustrum in Parkinson's disease and dementia with Lewy bodies.

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Neurosci Lett 2009 Sep; 461(1):12-5

Authors: M E Kalaitzakis, R K B Pearce, S M Gentleman

Department of Clinical Neuroscience, Neuropathology Unit, Division of Neuroscience and Mental Health, Imperial College Healthcare NHS Trust, London, UK. michail.kalaitzakis03@imperial.ac.uk

Dementia and visual hallucinations are common complications of Parkinson's disease (PD), yet their patho-anatomical bases are poorly defined. We studied alpha-synuclein (alphaSyn), tau and amyloid-beta (Abeta) pathology in the claustrum of 20 PD cases without dementia, 12 PD cases with dementia (PDD) and 7 cases with dementia with Lewy bodies (DLB). alphaSyn positivity was observed in 75% of PD cases without dementia and in 100% of PDD and DLB cases. Abeta was observed in the claustrum in 25% of PD, 58% of PDD and 100% of DLB cases. Tau was negligible in all cases restricting further analysis. Compared to PD cases without dementia, PDD cases demonstrated a significantly greater alphaSyn burden in the claustrum (p=0.0003). In addition, DLB cases showed a significantly increased alphaSyn deposition when compared to PDD (p=0.02) and PD without dementia (p=0.0002). A similar hierarchy, PD

PMID: 19523504 [PubMed - as supplied by publisher]

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