Neurotoxicity in Diabetes Mellitus: The Role of Mitochondrial Dysfunction and Redox-Sensitive Signalling Pathways
Mugo Moses H.
School of Natural and Applied Sciences Kampala International University Uganda
ABSTRACT
Diabetes mellitus (DM) is a metabolic disorder characterized by chronic hyperglycemia, which exerts profound effects on multiple organ systems, including the nervous system. Neurotoxicity in diabetes is increasingly recognized as a consequence of mitochondrial dysfunction and activation of redox-sensitive signalling pathways. Persistent hyperglycemia induces excessive production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), leading to oxidative stress, mitochondrial damage, and dysregulated cellular signalling. These alterations compromise neuronal bioenergetics, promote inflammation, and precipitate axonal degeneration and synaptic dysfunction. Redox-sensitive transcription factors, including NF-kB, Nrf2, and AP-1, mediate inflammatory and antioxidant responses, while mitochondrial permeability transition, calcium dysregulation, and apoptotic signalling contribute to neuronal death. This review integrates current understanding of the mechanisms underlying diabetic neurotoxicity, highlighting the interplay between mitochondrial impairment and oxidative stress-mediated signalling pathways. Therapeutic strategies targeting mitochondrial function, redox balance, and downstream signalling are discussed, emphasizing their potential to prevent or mitigate diabetic neuropathy and cognitive dysfunction.
Keywords: Diabetes mellitus, neurotoxicity, mitochondrial dysfunction, oxidative stress, redox signaling
CITE AS: Mugo Moses H. (2026). Neurotoxicity in Diabetes Mellitus: The Role of Mitochondrial Dysfunction and Redox-Sensitive Signalling Pathways. IDOSR JOURNAL OF BIOCHEMISTRY, BIOTECHNOLOGY AND ALLIED FIELDS 11(1):6-10. https://doi.org/10.59298/IDOSR/JBBAF/2026/102610