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Neuroprotective Effects of Roots and Its Active Constituents on Scopolamine-Induced Memory Impairment in In Vivo and In Vitro Studies. | LitMetric

Beta-amyloid (Aβ) proteins, major contributors to Alzheimer's disease (AD), are overproduced and accumulate as oligomers and fibrils. These protein accumulations lead to significant changes in neuronal structure and function, ultimately resulting in the neuronal cell death observed in AD. Consequently, substances that can inhibit Aβ production and/or accumulation are of great interest for AD prevention and treatment. In the course of an ongoing search for natural products, the roots of T. Moore ex Baker were selected as a promising candidate with anti-amyloidogenic effects. The ethanol extract of roots, along with its active constituents, not only markedly reduced Aβ production by decreasing β-secretase expression in APP-CHO cells (Chinese hamster ovary cells which stably express amyloid precursor proteins), but also exhibited the ability to diminish Aβ aggregation while enhancing the disaggregation of Aβ aggregates, as determined through the Thioflavin T (Th T) assay. Furthermore, in an in vivo study, the extract of roots showed potential (a tendency) for mitigating scopolamine-induced memory impairment, as evidenced by results from the Morris water maze test and the passive avoidance test, which correlated with reduced Aβ deposition. Additionally, the levels of acetylcholine were significantly elevated, and acetylcholinesterase levels significantly decreased in the brains of mice (whole brains). The treatment with the extract of roots also led to upregulated brain-derived neurotrophic factor (BDNF) and phospho-cAMP response element-binding protein (p-CREB) in the hippocampal region. These findings suggest that the extract of roots, along with its active constituents, may offer neuroprotective effects against AD. Consequently, there is potential for the development of the extract of roots and its active constituents as effective therapeutic or preventative agents for AD.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10675602PMC
http://dx.doi.org/10.3390/ph16111606DOI Listing

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