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Polysaccharide alleviates neurodegeneration and behavioral deficit by enhancing mitochondrial autophagy in chronic methamphetamine mice.

Han Yang,Yuanhe Wang,Shan Liu,Shan Zhang,Yuemeng Chen,Jiuyang Ding,Shunqin Chen,Faze Zhu,Bing Xia,Peng Luo,Yubo Liu

Published 2025 in Neurotoxicology

ABSTRACT

Methamphetamine (METH) is a psychostimulant drug widely abused because of its addictive properties.Its impact on the central nervous system is a major area of interest due to its unique ability to cross the blood-brain barrier, facilitated by its dual water and lipid solubility. Studies have indicated that oxidative stress, neuroinflammation, neuronal apoptosis, and mitochondrial dysfunction are primary mechanisms of METH-induced neurotoxicity. Mitophagy, a process regulated by the phosphatase and tensin homolog deleted on chromosome 10 (PTEN) induced kinase 1 (PINK1)/Parkin signaling pathway, has emerged as a critical mechanism for preserving mitochondrial function. Polysaccharides derived from bamboo fungus have shown potential in mitigating neurotoxicity. However, the role of these polysaccharides in ameliorating methamphetamine-induced neurotoxicity remains unclear. This study aimed to investigate whether polysaccharides could alleviate neurodegeneration in a chronic METH mice model and elucidate the underlying mechanisms and elucidate the mechanisms underlying METH-induced neuronal damage. Keywords: Polysaccharide; methamphetamine; neurodegeneration; mitochondrial autophagy; forensic toxicology.

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