Peroxisome proliferator-activated receptor gamma (PPAR-γ) is one of the ligand-activated transcription factors which regulates a number of central events and considered as a promising target for various neurodegenerative disease conditions. Numerous reports implicate that PPAR-γ agonists have shown neuroprotective effects by regulating genes transcription associated with the pathogenesis of neurodegeneration. In regards, this review critically appraises the recent knowledge of PPAR-γ receptors in neuroprotection in order to hypothesize potential neuroprotective mechanism of PPAR-γ agonism in chronic neurological conditions. Of note, the PPAR-γ′s interaction dynamics with PPAR-γ coactivator-1α (PGC-1α) has gained significant attention for neuroprotection. Likewise, a plethora of studies suggest that the PPAR-γ pathway can be actuated by the endogenous ligands present in the CNS and thus identification and development of novel agonist for the PPAR-γ receptor holds a vow to prevent neurodegeneration. Together, the critical insights of this review enlighten the translational possibilities of developing novel neuroprotective therapeutics targeting PPAR-γ for various neurodegenerative disease conditions.

过氧化物酶体增殖物激活受体 γ (PPAR-γ) 是配体激活的转录因子之一，可调节许多中心事件，并被认为是各种神经退行性疾病的有希望的靶标。许多报告表明 PPAR-γ 激动剂通过调节与神经变性发病机制相关的基因转录显示出神经保护作用。在这方面，这篇综述批判性地评价了 PPAR-γ 受体在神经保护中的最新知识，以假设 PPAR-γ 激动在慢性神经系统疾病中的潜在神经保护机制。值得注意的是，PPAR-γ 与 PPAR-γ 辅激活因子-1α (PGC-1α) 的相互作用动力学在神经保护方面受到了极大的关注。同样地，大量研究表明，PPAR-γ 通路可以被 CNS 中存在的内源性配体激活，因此鉴定和开发 PPAR-γ 受体的新型激动剂有望防止神经变性。总之，这篇综述的重要见解启发了开发针对各种神经退行性疾病的 PPAR-γ 的新型神经保护疗法的转化可能性。