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Autophagic- and Lysosomal-Related Biomarkers for Parkinson’s Disease: Lights and Shadows

by Helena Xicoy 1,2,3,†, Núria Peñuelas 1,†, Miquel Vila 1,4,5 and Ariadna Laguna 1,*
Neurodegenerative Diseases Research Group, Vall d’Hebron Research Institute (VHIR)-Center for Networked Biomedical Research on Neurodegenerative Diseases (CIBERNED), 08035 Barcelona, Spain
Department of Cell biology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Centre, 6525 GA Nijmegen, The Netherlands
Department of Molecular Animal Physiology, Donders Institute for Brain, Cognition and Behaviour, Donders Centre for Neuroscience, Faculty of Science, 6525 GA Nijmegen, The Netherlands
Department of Biochemistry and Molecular Biology, Autonomous University of Barcelona, 08193 Barcelona, Spain
Catalan Institution for Research and Advanced Studies (ICREA), 08010 Barcelona, Spain
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Cells 2019, 8(11), 1317;
Received: 8 October 2019 / Revised: 21 October 2019 / Accepted: 22 October 2019 / Published: 25 October 2019
(This article belongs to the Special Issue Autophagy in Neurodegenerative Diseases)
Parkinson’s disease (PD) is a neurodegenerative disorder that currently affects 1% of the population over the age of 60 years, for which no disease-modifying treatments exist. This lack of effective treatments is related to the advanced stage of neurodegeneration existing at the time of diagnosis. Thus, the identification of early stage biomarkers is crucial. Biomarker discovery is often guided by the underlying molecular mechanisms leading to the pathology. One of the central pathways deregulated during PD, supported both by genetic and functional studies, is the autophagy-lysosomal pathway. Hence, this review presents different studies on the expression and activity of autophagic and lysosomal proteins, and their functional consequences, performed in peripheral human biospecimens. Although most biomarkers are inconsistent between studies, some of them, namely HSC70 levels in sporadic PD patients, and cathepsin D levels and glucocerebrosidase activity in PD patients carrying GBA mutations, seem to be consistent. Hence, evidence exists that the impairment of the autophagy-lysosomal pathway underlying PD pathophysiology can be detected in peripheral biosamples and further tested as potential biomarkers. However, longitudinal, stratified, and standardized analyses are needed to confirm their clinical validity and utility. View Full-Text
Keywords: Parkinson’s disease; biomarker; autophagy; lysosome; glucocerebrosidase; alpha synuclein Parkinson’s disease; biomarker; autophagy; lysosome; glucocerebrosidase; alpha synuclein
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Xicoy, H.; Peñuelas, N.; Vila, M.; Laguna, A. Autophagic- and Lysosomal-Related Biomarkers for Parkinson’s Disease: Lights and Shadows. Cells 2019, 8, 1317.

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