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Amyotrophic lateral sclerosis (ALS) is one of the most common adult-onset debilitat‐ ing neurodegenerative diseases (NDs) which is characterized by a chronic progres‐ sive degeneration of upper and lower motor neurons, resulting in muscular atrophy, paralysis and ultimately death. It has been established that in ALS, the canonical Wnt/ beta-catenin pathway is upregulated. Peroxisome proliferator-activated receptor gamma (PPAR gamma) generally varies in opposite way compared with the Wnt/betacatenin signaling. Several studies carried out on ALS transgenic mice have shown the beneficial effects induced after treatment by PPAR agonists partly due to antiinflammatory effects induced by PPAR gamma. The coupling between the Wnt/betacatenin signaling and PPAR gamma has led to divide NDs into two classes: NDs in which the Wnt/beta-catenin pathway is upregulated whereas PPAR gamma is downregulated (ALS, Parkinson’s disease, Huntington’s disease and Friedreich’s ataxia); and NDs in which the Wnt-beta-catenin pathway is downregulated while PPAR gamma is upregulated (Alzheimer’s disease, bipolar disorder and schizophrenia).

Amyotrophic Lateral Sclerosis: Role of the Canonical Wnt/Beta- Catenin Pathway and PPAR Gamma