**1. Introduction**

Neurodegenerative diseases (NDs) are frequent and often present a pejorative prognosis. Two major systems play a key role in the pathophysiology of NDs, i.e., the canonical Wnt/betacatenin pathway and PPAR gamma. Several studies have demonstrated the opposite interac‐ tion between the canonical Wnt/beta-catenin pathway and the PPAR gamma [1–7]. It has recently been shown that certain NDs can be divided into two classes [8]: on one hand, NDs

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in which the Wnt/beta-catenin pathway is upregulated whereas PPAR gamma is downregu‐ lated. Among these NDs, we find amyotrophic lateral sclerosis (ALS), Parkinson's disease, Huntington's disease and Friedreich's ataxia. PPAR agonists exert protective effects in ALS neurons of transgenic mice and may represent therapeutic targets in human ALS. On the other hand, NDs in which the Wnt-beta-catenin pathway is downregulated while PPAR gamma is upregulated. Among these NDs, we find Alzheimer's disease, bipolar disorder and schizo‐ phrenia. This list is not exhaustive.
