About this Journal Submit a Manuscript Table of Contents

Implication of Autophagy in Parkinson's Disease

Call for Papers

Parkinson's disease (PD) is a disorder characterised by a progressive degeneration of midbrain neurons in the substantia nigra and by the presence of cytoplasmic protein inclusions. Therefore, the pathogenesis of this disease has been linked to dysfunctions of cellular degradation.

Autophagic dysfunction is emerging as an important topic in the study of neurodegenerative diseases, including PD, in which aggregated proteins appear to play a major role. In this sense, different studies have shown that in the substantia nigra of PD patients there is increased formation of autophagic vacuoles. Paradoxically, although autophagy is an initial process of protection for the cells involved, the recycling of aggregates of proteins that could be toxic to the cell may also play a key role in triggering cell death by execution of an irreversible self-destruction program.

Reflecting a multifactorial disease process, the pattern of cell death in PD is complex, with characteristics of apoptosis and necrosis as well as accumulations of autophagosome-like structures. Interestingly, different types of mutant genes that trigger familial PD encode proteins that act in ubiquitin-dependent proteasomal system, underlining the pathogenic importance of failure of proteolysis in PD.

We invite investigator to contribute original research as well as review articles on research of the role of autophagy in the pathogenesis of PD, and the study of the regulation of the interaction between environmental agents and genes mutations can open new lines of research to improve human health and to clarify different alternatives of therapeutic potential in PD. Potential topics include, but are not limited to:

  • Dysregulation of autophagy in PD
  • Alpha-synuclein degradation by autophagy
  • Impact of glucocerebrosidase-1 mutations in autophagy
  • Mitophagy and PD
  • Pink-1/Parkin and mitophagy deregulation
  • Pesticide-mediated autophagy
  • Involvement of LRRK2 mutants in autophagy changes
  • Autophagy as a possible neuroprotective mechanism in PD

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/pd/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/ according to the following timetable:

Manuscript DueFriday, 26 October 2012
First Round of ReviewsFriday, 18 January 2013
Publication DateFriday, 15 March 2013

Lead Guest Editor

  • Rosa Ana González Polo, Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Departamento de Bioquímica y Biología Molecular y Genética, E. Enfermería y Terapia Ocupacional, Universidad de Extremadura, 10003 Cáceres, Spain

Guest Editors

  • José Manuel Fuentes Rodríguez, Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Departamento de Bioquímica y Biología Molecular y Genética, E. Enfermería y Terapia Ocupacional, Universidad de Extremadura, 10003 Cáceres, Spain
  • Mireia Niso Santano, INSERM, U848, Institut Gustave Roussy, Université Paris Sud, Paris 11, Villejuif, France
  • Lydia Álvarez-Erviti, University Department of Clinical Neurosciences, Institute of Neurology, University College London, London, UK