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<p>Non-Alcoholic Fatty Liver Disease (NAFLD) is increasingly recognized as a systemic disorder with implications far beyond the liver, notably in the progression of cognitive decline and neurodegenerative disorders such as Alzheimer’s disease (AD) and traumatic brain injury (TBI). At the center of this liver-brain axis lies Saroglitazar (SGZ), a dual PPAR-α/γ agonist initially developed for diabetic dyslipidemia. Emerging evidence suggests that SGZ exerts neuroprotective effects via multiple molecular mechanisms, including modulation of oxidative stress, inflammation, and mitochondrial integrity. This review critically evaluates the mechanistic intersections of SGZ’s hepatic and neural actions and proposes a unified framework for its therapeutic impact. We contextualize SGZ’s role alongside alternative therapies, explore its translational readiness, and propose testable hypotheses to guide future research. While preclinical evidence is promising, robust human studies are essential to validate SGZ’s potential in mitigating NAFLD-associated cognitive impairment. This article aims to advance a novel conceptual synthesis and call for integrative strategies targeting the hepato-neuro axis.</p>

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Saroglitazar at the Crossroads of Metabolic and Neurodegenerative Disease: A Critical Review of the Hepato-Neuro Axis and Translational Horizons

  • 期刊论文

  • 发表日期：

    2025年11月5日

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  • Himanshu Kumar,
  • Kanika Vashisht,
  • Shiv Kumar Kushawaha,
  • Vandana Bhatia,
  • Mahendra Singh Ashawat,
  • Rimpi Arora,
  • Ashish Baldi

摘要

Non-Alcoholic Fatty Liver Disease (NAFLD) is increasingly recognized as a systemic disorder with implications far beyond the liver, notably in the progression of cognitive decline and neurodegenerative disorders such as Alzheimer’s disease (AD) and traumatic brain injury (TBI). At the center of this liver-brain axis lies Saroglitazar (SGZ), a dual PPAR-α/γ agonist initially developed for diabetic dyslipidemia. Emerging evidence suggests that SGZ exerts neuroprotective effects via multiple molecular mechanisms, including modulation of oxidative stress, inflammation, and mitochondrial integrity. This review critically evaluates the mechanistic intersections of SGZ’s hepatic and neural actions and proposes a unified framework for its therapeutic impact. We contextualize SGZ’s role alongside alternative therapies, explore its translational readiness, and propose testable hypotheses to guide future research. While preclinical evidence is promising, robust human studies are essential to validate SGZ’s potential in mitigating NAFLD-associated cognitive impairment. This article aims to advance a novel conceptual synthesis and call for integrative strategies targeting the hepato-neuro axis.