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Throughout our evolutionary history, physical activity has played a significant role in shaping our physiology. Advances in exercise science have further reinforced this concept by highlighting how exercise can change gene expression and molecular signaling to achieve various beneficial outcomes. Several studies have shown that exercise can alter neuronal functions to prevent neurodegenerative conditions like Parkinson's and Alzheimer's diseases. However, individual genotypes, phenotypes, and varying exercise protocols hinder the prescription of exercise as standard therapy. Moreover, exercise-induced molecular signaling targets can be double-edged swords, making it difficult to use exercise as the primary candidate for beneficial effects. For example, activating PGC-1 alpha and BDNF through exercise could produce several benefits in maintaining brain health, such as plasticity, neuronal survival, memory formation, cognition, and synaptic transmission. However, higher expression of BDNF might playa negative role in bipolar disorder. Therefore, further understanding of a specific mechanistic approach is required. This review focuses on how exercise-induced activation of these molecules could support brain health and discusses the potential underlying mechanisms of the effect of exercise-induced PGC-1 alpha and BDNF on brain health. [ABSTRACT FROM AUTHOR]

Simple Summary: Advances in exercise science have revealed how physical exercise performance can help to shape our physiology. However, individual genetic traits, physical characteristics, and different exercise protocols can affect each molecular target to achieve exercise-induced benefits, and this challenge causes exercise to be prescribed as standard therapy for several pathological conditions. Therefore, each exercise protocol must be thoroughly investigated. Sprint interval training (SIT) influences the brain-derived neurotrophic factor (BDNF) response for maintaining brain health through several possible forms of molecular signaling, which leads to crosstalk that can improve BDNF response. In addition, regulating BDNF levels can provide a protective effect on bipolar disorders since BDNF elevation is associated with bipolar disorders. For example, SNP rs6265 is a single nucleotide substitution that disrupts BDNF secretion and transports and affects its functions to cause neurocognitive impairments. Moderate intensity possesses a protective effect in reducing depression by impacting SNP rs6265 for BDNF secretion, while high-intensity exercise improves locomotor learning by influencing SNP rs6265. This is crucial in terms of reducing depression, schizophrenia, and bipolar disorders and improving mood and cognitive functions. Although no studies have established the link between these genetic variants by SIT protocols for BDNF regulation, HIT protocols are considered to be the same as SIT, which can support SIT, which may affect this genetic variant for BDNF regulation. Moreover, BDNF induces a fatigue mechanism by increasing beta-hydroxybutyrate. This could affect the individual's SIT performance and mood. Physical exercise can significantly impact our bodies, affecting our functional capacity, structure establishment, and molecular makeup. The magnitude of these changes depends on the specific exercise protocols used. For instance, low-to-moderate-intensity exercise can activate important molecular targets in the short term, such as BDNF-mediated signaling, while high-intensity exercise can maintain these signaling molecules in the active state for a longer term. This makes it challenging to recommend specific exercises for obtaining BDNF-induced benefits. Additionally, exercise-induced molecular signaling targets can have positive and negative effects, with some exercises blunting these targets and others activating them. For example, increasing BDNF concentration through exercise can be beneficial for brain health, but it may also have a negative impact on conditions such as bipolar disorder. Therefore, a deeper understanding of a specific exercise-mediated mechanistic approach is required. This review will delve into how the sprint exercise-mediated activation of BDNF could help maintain brain health and explore potential molecular interventions. [ABSTRACT FROM AUTHOR]

A member of the Phyllanthaceae family, Flueggea leucopyrus is a well-known plant in the tribal areas of Sri Lanka, India's Shaurastra region, Australia, and Malaysia. This study provides information about Flueggea leucopyrus, a plant with a wide range of therapeutic uses in India. Different extracts from the leaves and roots of Flueggea leucopyrus were evaluated for their physical and chemical properties, preliminary phytochemical parameters, and pharmacological activities in the current study, followed by their fourier transform infrared spectroscopy (FTIR), gas chromatography-mass spectrometry (GC–MS), antioxidant, and anti-inflammatory properties. The aqueous extract of Flueggea leucopyrus leaves and roots have more different phytochemical elements than other solvent extracts, according to physico-chemical tests and phytochemical screening. As a result, the FT-IR, GC–MS, antioxidant, and anti-inflammatory activities of an aqueous extract were tested. Studies on hind paw edemas caused by carrageenan in albino rats examined the mean increase in paw volume and the percentage inhibition in paw volume at various time points following the injection of carrageenan (1% w/v). In comparison to the norm, these inhibitions were statistically significant (p < 0.001). The aqueous extract of Flueggea leucopyrus leaves and roots have both antioxidative and anti-inflammatory activities, indicating that it has the potential to be used in the formulation of antioxidant and anti-inflammatory medications in the future. [ABSTRACT FROM AUTHOR]