Molecular Pathology of Lewy Body Diseases

Overview

Journal Int J Mol Sci

Publisher MDPI

Specialties Biochemistry
Chemistry
Molecular Biology

Date 2009 Apr 29

PMID 19399218

Citations 57

Authors

Katrin Beyer

Montserrat Domingo-Sabat

Aurelio Ariza

Affiliations

Soon will be listed here.

Abstract

Lewy body diseases are characterized by the presence of Lewy bodies, alpha-synuclein(AS)-positive inclusions in the brain. Since their main component is conformationally modified AS, aggregation of the latter is thought to be a key pathogenic event in these diseases. The analysis of inclusion body constituents gives additional information about pathways also involved in the pathology of synucleinopathies. Widespread mitochondrial dysfunction is very closely related to disease development. The impairment of protein degradation pathways, including both the ubiquitin-proteasome system and the autophagy-lysosome pathway also play an important role during the development of Lewy body diseases. Finally, differential expression changes of isoforms corresponding to genes primarily involved in Lewy body formation point to alternative splicing as another important mechanism in the development of Parkinson's disease, as well as dementia with Lewy bodies. The present paper attempts to give an overview of recent molecular findings related to the pathogenesis of Lewy body diseases.

Citing Articles

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Modulation of α-synuclein in vitro aggregation kinetics by its alternative splice isoforms.

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Autophagy Markers Are Altered in Alzheimer's Disease, Dementia with Lewy Bodies and Frontotemporal Dementia.

Longobardi A, Catania M, Geviti A, Salvi E, Vecchi E, Bellini S Int J Mol Sci. 2024; 25(2).

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Differential methylation analysis in neuropathologically confirmed dementia with Lewy bodies.

Reho P, Saez-Atienzar S, Ruffo P, Solaiman S, Shah Z, Chia R Commun Biol. 2024; 7(1):35.

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