Lysosomal dysfunction in neurodegenerative diseases

COMMENTARY ON THE LAW

Lysosomal dysfunction in neurodegenerative diseases

Klaudia Tomala 1 , Bożena Gabryel 2

1. Katedra i Zakład Farmacji Fizycznej, Wydział Farmaceutyczny z Oddziałem Medycyny Laboratoryjnej w Sosnowcu, Śląski Uniwersytet Medyczny w Katowicach
2. Zakład Farmakologii Katedry Farmakologii, Wydział Lekarski w Katowicach, Śląski Uniwersytet Medyczny w Katowicach

Published: 2017-05-04
DOI: 10.5604/01.3001.0010.3814
GICID: 01.3001.0010.3814
Available language versions: en pl
Issue: Postepy Hig Med Dosw 2017; 71 : 291-306

 

Abstract

Recent data advocate for the implication of lysosomes in the development of programmed cell death. Lysosomal dysfunction decreased the efficiency of autophagosome/lysosome fusion that leads to vacuolation of cells. Autophagic vacuoles containing damaged organelles and altered proteins are hallmarks in most neurodegenerative disorders. These aggregates consequently disrupt cellular homeostasis causing neuronal cell death due apoptosis or necrosis. Moreover calpain mediated or mutation inducted lysosomal rupture result in release of lysosomal cathepsins into the cytoplasm and inducing neuronal cell death. In this review we emphasize the pathophysiological mechanism connecting disrupting autophagy – lysosomal pathway and lysosomal dysfunction in neuronal cell death called lysosomal cell death.

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