AI Article Synopsis

  • Cognitive impairments can significantly hinder daily life and work performance, and despite many drug developments, most have failed in clinical trials, prompting interest in herbal remedies as a potential treatment for dementia.
  • The study investigated the cognitive effects of a specific herbal remedy and its compounds through various behavioral tests and their influence on key pathological targets in Alzheimer's disease, including amyloid deposition and tau hyperphosphorylation.
  • Findings suggest that the herbal remedy and its active components help improve cognitive function by reducing oxidative damage, regulating neuroinflammation, preventing cell death, and enhancing neural growth, indicating potential for future treatments in neurological disorders.

Article Abstract

Objectives: Cognitive impairments, ranging from mild to severe, adversely affect daily functioning, quality of life, and work capacity. Despite significant efforts in the past decade, more than 200 promising drug candidates have failed in clinical trials. Herbal remedies are gaining interest as potential treatments for dementia due to their long history and safety, making them valuable for drug development. This review aimed to examine the mechanisms behind the effect of on cognitive function.

Methods: This study focused primarily on the effects of and its chemical constituents on cognitive behavioral outcomes including the Morris water maze, the passive avoidance test, and the Y maze, as well as pathogenic targets of cognitive impairment and Alzheimer's disease (AD) like amyloid deposition, amyloid precursor protein, tau hyperphosphorylation, and cognitive decline. Additionally, a thorough evaluation of the mechanisms behind 's impact on cognitive function was conducted. We reviewed the most recent data from preclinical research done on experimental models, particularly looking at 's effects on cognitive decline and AD.

Results: According to recent research, and its bioactive components, stilbene, and emodin, influence cognitive behavioral results and regulate the pathological target of cognitive impairment and AD. Their mechanisms of action include reducing oxidative and mitochondrial damage, regulating neuroinflammation, halting apoptosis, and promoting increased neurogenesis and synaptogenesis.

Conclusion: This review serves as a comprehensive compilation of current experiments on AD and other cognitive impairment models related to the therapeutic effects of . We believe that these findings can serve as a basis for future clinical trials and have potential applications in the treatment of human neurological disorders.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11194523PMC
http://dx.doi.org/10.3831/KPI.2024.27.2.70DOI Listing

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