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Intracortical microelectrodes (IMEs) can be used to restore motor and sensory function as a part of brain-computer interfaces in individuals with neuromusculoskeletal disorders. However, the neuroinflammatory response to IMEs can result in their premature failure, leading to reduced therapeutic efficacy. Mechanically-adaptive, resveratrol-eluting (MARE) neural probes target two mechanisms believed to contribute to the neuroinflammatory response by reducing the mechanical mismatch between the brain tissue and device, as well as locally delivering an antioxidant therapeutic. To create the mechanically-adaptive substrate, a dispersion, casting, and evaporation method is used, followed by a microfabrication process to integrate functional recording electrodes on the material. Resveratrol release experiments were completed to generate a resveratrol release profile and demonstrated that the MARE probes are capable of long-term controlled release. Additionally, our results showed that resveratrol can be degraded by laser-micromachining, an important consideration for future device fabrication. Finally, the electrodes were shown to have a suitable impedance for single-unit neural recording and could record single units .
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http://dx.doi.org/10.1088/1361-6439/ad27f7 | DOI Listing |
Annu Rev Med
September 2025
3Department of Anatomy and Physiology, University of Melbourne, Victoria, Australia.
Chronic cough can coexist with or without pulmonary and extrapulmonary conditions and can be refractory to therapies that improve these associated conditions. It is underlined by cough hypersensitivity, which is characterized by increased cough responses to stimuli that affect the airways and vagally innervated tissues as well as by excessive cough responses to innocuous stimuli, and it is caused by neuroinflammatory and neuropathic mechanisms at both peripheral and central levels. The management of chronic cough starts with exclusion of associated conditions, followed by use of neuromodulators and speech and language therapy.
View Article and Find Full Text PDFPLoS Pathog
September 2025
National Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, China.
Neuroinflammation within the central nervous system (CNS) is recognized as a critical pathological process in meningitic Escherichia coli (E. coli) infection, leading to severe neurodegenerative disorders and long-term sequelae. Astrocyte reactivity plays a pivotal role in driving the neuroinflammatory cascade in response to pathological stimuli from peripheral sources or other cellular components of the CNS.
View Article and Find Full Text PDFInflammopharmacology
September 2025
Department of Pharmacology and Toxicology, Faculty of Pharmacy, October University for Modern Sciences and Arts (MSA University), Giza, Egypt.
The neuroprotective potential of tyrosine kinase inhibitors (TKIs), potent anticancer drugs, was verified against various neurodegenerative insults, but not Huntington's disease (HD). These promising outcomes were due to their ability to modulate various intracellular signalling pathways. Hence, the current study aimed to evaluate the neuroprotective effects of lapatinib and pazopanib in the 3-nitropropionic (3-NP)-induced HD model in rats.
View Article and Find Full Text PDFCNS Drugs
September 2025
Global Health Neurology Lab, Sydney, NSW, 2150, Australia.
Acute ischemic stroke (AIS) remains a leading cause of mortality and long-term disability globally, with survivors at high risk of recurrent stroke, cardiovascular events, and post-stroke dementia. Statins, while widely used for their lipid-lowering effects, also possess pleiotropic properties, including anti-inflammatory, endothelial-stabilizing, and neuroprotective actions, which may offer added benefit in AIS management. This article synthesizes emerging evidence on statins' dual mechanisms of action and evaluates their role in reducing recurrence, improving survival, and mitigating cognitive decline.
View Article and Find Full Text PDFMol Biol Rep
September 2025
Chitkara College of Pharmacy, Chitkara University, Rajpura, 140401, Punjab, India.
Neuroinflammation, a vital protective response for tissue homeostasis, becomes a detrimental force when chronic and dysregulated, driving neurological disorders like Alzheimer's, Parkinson's, and Huntington's diseases. Potassium (K) channels maintain membrane potential and cellular excitability in neurons and glia within the intricate CNS signaling network. Neuronal injury or inflammation can disrupt K channel activity, leading to hyperexcitability and chronic pain.
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