Autophagy (from Greek, “auto” - oneself, “phagy” - to eat) is an evolutionarily conserved lysosomal degradation and recycling pathway in eukaryotic cells by which cytoplasmic content (proteins, lipids, nucleic acids and polysaccharides) and subcellular organelles such as mitochondria (mitophagy) are delivered to the lysosome. It is induced under conditions such as nutrient starvation, low oxygen levels and absence of growth factors and is essential for cell survival, differentiation, development, homeostasis and, in particular circumstances, triggers programmed cell death. Autophagy dysfunction has previously been associated with a variety of diseases such as cancer, muscular disorders (Danon's disease), pathogen infections (Listeria monocytogenes), cerebral ischemia, neurodegeneration, psychiatric disorders and more. The currently Research Topic will focus on autophagy and its dual role - in cell survival and in cell death in the central nervous system (CNS), namely, in neurodegenerative [Alzheimer's disease (AD)], Parkinson's disease (PD), Amyotrophic Lateral Sclerosis (ALS) and Huntington’s disease (HD)], neurodevelopmental [autism spectrum disorders (ASD) and Fragile X syndrome] and psychiatric disorders [schizophrenia, bipolar disorder and unipolar depression].
Postmortem brain findings such as accumulation of double-membrane vesicles resembling autophagosomes in the axonal dystrophic terminals of dysfunctional or degenerating neurons in patients with neurodegenerative diseases, a shift in the expression of autophagy-related proteins in schizophrenia patients and studies indicating that autophagy enhancers induce an anti-depressant-like effect in rodents raise the possibility that aberrant autophagy is involved in the pathogenesis of these disorders and that enhancing the process protects against them.
Given the 2016 Nobel Prize in Physiology/Medicine to Yoshinori Ohsumi for his discoveries of mechanisms of autophagy, we believe such a Research Topic is timely.
Autophagy (from Greek, “auto” - oneself, “phagy” - to eat) is an evolutionarily conserved lysosomal degradation and recycling pathway in eukaryotic cells by which cytoplasmic content (proteins, lipids, nucleic acids and polysaccharides) and subcellular organelles such as mitochondria (mitophagy) are delivered to the lysosome. It is induced under conditions such as nutrient starvation, low oxygen levels and absence of growth factors and is essential for cell survival, differentiation, development, homeostasis and, in particular circumstances, triggers programmed cell death. Autophagy dysfunction has previously been associated with a variety of diseases such as cancer, muscular disorders (Danon's disease), pathogen infections (Listeria monocytogenes), cerebral ischemia, neurodegeneration, psychiatric disorders and more. The currently Research Topic will focus on autophagy and its dual role - in cell survival and in cell death in the central nervous system (CNS), namely, in neurodegenerative [Alzheimer's disease (AD)], Parkinson's disease (PD), Amyotrophic Lateral Sclerosis (ALS) and Huntington’s disease (HD)], neurodevelopmental [autism spectrum disorders (ASD) and Fragile X syndrome] and psychiatric disorders [schizophrenia, bipolar disorder and unipolar depression].
Postmortem brain findings such as accumulation of double-membrane vesicles resembling autophagosomes in the axonal dystrophic terminals of dysfunctional or degenerating neurons in patients with neurodegenerative diseases, a shift in the expression of autophagy-related proteins in schizophrenia patients and studies indicating that autophagy enhancers induce an anti-depressant-like effect in rodents raise the possibility that aberrant autophagy is involved in the pathogenesis of these disorders and that enhancing the process protects against them.
Given the 2016 Nobel Prize in Physiology/Medicine to Yoshinori Ohsumi for his discoveries of mechanisms of autophagy, we believe such a Research Topic is timely.