There are currently few clinical strategies in place, which provide effective neuroprotection and repair, despite an intense international effort over the past decades. One possible explanation for this is that a deeper understanding is required of how endogenous mechanisms act to confer neuroprotection. This mini-review reports the proceedings of a recent workshop "Neuroprotection and Neurorepair: New Strategies" (Iguazu Falls, Misiones, Argentina, April 11-13, 2011, Satellite Symposium of the V Neurotoxicity Society Meeting, 2011) in which four areas of active research were identified to have the potential to generate new insights into this field. Topics discussed were (i) metallothionein and other multipotent neuroprotective molecules; (ii) oxidative stress and their signal mediated pathways in neuroregeneration; (iii) neurotoxins in glial cells, and (iv) drugs of abuse with neuroprotective effects.
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http://dx.doi.org/10.1007/s12640-011-9265-8 | DOI Listing |
Brain Commun
January 2025
Neuromuscular Department, Motor Neuron Disease Centre, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.
Neuroinflammation impacts on the progression of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disorder. Specialized pro-resolving mediators trigger the resolution of inflammation. We investigate the specialized pro-resolving mediator blood profile and their receptors' expression in peripheral blood mononuclear cells in relation to survival in ALS.
View Article and Find Full Text PDFToxicol Rep
June 2025
Era College of Pharmacy, Era University, Sarfarajgung, Lucknow-Hardoi Road, Lucknow, Uttar Pradesh, India.
Copper (Cu) dysregulation, often stemming from ATP7B gene mutations, exacerbates neurological disorders like Huntington's, Alzheimer's, and Parkinson's diseases. Monoisoamyl 2,3-dimercaptosuccinic acid (MiADMSA) shows promise in mitigating Cu induced neurotoxicity by chelating intracellular Cu ions, reducing oxidative stress, and restoring antioxidant enzyme function. However, challenges such as poor bioavailability hinder its therapeutic efficacy.
View Article and Find Full Text PDFJ Int Soc Sports Nutr
December 2025
Department of Health and Human Performance, Nova Southeastern University, Davie, FL, USA.
Position Statement: The International Society of Sports Nutrition (ISSN) presents this position based on a critical examination of the literature surrounding the effects of long-chain omega-3 polyunsaturated fatty acid (ω-3 PUFA) supplementation on exercise performance, recovery, and brain health. This position stand is intended to provide a scientific foundation for athletes, dietitians, trainers, and other practitioners regarding the effects of supplemental ω-3 PUFA in healthy and athletic populations. The following conclusions represent the official position of the ISSN: Athletes may be at a higher risk for ω-3 PUFA insufficiency.
View Article and Find Full Text PDFNeuroscience
January 2025
Narula Research, LLC, 107 Boulder Bluff, Chapel Hill, NC 27516, USA.
Neurological disorders significantly impact the central nervous system, contributing to a growing public health crisis globally. The spectrum of these disorders includes neurodevelopmental and neurodegenerative diseases. This manuscript reviews the crucial roles of cellular signalling pathways in the pathophysiology of these conditions, focusing primarily on glutaminase/glutamate/NMDA receptor signalling, alongside the mitogen-activated protein kinase (MAPK) pathways-ERK1/2, C-JNK, and P38 MAPK.
View Article and Find Full Text PDFInflammopharmacology
January 2025
Department of Pharmacology, Central University of Punjab, Bathinda, 151001, Punjab, India.
Alzheimer's Disease (AD), a progressive and age-associated neurodegenerative disorder, is primarily characterized by amyloid-beta (Aβ) plaques and neurofibrillary tangles. Despite advances in targeting Aβ-mediated neuronal damage with anti-Aβ antibodies, these treatments provide only symptomatic relief and fail to address the multifactorial pathology of the disease. This necessitates the exploration of novel therapeutic approaches and a deeper understanding of molecular signaling mechanisms underlying AD.
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