Neuroprotective Effects of a Multi-Herbal Extract on Axonal and Synaptic Disruption and Cognitive Impairment .

BACKGROUND

Alzheimer's disease (AD) is a multifactorial disorder characterized by cognitive decline. Current available therapeutics for AD have limited clinical benefit. Therefore, preventive therapies for interrupting the development of AD are critically needed. Molecules targeting multifunction to interact with various pathlogical components have been considered to improve the therapeutic efficiency of AD. In particular, herbal medicines with multiplicity of actions produce cognitive benefits on AD. Bugu-M is a multi-herbal extract composed of (Antler form), Gaertn., Mill., and with the ability of its various components to confer resilience to cognitive deficits.

OBJECTIVE

To evaluate the potential of Bugu-M on amyloid-β (Aβ) toxicity and its mechanisms and on cognitive function.

METHODS

We illustrated the effect of Bugu-M on Aβ-evoked toxicity as well as its possible mechanisms to diminish the pathogenesis of AD in rat cortical neurons. For cognitive function studies, 2-month-old female 3×Tg-AD mice were administered 400 mg/kg Bugu-M for 30 days. Behavioral tests were performed to assess the efficacy of Bugu-M on cognitive impairment.

RESULTS

In primary cortical neuronal cultures, Bugu-M mitigated Aβ-evoked toxicity by reducing cytoskeletal aberrations and axonal disruption, restoring presynaptic and postsynaptic protein expression, suppressing mitochondrial damage and apoptotic signaling, and reserving neurogenic and neurotrophic factors. Importantly, 30-day administration of Bugu-M effectively prevented development of cognitive impairment in 3-month-old female 3×Tg-AD mice.

CONCLUSION

Bugu-M might be beneficial in delaying the progression of AD, and thus warrants consideration for its preventive potential for AD.