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Updated: Aug 14, 2026

Studying Pre-formed Fibril Induced α-Synuclein Accumulation in Primary Embryonic Mouse Midbrain Dopamine Neurons
Published on: August 16, 2020
Pathophysiology of synuclein aggregation in Lewy body disease
Elizabeta B Mukaetova-Ladinska1, Ian G McKeith
1Institute 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.
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