Version 1
: Received: 31 January 2022 / Approved: 1 February 2022 / Online: 1 February 2022 (12:49:48 CET)
How to cite:
Espina-Zambrano, Á.G. P53 Protein Modulates Muscle Metabolism and Generates a Non-Genetic Risk Environment that Contributes to Triggering Amyotrophic Lateral Sclerosis. Preprints2022, 2022020013. https://doi.org/10.20944/preprints202202.0013.v1
Espina-Zambrano, Á.G. P53 Protein Modulates Muscle Metabolism and Generates a Non-Genetic Risk Environment that Contributes to Triggering Amyotrophic Lateral Sclerosis. Preprints 2022, 2022020013. https://doi.org/10.20944/preprints202202.0013.v1
Espina-Zambrano, Á.G. P53 Protein Modulates Muscle Metabolism and Generates a Non-Genetic Risk Environment that Contributes to Triggering Amyotrophic Lateral Sclerosis. Preprints2022, 2022020013. https://doi.org/10.20944/preprints202202.0013.v1
APA Style
Espina-Zambrano, Á.G. (2022). P53 Protein Modulates Muscle Metabolism and Generates a Non-Genetic Risk Environment that Contributes to Triggering Amyotrophic Lateral Sclerosis. Preprints. https://doi.org/10.20944/preprints202202.0013.v1
Chicago/Turabian Style
Espina-Zambrano, Á.G. 2022 "P53 Protein Modulates Muscle Metabolism and Generates a Non-Genetic Risk Environment that Contributes to Triggering Amyotrophic Lateral Sclerosis" Preprints. https://doi.org/10.20944/preprints202202.0013.v1
Abstract
Amyotrophic lateral sclerosis (ALS) is also called "motor neuron disease”. In this review, we propose that ALS is not just a neuromotor disorder, but begins as a disorder of P53-modulated skeletal muscle metabolism, leading to failures at the energy state of the cells, incorrect redox states, motor denervation, and a loss of muscle fibers. Motoneurons die as a consequence of the lack of muscular feedback, and the oligomeric TDP43 aggregates progressively and relentlessly lead to mistakes in peripheral immune self-tolerance sustained over time. An effective treatment has not been found for this devastating pathology, as for 152 years the target has not been accurately defined. Scientists and doctors should consider new knowledge regarding ALS and consider immunomodulatory therapies that, based on genetic analysis and symptoms, can be combined with compounds that regulate metabolism and promote the elimination of useless organelles and cells. What if ALS could be cured as a result of seeing motor neuron disease differently? This review aims to develop that goal and change the paradigm of our understanding of ALS.
Medicine and Pharmacology, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
