Cellular and Molecular Mechanisms of Amyotrophic Lateral Sclerosis
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".
Deadline for manuscript submissions: closed (5 November 2021) | Viewed by 8431
Special Issue Editors
Interests: neurodegeneration; neuromuscular disorders; amyotrophic lateral sclerosis; electromyography
Special Issue Information
Dear colleagues,
Amyotrophic lateral sclerosis (ALS), although described as early as 1869, still remains a fatal, minimally treatable disease. The etiology of this disease, which causes degeneration of the upper and lower motoneurons, remains unclear. However, recent years have also brought a significant shift in this issue and more molecular and cellular mechanisms involved in the pathogenesis of ALS are known, which is a necessary prerequisite for finding a relevant therapy.
The era of molecular discovery began in 1993 with the identification of a mutation in the SOD1 gene, and since then more than 30 genes have been discovered whose mutations are involved in the pathogenesis of ALS and which are found in approximately 20% of patients. Molecular mechanisms then intersect with a variety of cellular processes. The most studied cellular processes and mechanisms involved in the pathogenesis of ALS are as follows:
- Mitochondrial dysfunction;
- Oxidative stress;
- Glutamate receptor-mediated excitotoxicity;
- Spinal inhibitory circuits and its disruption;
- Neuroinflammation;
- Intracellular trafficking defects;
- Energy failure;
- Intracellular Ca2+dyshomeostasis;
- Protein misfolding and aggregation;
- Astrocyte alterations.
Knowledge of these processes very slowly brings the possibility of other therapies than just medication with riluzole, which prolongs survival by several months. This is, for example, edaravone targeting oxidative stress, i.e., acting as a free radical scavenger. Another example is the antisense oligonucleotide Tofersen, which is the subject of clinical trials in SOD1 ALS, or the monoclonal antibody ANX005, which targets the inhibition of the classical complement cascade.
The aim of this Special Issue is to update these issues, ideally with a link to clinical practice—i.e., drugs in research that could slowly reach our patients, or the possibility of influencing the damaged cellular process by an alternative method (e.g., supplementation with natural antioxidants if it concerns oxidative stress or nicotinamide riboside supplementation if it is a matter of mitochondrial dysfunction).
We look forward to your contributions.
Dr. Martin Vališ
Dr. Pavlína Hemerková
Guest Editors
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