Topic: mitochondrial dysfunction

Meagan McManus examines mitochondrial dysfunction as an early driver of brain ageing and neurodegeneration. Reactive oxygen species and other mitochondrial stress signals connect impaired energy metabolism with glial activation. The talk presents preclinical evidence for [18F]ROStrace PET, a redox-sensitive tracer that crosses the blood–brain barrier, as a non-invasive way to detect mitochondrial and immune distress before overt pathology in models relevant to late-onset Alzheimer’s and Parkinson’s diseases. Online via the University of Arizona Zoom meeting. Use the Zoom link published on the

Cancer-related fatigue is a prominent and debilitating side effect of cancer and its treatment. It can develop prior to diagnosis, generally peaks during cancer treatment, and can persist long after treatment completion. Its mechanisms are multifactorial, and its expression is highly variable. Unfortunately, treatment options are limited. Our research uses syngeneic murine models of cancer and cisplatin-based chemotherapy to better understand these mechanisms. Our data indicate that both peripherally and centrally processes may contribute to the developmental of fatigue. These processes includ

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease, defined by motor neuron loss, muscle paralysis, and death. ALS individuals often present alterations in cardiovascular function that may evolve into heart failure and death. Mitochondrial dysfunction and oxidative stress are key players in ALS pathophysiology. Thus, improving mitochondrial function and/or antioxidant capacity constitute promising therapeutic strategies to delay ALS progression. We hypothesized that mitochondria-targeted antioxidant AntiOxCIN4 can reduce cardiac oxidative/nitrosative stress in SOD1G93A ALS mice

Arginase 2 (Arg2), an arginine-metabolizing, mitochondrial enzyme, has been recently found to be enriched in the striatum, and progressive loss of Arg2 has been proposed as a potential factor contributing to the pathogenesis of Huntington’s disease (HD), a disorder primarily involving this region of the brain. Although direct metabolic role of Arg2 is well established, the importance of this enzyme for striatal function and dysfunction is not known. The purpose of this work was to identify cellular pathways potentially controlled by Arg2 in the striatum. In our experiments, we have used wild-t

Oxidative stress and neuroinflammation are crucial phenomena in the pathogenesis of Alzheimer disease (AD). Oxotremorine-M (Oxo), a non-selective muscarinic acetylcholine receptors agonist, exerts neurotrophic functions in primary neurons and modulates oxidative stress and neuroinflammation phenomena in rat brain. Based on this, our study investigates Oxo positive effects on differentiated SH-SY5Y neuroblastoma cells, revealing that Oxo treatment a) enhances cell survival, b) increases neurite length and c) upregulates HSP70 and pHSF1 expression. Moreover, Oxo counteracts tert–Butyl hydroperox