Alpha lipoic acid ameliorates scopolamine induced memory deficit and neurodegeneration in the cerebello-hippocampal cortex. - GreenMedInfo Summary
Alpha lipoic acid ameliorates scopolamine induced memory deficit and neurodegeneration in the cerebello-hippocampal cortex.
Metab Brain Dis. 2021 May 22. Epub 2021 May 22. PMID: 34021876
Adejoke Elizabeth Memudu
Scopolamine- induced memory loss is used to study new drug discovery in Alzheimer's disease (AD) pathogenesis. This study was aimed at evaluating the role of an antioxidant supplement alpha-lipoic acid (AHA), in ameliorating the oxidative damaging effects of scopolamine on cognition, memory, and the neurohistology of the cerebello-hippocampal cortex. Twenty adult male Wistar rats used were categorized into four (4) groups (n = 5): Group A- Control, Group B- 200 mg/kg of AHA, Group C- Scopolamine (memory-impaired model), and Group D- Neurodegenerative repair model (Scopolamine + AHA). The treatment lasted for fourteen (14) days. Y-maze and hang-wire (limb use test) were used as behavioural index to assess memory and motor function while brain tissues were processed for histology (H and E stain), histochemistry using Cresyl Fast violet stain for Nissl bodies, and immunohistochemistry of astrocytes using glial fibrillary acidic protein (GFAP). Results showed that scopolamine led to a decline in brain weight, impaired memory and motor function, induced oxidative tissue damage cumulating in loss of neuronal cells, chromatolysis, the proliferation of reactive astrocytes (neuroinflammation biomarker) in the cerebello-hippocampal cortex; but upon administration of AHA these neuropathological characterizationswere inhibited and reversed by AHA demonstrating its antioxidant and neuro- repair potential. In conclusion, AHA is a useful therapeutic agent against scopolamine-induced cognitive and memory deficit because it has the ability to ameliorate oxidative tissue damage by attenuating reactive astrocytesproliferation and neuron chromatolysis thereby improving memory and motor function.