Glutathione (GSH) is a master antioxidant that counters oxidative stress. Clinical studies have confirmed significant depletion of GSH in the hippocampus and the substantia nigra as an early diagnostic biomarker for Alzheimer's disease (AD) and Parkinson disease (PD), respectively. External agents like anesthetics (inhaled and intravenous) have a different impact on GSH.
View Article and Find Full Text PDFJ Assoc Physicians India
November 2024
In heart failure, sympathetic overdrive is evidenced by norepinephrine spillover, receptor level changes, etc. Beta-blockers continue to be the cornerstone of treatment in patients with chronic heart failure due to their ability to counteract sympathetic overdrive. Extensive clinical research has demonstrated that long-term beta-blocker treatment with metoprolol succinate, carvedilol, or bisoprolol enhances left ventricular function and reverses left ventricular remodeling, decreases hospitalization risk, and increases survival.
View Article and Find Full Text PDFGlutathione (GSH) is a master antioxidant which primarily protects cells from oxidative stress. Clinical studies have found significant depletion of GSH from the hippocampus in patients with mild cognitive impairment (MCI), a transitional stage before conversion to Alzheimer's disease (AD). Significant depletion of GSH is considered an early diagnostic biomarker of AD.
View Article and Find Full Text PDFAlzheimer's disease (AD) is a major neurodegenerative disorder impacting millions of people with cognitive impairment and affecting activities of daily living. The deposition of neurofibrillary tangles of hyperphosphorylated tau proteins and accumulation of amyloid-β (Aβ) are the main pathological characteristics of AD. However, the actual causal process of AD is not yet identified.
View Article and Find Full Text PDFTranscranial electrical stimulation (tES) is increasingly recognized for its potential to modulate cerebral blood flow (CBF) and evoke cerebrovascular reactivity (CVR), which are crucial in conditions like mild cognitive impairment (MCI) and dementia. This study explores the impact of tES on the neurovascular unit (NVU), employing a physiological modeling approach to simulate the vascular response to electric fields generated by tES. Utilizing the FitzHugh-Nagumo model for neuroelectrical activity, we demonstrate how tES can initiate vascular responses such as vasoconstriction followed by delayed vasodilation in cerebral arterioles, potentially modulated by a combination of local metabolic demands and autonomic regulation (pivotal locus coeruleus).
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