Molecular Pathology of Amyotrophic Lateral Sclerosis
A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".
Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 2539
Special Issue Editor
Special Issue Information
Dear Colleagues,
Amyotrophic lateral sclerosis (ALS) is a chronic, progressive, degenerative neurological disease affecting motor neurons. Sporadic ALS, which is the most common form of ALS, develops symptoms in early or mid-life, eventually hindering the ability to move, eat, or breathe independently. About 5–10% of ALS cases are genetically inherited (familial ALS), while 90–95% of the cases develop “sporadic” ALS (sALS) in people with no prior family history. Existing evidence supports the conclusion that people who have served in the military are at a greater risk of developing ALS and dying from the disease than those with no history of military service. The recognition of autoimmunity with IL-17 in the blood and spinal fluid is important for diagnosis and therapy. The cause of familial ALS is attributed to the mutations in the senataxin (SETX) gene, TAR DNA Binding Protein 43 kDa (TDP-43), and in the FUS gene on chromosome 16. The sporadic ALS pathogenesis includes autoimmunity, inflammation, and activation of the cGAS/STING pathway. Ultimately, the therapy for sporadic ALS refers to inhibitors of cGAS/STING pathway; inhibitors of NfkappaB, dimethylfumarate; and the inhibitor of PD1.
Dr. Milan Fiala
Guest Editor
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Keywords
- familial ALS
- SETX
- TDP43
- FUS
- sporadic ALS
- trauma
- extranuclear DNA
- autoimmunity
- inflammation
- cGAS/STING pathway
- NikappB
- PD1/PDL1
- dimethylfumarate
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