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RESEARCH PRODUCT
Oxidative Stress, Neuroinflammation and Mitochondria in the Pathophysiology of Amyotrophic Lateral Sclerosis
Ali Jihad-jebbarElena ObradorRafael López-blanchRosario SalvadorJosé M. EstrelaSoraya L. Vallessubject
0301 basic medicineamyotrophic lateral sclerosisPhysiologyClinical BiochemistryReviewDiseaseMitochondrionmedicine.disease_causeBiochemistryneuroinflammationNeurologia03 medical and health sciences0302 clinical medicineoxidative stressMedicineAmyotrophic lateral sclerosisMolecular BiologyNeuroinflammationMicrogliabusiness.industrylcsh:RM1-950NeurodegenerationCell Biologymedicine.diseasePatologiaPathophysiologymitochondrialcsh:Therapeutics. Pharmacology030104 developmental biologymedicine.anatomical_structuremotor neuron diseasebusinessNeuroscience030217 neurology & neurosurgeryOxidative stressdescription
Amyotrophic lateral sclerosis (ALS) is a progressive motor neuron (MN) disease. Its primary cause remains elusive, although a combination of different causal factors cannot be ruled out. There is no cure, and prognosis is poor. Most patients with ALS die due to disease-related complications, such as respiratory failure, within three years of diagnosis. While the underlying mechanisms are unclear, different cell types (microglia, astrocytes, macrophages and T cell subsets) appear to play key roles in the pathophysiology of the disease. Neuroinflammation and oxidative stress pave the way leading to neurodegeneration and MN death. ALS-associated mitochondrial dysfunction occurs at different levels, and these organelles are involved in the mechanism of MN death. Molecular and cellular interactions are presented here as a sequential cascade of events. Based on our present knowledge, the discussion leads to the idea that feasible therapeutic strategies should focus in interfering with the pathophysiology of the disease at different steps.
year | journal | country | edition | language |
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2020-01-01 | Antioxidants |