Spedding M (2025) Does amyotrophic lateral sclerosis (als) have metabolic causes from human evolution?. Cells 14(21):1734. doi: 10.3390/cells14211734 PMID: 41227379
Objective: To evaluate if recent human genetic variants play major roles in Amyotrophic Lateral Sclerosis (ALS), changing metabolism.
Summary: The authors reviewed Cholera Toxin B (CTB) binding as a tool to study GM1 and fucosylated structures, and to cause denervation. Findings suggest CTB may be used as a surrogate marker of GM1. CTB-SAP causes specific motor neuron death, presumably by binding to and downregulating GM1, and possibly other fucosylated targets; powerful evidence linking loss of GM1 to denervation in ALS.
Related Products: CTB-SAP (Cat. #IT-14)
See Also:
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