Title : Investigating brahmi's neuroprotective effects in chronic traumatic encephalopathy: Insights from a mouse model
Abstract:
Introduction: Chronic Traumatic Encephalopathy (CTE) is a progressive neurodegenerative disorder resulting from repetitive head injuries, often seen in athletes and military personnel. The condition is characterized by the accumulation of hyperphosphorylated tau protein, leading to cognitive decline, memory loss, and behavioral changes. Current therapeutic options are limited, necessitating the exploration of alternative treatments. Brahmi (Bacopa monnieri), a traditional herb renowned for its neuroprotective properties, has shown promise in enhancing cognitive function and promoting neurogenesis. This study investigates the biochemical mechanisms underlying neurogenesis in a mouse model of CTE and evaluates the therapeutic potential of Brahmi in reducing tau pathology.
Objective: The primary objective of this study is to assess the effects of Brahmi on phosphorylated tau protein levels and neurogenic markers in a CTE mouse model. Specifically, we aim to determine whether Brahmi treatment can mitigate tau accumulation and enhance neurogenesis, thereby improving cognitive outcomes.
Methodology: We utilized a well-established mouse model of CTE, inducing chronic neurodegeneration through repeated mild traumatic brain injuries (mTBI). Mice were randomly divided into two groups: one receiving Brahmi extract and the other receiving a placebo. The treatment period lasted eight weeks, during which we conducted biochemical analyses to measure levels of tau protein and P-Tau. Immunohistochemical analysis was performed to assess neuronal proliferation in the hippocampus, utilizing markers such as doublecortin (DCX) to visualize newly formed neurons. Additionally, we conducted behavioral assessments, including the Barnes maze and novel object recognition tests, to evaluate cognitive function and memory retention.
Results: Our findings revealed that CTE induction significantly increased tau protein levels in the brains of control mice, correlating with the expected neurodegenerative pathology. In contrast, the Brahmi-treated group exhibited a notable reduction in tau levels, suggesting a protective effect against tau accumulation. Furthermore, levels of neurotrophic factors such as NeuN and BDNF were elevated in the Brahmi group, indicating enhanced neurogenesis. Immunohistochemical analysis demonstrated increased neuronal proliferation in the hippocampus of Brahmi-treated mice compared to the placebo group, corroborating the biochemical findings. Behavioral assessments revealed that Brahmi treatment led to significant improvements in cognitive function, as evidenced by enhanced performance in both the Morris water maze and novel object recognition tests. Additionally, Brahmi treatment was associated with a reduction in markers of neuroinflammation and oxidative stress in the brains of the treated mice.
Conclusion: These results suggest that Brahmi not only enhances neurogenesis but also provides neuroprotective benefits in the context of CTE by mitigating tau pathology. The reduction in tau levels, alongside improved cognitive function and neurogenic markers, highlights Brahmi's potential as a therapeutic agent for CTE. This study underscores the importance of further investigating herbal treatments in neurodegenerative disorders and supports the need for clinical research into the efficacy of Brahmi in human populations affected by CTE. By establishing a foundation for future studies, this research may pave the way for innovative treatment strategies to combat the effects of CTE and improve patient outcomes.
