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Review
. 2019 Jul 31:13:1177392819866412.
doi: 10.1177/1177392819866412. eCollection 2019.

Bacopa monnieri, a Neuroprotective Lead in Alzheimer Disease: A Review on Its Properties, Mechanisms of Action, and Preclinical and Clinical Studies

Affiliations
Review

Bacopa monnieri, a Neuroprotective Lead in Alzheimer Disease: A Review on Its Properties, Mechanisms of Action, and Preclinical and Clinical Studies

Aimi Syamima Abdul Manap et al. Drug Target Insights. .

Abstract

Alzheimer disease is a neurodegenerative disease that is signified by cognitive decline, memory loss, and erratic behavior. Till date, no cure for Alzheimer exists and the current Alzheimer medications have limited effectiveness. However, herbal medicines may slow down the disease's progression, which may hopefully reduce the number of cases in the years to come. Numerous studies have been done on characterizing the neuroprotective properties from plants belonging to Scrophulariaceae family, particularly Bacopa monnieri and its polyphenolic compounds known as bacosides. This review presents the findings on bacosides in therapeutic plants and their impact on Alzheimer disease pathology. These reports present data on the clinical, cellular activities, phytochemistry, and biological applications that may be used in new drug treatment for Alzheimer disease.

Keywords: Alzheimer; Bacopa monnieri; aging; bacosides; therapeutic plant.

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Conflict of interest statement

Declaration of conflicting interests:The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Figures

Figure 1.
Figure 1.
Clinical symptoms of Alzheimer disease.
Figure 2.
Figure 2.
Bacopa monnieri plants.
Figure 3.
Figure 3.
Chemical structure of Bacoside A.
Figure 4.
Figure 4.
Neuroprotective effects of bacoside from Bacopa monnieri.
Figure 5.
Figure 5.
The action mechanism of bacoside against ROS induces mitochondrial damage. ROS indicates reactive oxygen species; SOD, superoxide dismutase.
Figure 6.
Figure 6.
Mechanism of action of bacoside against beta-amyloid (adaptation and modifications from previous works,). However, Bacoside A exhibited anti-amyloid toxicity properties upon membrane interactions and bilayer-induced fibrillation of pathogenic substance prion protein (PrP). The experimental data revealed that preincubation of PrP (106-126) with Bacoside A before addition to vesicle bilayers might possibly enhance fibril formation and in parallel had inhibited membrane interactions of the peptide assemblies. The findings from this study revealed a significant interaction of the compound with the amyloidogenic determinant of PrP and noticeable effects upon the structural and functional properties of the peptide even though Bacoside A has not been explored yet in conjunction with the prion protein. In a more extensive context, the anti-amyloid properties of Bacoside A might be discovered to its impact in ameliorating the amyloid protein toxicity via stimulating and enhancing fibrillation.

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