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Free Content Connecting Ca2 + and Lysosomes to Parkinson Disease

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The neurodegenerative movement disorder Parkinson disease (PD) is prevalent in the aged population. However, the underlying mechanisms that trigger disease are unclear. Increasing work implicates both impaired Ca2+ signalling and lysosomal dysfunction in neuronal demise. Here I aim to connect these distinct processes by exploring the evidence that lysosomal Ca2+ signalling is disrupted in PD. In particular, I highlight defects in lysosomal Ca2+ content and signalling through NAADP-regulated two-pore channels in patient fibroblasts harbouring mutations in the PD-linked genes, GBA1 and LRRK2. As an emerging contributor to PD pathogenesis, the lysosomal Ca2+ signalling apparatus could represent a novel therapeutic target.

Keywords: CA2+; GBA1; LRRK2; LYSOSOMES; NAADP; PARKINSON DISEASE; TPC1; TPC2; TRPML1

Document Type: Review Article

Publication date: June 1, 2016

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  • The MESSENGER is an international peer-reviewed journal, focused on all aspects of messenger-signaling. The MESSENGER is devoted to all aspects of messenger- signaling, from the upstream activation of the receptors of the first messengers to the downstream signaling cascades. Undoubtedly, more novel second messengers will be discovered, expanding the scope of the journal appropriately. The MESSENGER publishes review articles, full research articles and short communications of important new scientific findings on all research aspects of messengers.
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