Publications by authors named "M L Hefti"
Introduction: Efficacy of deep brain stimulation (DBS) is established for several movement and psychiatric disorders. However, the mechanism of action and local tissue changes are incompletely described. We describe neurohistopathological findings of 9 patients who underwent DBS for parkinsonism and performed a systematic literature review on postmortem pathologic reports post-DBS.
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- * Researchers have created a new mouse model that mimics chronic hydrocephalus with normal pressure, displaying similar symptoms to human NPH, including unsteady gait and subtle learning difficulties.
- * This model allows scientists to investigate the underlying neural mechanisms of NPH symptoms using advanced genetic techniques, potentially leading to new treatments.
Article Synopsis
- Excessive production of aldosterone is linked to serious health risks, including heart disease, stroke, dementia, and increased mortality, primarily by promoting sodium retention and consumption.
- Researchers identified specific neurons in the human brain that are sensitive to aldosterone and express a genetic regulator called HSD2, which play a crucial role in salt intake.
- Experimental studies in mice confirmed that these HSD2 neurons are essential for aldosterone-induced salt consumption, suggesting they could be a potential target for treatments aimed at controlling dietary sodium intake.
Article Synopsis
- - Epilepsy and Alzheimer's disease exhibit shared neurodegenerative features, including seizures and cognitive decline; however, the underlying molecular mechanisms are not fully understood.
- - The study highlights the significant increase in Fyn-tau interactions following seizure induction, indicating potential therapeutic targets for modifying brain pathology in both conditions.
- - Findings suggest that inhibiting Fyn via saracatinib can reduce pathological interactions and phosphorylation in models of epilepsy, pointing to promising avenues for treatment in human cases.
Introduction: Swine exhibit cerebral cortex mitochondrial dysfunction and neuropathologic injury after hypoxic cardiac arrest treated with hemodynamic-directed CPR (HD-CPR) despite normal Cerebral Performance Category scores. We analyzed the temporal evolution of plasma protein biomarkers of brain injury and inflammatory cytokines, as well as cerebral cortical mitochondrial injury and neuropathology for five days following pediatric asphyxia-associated cardiac arrest treated with HD-CPR.
Methods: One-month-old swine underwent asphyxia associated cardiac arrest, 10-20 min of HD-CPR (goal SBP 90 mmHg, coronary perfusion pressure 20 mmHg), and randomization to post-ROSC survival duration (24, 48, 72, 96, 120 h; n = 3 per group) with standardized post-resuscitation care.