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Mech Ageing Dev. 2006 Feb;127(2):188-202. Epub 2005 Nov 16.

Pathophysiology of synuclein aggregation in Lewy body disease.

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1
Institute for Ageing and Health, University of Newcastle, Newcastle General Hospital, Westgate Road, Newcastle upon Tyne NE4 6BE, UK. Elizabeta.Mukaetova-Ladinska@ncl.ac.uk

Abstract

We provide an overview of synaptic pathology in dementia with Lewy bodies (DLB) and related neurodegenerative disorders that are characterised by intraneuronal accumulation of alpha-synuclein aggregates. The review addresses the clinico-neuropathological correlates of synaptic pathology in Lewy body disease, and concentrates on: altered alpha-synuclein metabolism, mechanisms leading to alpha-synuclein fibril formation (self-polymerisation, alpha-synuclein mutations and post-translational modifications) and how these influence the axonal transport and synaptic network in ageing and disease process. Understanding the mechanisms leading to intraneuronal alpha-synuclein accumulation are crucial for the development of novel therapies for treatment of Lewy body disease.

PMID:
16297436
DOI:
10.1016/j.mad.2005.09.014
[Indexed for MEDLINE]
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