Is Innate Immunity and Inflammasomes Involved in Pathogenesis of Amyotrophic Lateral Sclerosis (ALS)?

Area of Science:

• Neuroscience
• Immunology
• Biochemistry

Background:

• Amyotrophic Lateral Sclerosis (ALS) is a progressive, irreversible neurodegenerative disease affecting motor neurons.
• Both sporadic (sALS) and familial (fALS) forms share similar pathology, with potential roles for oxidative stress and neuroinflammation.

Purpose of the Study:

• To review biochemical and immunological biomarkers and pathogenic mechanisms in ALS.
• To evaluate the role of inflammasomes and related pathways in ALS pathogenesis.
• To discuss recent patents related to ALS treatment and therapeutic targets.

Main Methods:

• Literature review focusing on biochemical and immunological aspects of ALS.
• Analysis of proposed pathogenic mechanisms including oxidative stress, protein aggregation, and neuroinflammation.
• Summary and evaluation of relevant patents from 2014.

Main Results:

• Key biochemical and immunological factors implicated in ALS include regulatory T cells, pro-inflammatory cytokines, and inflammasome activation (NLRP3, IL-18, IL-1β, caspase-1).
• HMGB-1 (DAMP) and Toll-like receptors/RAGE signaling are also suggested to be involved.
• Numerous patents from 2014 suggest novel therapeutic strategies and targets for ALS.

Conclusions:

• ALS pathogenesis involves complex biochemical and immunological dysregulation.
• Inflammasome activation and associated pathways are critical components of ALS pathology.
• Recent patents offer promising avenues for future ALS therapeutic development.