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<p>Parkinson’s disease (PD) is characterized by the development of chronic neuroinflammation and energy metabolism impairment in the substantia nigra. Here we investigated the role of the lactate receptor GPR81 (HCAR1) and lactate metabolism in the inflammatory cascade in vivo in the lipopolysaccharide (LPS)-induced experimental model of PD. The data obtained suggest that GPR81/HCAR1 and MCT1 are dynamically regulated during the inflammatory response in the substantia nigra and may represent part of a compensatory interaction between lactate signaling and glial activation.</p> Graphical abstract <p></p>

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Early GPR81/MCT1 rise and late lactate–NAD(H) Build-up in an LPS model of PD

  • 期刊论文

  • 发表日期：

    2026年6月1日

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  • Arseniy K. Berdnikov,
  • Natalia A. Kolotyeva,
  • Natalia A. Rozanova ,
  • Svetlana V. Novikova,
  • Anastasia K. Pavlova,
  • Artyom S. Olshanskiy,
  • Alla V. Stavrovskaya,
  • Yulia K. Komleva,
  • Alla B. Salmina

摘要

Parkinson’s disease (PD) is characterized by the development of chronic neuroinflammation and energy metabolism impairment in the substantia nigra. Here we investigated the role of the lactate receptor GPR81 (HCAR1) and lactate metabolism in the inflammatory cascade in vivo in the lipopolysaccharide (LPS)-induced experimental model of PD. The data obtained suggest that GPR81/HCAR1 and MCT1 are dynamically regulated during the inflammatory response in the substantia nigra and may represent part of a compensatory interaction between lactate signaling and glial activation.

Graphical abstract