Identified Potential Causes of Amyotrophic Lateral Sclerosis and Related Possible Treatments

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Degeneration and impaired regeneration of gray matter oligodendrocytes in amyotrophic lateral sclerosis

A specific cause of amyotrophic lateral sclerosis has yet to be determined. This primary article presented evidence for degeneration of oligodendrocytes and a decrease in number of oligodendrocytes present in sufferers of ALS. It aimed to argue that the genes linked with ALS would further increase harm to motor neurons and quicken progression of the disease by targeting oligodendrocyte functionality. In vivo imaging was used to trace oligodendrocytes and progenitor cells in the spinal cord of mice with ALS. It was indeed found that an important glial cell progenitor, known as NG2 sup+ cells, which should normally differentiate into oligodendrocytes, were dysfunctional in the mice with ALS. Furthermore, when deleting the mutation SOD1 from these NG2 sup+ cells, disease onset was considerably delayed. Hence, the study suggested a strong relationship between SOD1 and oligodendrocyte degeneration, and ALS.

Basal ganglia involvement in amyotrophic lateral sclerosis

This primary article aimed to determine whether brain structures – more specifically the basal ganglia – had any role or link with the development of ALS. The study used 44 healthy controls and 39 ALS patients and employed MRI technology to observe 15 structures within the basal ganglia, and to determine any differences in these structures compared to the healthy controls. The results confirmed a link between these structures and ALS with volume decrease in the left caudate nucleus, left hippocampus and right accumbens nucleus. Furthermore, the shape of the bilateral thalami, left hippocampus and left caudate were all affected. These impairments to the basal ganglia were even more pronounced in those patients with the specific C9orf72 hexanucleotide repeat expansion. It is important to note that this article most likely illustrated symptoms of ALS and not causes.

Therapeutic neuroprotective agents for amyotrophic lateral sclerosis

This review aimed to give an overview of possible therapies for amyotrophic lateral sclerosis. This was done by examining the known mechanisms linked with ALS onset and development, and attempting to find neuroprotective agents that might help counter that. The only drug currently available for treatment of ALS has very restricted efficacy, hence new treatments are urgently required. The review collated numerous possible treatments and agents to counter the toxicity, oxidative stress, mitochondrial dysfunction, protein degradation, apoptosis and inflammation that are all typical of the disease. It concludes that these molecules may be effective, and that they should be trialled in drugs to test for any improvements or slowing down/reversing of symptoms. Hence, there appears to be a large variety of directions for ALS treatment research.