There are a variety of types of amyotrophic lateral sclerosis (ALS). Most patients with ALS (90%) are classified into the sporadic type (SALS) without heredity. 5% of SALS and 3%of familial type (FALS) are caused by mutations in the 43-kDa trans-activating response region DNA-binding protein (TDP-43). 20%of FALS are caused by the mutation of Cu, Zn superoxide dismutase (SOD1). Superoxide dismutases (SODs) catalyze the dismutation which reaction breaks down harmful radicals into non-reactive molecules in the cells. Mutated SOD1 leads to the production of ROS that causes neuronal death. Recently, a number of new causal factors have been found to link to the pathogenesis of ALS. Characteristic pathological mechanism of ALS is the function of cytosolic protein aggregates. Normal cell functions are disturbed in the cytosol and lead to abnormal cellular processes such as oxidative stress, excitotoxicity, mitochondrial dysfunction. Matrix metalloproteinases (MMPs) and Tissue inhibitors of metalloproteinases (TIMPs) process physiological tissue remodeling and pathological conditions, both of which include vascular and fibrotic regenerations, angiogenesis and destructive diseases such as ALS and cancers. The Receptor for Advanced Glycation End Products (RAGE) plays an important role in ALS causing inflammation oxidative stress and cellular dysfunction. RAGE is also expressed in neurons, vascular cells, microglia, and astrocytes in the central nervous system (CNS). β-N-methylamino-L-alanine (BMAA) is a potential environmental factor in ALS, which is derived from the cycad plant synthesized by cyanobacteria. BMAA is consumed mainly as cycad flour. Dysfunction of these factors are closely associated with nuclear factor-κB (NF-κB) and activator protein-1 (AP-1) The drugs that suppress activated NF-κB are currently thalidomide, celecoxib and valproic acid. These drugs might slow down the exacerbation of ALS as they are effective for cancers.
| Published in | American Journal of Biomedical and Life Sciences (Volume 10, Issue 5) |
| DOI | 10.11648/j.ajbls.20221005.13 |
| Page(s) | 146-154 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2024. Published by Science Publishing Group |
Amyotrophic Lateral Sclerosis, Thalidomide, Celecoxib, Valproic Acid, Probiotics
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APA Style
Masato Hada, Muhammad Akram. (2022). Prevention with Synbiosis and Treatment with Thalidomide and Celecoxib for Amyotrophic Lateral Sclerosis. American Journal of Biomedical and Life Sciences, 10(5), 146-154. https://doi.org/10.11648/j.ajbls.20221005.13
ACS Style
Masato Hada; Muhammad Akram. Prevention with Synbiosis and Treatment with Thalidomide and Celecoxib for Amyotrophic Lateral Sclerosis. Am. J. Biomed. Life Sci. 2022, 10(5), 146-154. doi: 10.11648/j.ajbls.20221005.13
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Download@article{10.11648/j.ajbls.20221005.13,
author = {Masato Hada and Muhammad Akram},
title = {Prevention with Synbiosis and Treatment with Thalidomide and Celecoxib for Amyotrophic Lateral Sclerosis},
journal = {American Journal of Biomedical and Life Sciences},
volume = {10},
number = {5},
pages = {146-154},
doi = {10.11648/j.ajbls.20221005.13},
url = {https://doi.org/10.11648/j.ajbls.20221005.13},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajbls.20221005.13},
abstract = {There are a variety of types of amyotrophic lateral sclerosis (ALS). Most patients with ALS (90%) are classified into the sporadic type (SALS) without heredity. 5% of SALS and 3%of familial type (FALS) are caused by mutations in the 43-kDa trans-activating response region DNA-binding protein (TDP-43). 20%of FALS are caused by the mutation of Cu, Zn superoxide dismutase (SOD1). Superoxide dismutases (SODs) catalyze the dismutation which reaction breaks down harmful radicals into non-reactive molecules in the cells. Mutated SOD1 leads to the production of ROS that causes neuronal death. Recently, a number of new causal factors have been found to link to the pathogenesis of ALS. Characteristic pathological mechanism of ALS is the function of cytosolic protein aggregates. Normal cell functions are disturbed in the cytosol and lead to abnormal cellular processes such as oxidative stress, excitotoxicity, mitochondrial dysfunction. Matrix metalloproteinases (MMPs) and Tissue inhibitors of metalloproteinases (TIMPs) process physiological tissue remodeling and pathological conditions, both of which include vascular and fibrotic regenerations, angiogenesis and destructive diseases such as ALS and cancers. The Receptor for Advanced Glycation End Products (RAGE) plays an important role in ALS causing inflammation oxidative stress and cellular dysfunction. RAGE is also expressed in neurons, vascular cells, microglia, and astrocytes in the central nervous system (CNS). β-N-methylamino-L-alanine (BMAA) is a potential environmental factor in ALS, which is derived from the cycad plant synthesized by cyanobacteria. BMAA is consumed mainly as cycad flour. Dysfunction of these factors are closely associated with nuclear factor-κB (NF-κB) and activator protein-1 (AP-1) The drugs that suppress activated NF-κB are currently thalidomide, celecoxib and valproic acid. These drugs might slow down the exacerbation of ALS as they are effective for cancers.},
year = {2022}
}
TY - JOUR T1 - Prevention with Synbiosis and Treatment with Thalidomide and Celecoxib for Amyotrophic Lateral Sclerosis AU - Masato Hada AU - Muhammad Akram Y1 - 2022/10/28 PY - 2022 N1 - https://doi.org/10.11648/j.ajbls.20221005.13 DO - 10.11648/j.ajbls.20221005.13 T2 - American Journal of Biomedical and Life Sciences JF - American Journal of Biomedical and Life Sciences JO - American Journal of Biomedical and Life Sciences SP - 146 EP - 154 PB - Science Publishing Group SN - 2330-880X UR - https://doi.org/10.11648/j.ajbls.20221005.13 AB - There are a variety of types of amyotrophic lateral sclerosis (ALS). Most patients with ALS (90%) are classified into the sporadic type (SALS) without heredity. 5% of SALS and 3%of familial type (FALS) are caused by mutations in the 43-kDa trans-activating response region DNA-binding protein (TDP-43). 20%of FALS are caused by the mutation of Cu, Zn superoxide dismutase (SOD1). Superoxide dismutases (SODs) catalyze the dismutation which reaction breaks down harmful radicals into non-reactive molecules in the cells. Mutated SOD1 leads to the production of ROS that causes neuronal death. Recently, a number of new causal factors have been found to link to the pathogenesis of ALS. Characteristic pathological mechanism of ALS is the function of cytosolic protein aggregates. Normal cell functions are disturbed in the cytosol and lead to abnormal cellular processes such as oxidative stress, excitotoxicity, mitochondrial dysfunction. Matrix metalloproteinases (MMPs) and Tissue inhibitors of metalloproteinases (TIMPs) process physiological tissue remodeling and pathological conditions, both of which include vascular and fibrotic regenerations, angiogenesis and destructive diseases such as ALS and cancers. The Receptor for Advanced Glycation End Products (RAGE) plays an important role in ALS causing inflammation oxidative stress and cellular dysfunction. RAGE is also expressed in neurons, vascular cells, microglia, and astrocytes in the central nervous system (CNS). β-N-methylamino-L-alanine (BMAA) is a potential environmental factor in ALS, which is derived from the cycad plant synthesized by cyanobacteria. BMAA is consumed mainly as cycad flour. Dysfunction of these factors are closely associated with nuclear factor-κB (NF-κB) and activator protein-1 (AP-1) The drugs that suppress activated NF-κB are currently thalidomide, celecoxib and valproic acid. These drugs might slow down the exacerbation of ALS as they are effective for cancers. VL - 10 IS - 5 ER -
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