Neuroprotective Effects of Herbal Extracts in Chemically Induced Cognitive Dysfunction

Abstract

Background: Cognitive decline is a hallmark of Alzheimer's disease (AD), a complex condition. There is little clinical benefit to the current AD treatments. Preventive treatments are thus desperately required to stop AD from developing. It has been suggested that molecules that target several functions may interact with different pathological elements to increase the effectiveness of AD treatment. Herbal medications having a variety of effects, in particular, improve AD patients' cognitive function. With the capacity to provide resistance to cognitive deficiencies, Bugu-M is a multi-herbal extract made up of Ganoderma lucidum (Antler form), Nelumbo nucifera Gaertn., Ziziphus jujuba Mill., and Dimocarpus longan. Goal: To assess Bugu-M's potential effects on amyloid-β (Aβ) toxicity, its in vitro processes, and its impact on cognitive function in vivo.
Methods: In rat cortical neurons, we demonstrated Bugu-M's impact on Aβ25–35-evoked toxicity and its potential pathways to reduce the pathophysiology of AD. Two-month-old female 3×Tg-AD mice were given 400 mg/kg Bugu-M for 30 days in order to study cognitive performance. Behavioral assessments were conducted to evaluate Bugu-M's effectiveness in treating cognitive impairment.
Findings: By decreasing cytoskeletal abnormalities and axonal disruption, restoring presynaptic and postsynaptic protein expression, inhibiting mitochondrial damage and apoptotic signaling, and preserving neurogenic and neurotrophic factors, Bugu-M reduced Aβ-evoked toxicity in primary cortical neuronal cultures. Crucially, Bugu-M successfully stopped the development of cognitive impairment in 3-month-old female 3×Tg-AD mice after 30 days of dosing. In conclusion, Bugu-M merits attention for its potential as a preventative measure for AD as it may help slow the disease's course.