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A can convert molecular oxygen into HO by reducing divalent metal ions. Ainduced ROS accumulation results in lipid peroxidation and subsequent production of the cytotoxic HNE. Excessive intracellular calcium plays a central role in excitatory neurotoxicity.LTP was impaired in wildtype hippocampal slices treated with exogenous A and in slices from APPPS mutant mice that model AD.MitoQ, a mitochondriatargeted antioxidant, and EUK, a SOD and catalase mimetic, could prevent the impaired LTP. In a motor neuronlike cell system that was stabletransfected with wild type and mutant TDP, mutant TDP induced mitochondrial dysfunction and oxidative damage that was indicated by an increase in lipid peroxidation. Another way for ROS to bridge misfolded protein to cell death is its effect on the intracelluar andor extracellular clearance capability for aberrant proteins.The main intracellular pathways for the degradation and recycling of proteins are the ubiquitinproteasome system and the autophagylysosomal pathway.Under a pathological condition, such as in PD, the ubiquitinproteasome system and mitophagy are impacted by oxidative stress so that a decreased clearance rate results in the accumulation of alphasynuclein. Extracellular clearance pathways include interaction of neurons with astrocytes and microglia. Oxidative stress can result in microglial senescence in response to intracellular accumulation of iron.For example, the projections of microglia from aged mice, which surround A fibrillary aggregates, showed a diminished ability to Furosemide internalize A peptide.Thus, reduced clearance of A would contribute to the pathogenesis of AD, a lateonset disease.Although there is a great deal of scientific literature that describes the debilitating effects of ROS, oxidative stress may not readily contribute directly to cell death.However, if ER stress is prolonged or excessive in a disturbance, such as hypoxia, glucose deprivation or oxidative stress, the cells will elicit apoptotic processes to remove overstressed cells.ATF promotes folding of protein and removal of misfolded protein by upregulation of chaperones, foldases, and components of the ERAD machinery, while IRE and PERK are functionally involved in both reducing ER protein load and triggering apoptosis. Chemobrain can be very frustrating both for those who are living with cancer, and their loved ones who are L-α-Phosphatidylcholine trying to support them.Chemobrain can seriously affect quality of life and life itself in cancer patients.This toxicity can manifest itself in many ways, including encephalopathy syndromes and confusional states, seizure activity, headache, cerebrovascular complications and stroke, visual loss, cerebellar dysfunction, and spinal cord damage with myelopathy. There is reliable evidence that, as a result of treatment, a subset of cancer survivors experience cognitive problems that can last for many years following the completion of chemotherapy.These include attention deficits, memory loss, and confused thought processes.Up to of patients with cancer report that these cognitive difficulties persist well beyond the duration of treatment. Studies that have measured cognitive function using standardized neuropsychological assessments have found mild to moderate effects of chemotherapy on cognitive performance in of the survivors after treatment. Longitudinal studies have shown that, in a subset of survivors, cognitive difficulties can persist for between and years following the completion of chemotherapy. Crosssectional studies have found cognitive impairments lasting between and years following chemotherapy.

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