Therapeutic interventions of Amyotrophic Lateral Sclerosis (ALS)

Authors

  • Ashok Chakraborty AllExcel, Inc., Shelton, CT, USA
  • Anil Diwan

Keywords:

ALS, SOD1, Biomarkers, Glutamate, Protein Aggregation, Neurodegeneration

Abstract

Amyotrophic lateral sclerosis (ALS) is a non-demyelinating neurodegenerative disease mostly found in
adults between 40 to 60 years old. This disease is usually prevalent in males, however it’s irrespective
to the different genders. ALS is progressive and within 2-5 years of diagnosis ulimately ends with
death. The majority of ALS cases is sporadic (90%) and is recorded without any defined aetiology.
The other 10-12% of cases is recognized from mutations in more than 20 genes. The genes reported to
cause ALS are Superoxide Dismutase 1 (SOD1), TAR DNA Binding Protein (TDP), Fused in Sarcoma,
(FUS), Chromosome 9 Open Reading Frame 72 (c9orf72) and Vesicle-Associated Membrane-Protein-
Associated Protein B (VAPB). Furthermore, abnormal lipid metabolism with higher LDL/HDL ratio
was reported in ALS patients. The aetiology of ALS is shown in the schematic diagram below (Figure 1)
Due to the multi-nature of ALS causative factors and symptoms, there is no specific therapy for ALS
today. However, this paper will touch on potential therapies that are in practice or may come up in the
future. The goal is to maintain and improve the function of motor neuron, the well-being and quality
of life for ALS patients. Until then, we have to rely on the symptomatic treatment and rehabilitative
measures to support the patient’s quality of life.

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Published

2022-07-13

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Section

Articles