This Research Topic is the second volume of Research Topic "Molecular and Cellular pathways leading to Mitochondrial Dysfunction and Neurodegeneration: Lessons from in vivo models". Please see the first volume
here.
Mitochondria play essential roles in many cellular metabolic and signalling processes, most notably in the production of molecular energy in the form of ATP and in the regulation of cell death. Thus, any dysfunction triggers a plethora of downstream consequences. Impaired mitochondrial function is a pivotal element in many neurodegenerative diseases such as Parkinson´s, Alzheimer´s, Huntington´s as well as many ataxias. Interestingly, a growing body of evidence also indicates that mitochondrial dysfunction might be also a leading cause in schizophrenia, bipolar disorder and other psychiatric disorders. Although mitochondrial alterations might trigger a catastrophic failure, dysregulation of other processes, as a consequence or independently, will likely contribute to cell death. For this reason, it is of paramount importance to unveil and dissect other alterations such as loss of axonal projections and dendrites, problems with migration of neuronal progenitor cells during brain development, impaired glial protection, disruption of synapsis… These alterations might be underlying some of the phenotypic manifestations in many neurodegenerative and neuropsychiatric disorders and are therefore potential targets for pharmacological interventions.
We aim to bring together manuscripts, in the form of either Original Research or Reviews, that target the following topics:
1) mitochondrial metabolism and its role in neurological disorders and neurodevelopmental disorders;
2) mitochondrial homeostasis and axonal degeneration;
3) mitochondria quality control in neurons and glia;
4) oxidative stress signalling in the nervous system;
5) impact of organelle interplay in cellular death of neurons and glia;
6) mitochondria in homeostasis of iron, calcium and other metals;
7) therapeutic avenues in mitochondrial and neurodegenerative diseases.
We expect to collect manuscripts on the aforementioned topics that highlight the relevance of disease models (human, cellular, murine and invertebrate) in our understanding of the neurobiology of these diseases. Of particular interest would be manuscripts that shed light on new pathways involved in degenerative phenotypes by means of genetic or pharmacological screens. We also look forward to articles that review and/or investigate the relation between mitochondria and other cellular organelles in neurodegeneration as well as effects of aging and environmental factors on mitochondria-driven neurodegeneration.
We aim that our collection stimulates further research that will go beyond the state of the art in order to open new avenues for therapeutic approaches that will impact the progression of neurodevelopmental and neurodegenerative disorders.