Pascale Belenguer, João M N Duarte, Patrícia F Schuck, Gustavo C Ferreira. Neurotox Res 2019
Times Cited: 15
Times Cited: 15
Times Cited
Times Co-cited
Similarity
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Komal Panchal, Anand Krishna Tiwari. Mitochondrion 2019
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How Energy Metabolism Supports Cerebral Function: Insights from 13C Magnetic Resonance Studies In vivo.
Sarah Sonnay, Rolf Gruetter, João M N Duarte. Front Neurosci 2017
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Role of mitochondrial ROS in the brain: from physiology to neurodegeneration.
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Mitoautophagy: A Unique Self-Destructive Path Mitochondria of Upper Motor Neurons With TDP-43 Pathology Take, Very Early in ALS.
Mukesh Gautam, Edward F Xie, Nuran Kocak, P Hande Ozdinler. Front Cell Neurosci 2019
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Redox regulation by NRF2 in aging and disease.
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Mitochondrial dysfunction in neurodegenerative diseases and drug targets via apoptotic signaling.
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Therapeutic targeting of the NRF2 and KEAP1 partnership in chronic diseases.
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Compartmentalised energy metabolism supporting glutamatergic neurotransmission in response to increased activity in the rat cerebral cortex: A 13C MRS study in vivo at 14.1 T.
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Pathogenesis of brain damage in glutaric acidemia type I: Lessons from the genetic mice model.
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Glutamate uptake into astrocytes stimulates aerobic glycolysis: a mechanism coupling neuronal activity to glucose utilization.
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The effect of WIN 55,212-2 suggests a cannabinoid-sensitive component in the early toxicity induced by organic acids accumulating in glutaric acidemia type I and in related disorders of propionate metabolism in rat brain synaptosomes.
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A diet-induced mouse model for glutaric aciduria type I.
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Disturbance of redox homeostasis as a contributing underlying pathomechanism of brain and liver alterations in 3-hydroxy-3-methylglutaryl-CoA lyase deficiency.
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Calcium, mitochondria and cell metabolism: A functional triangle in bioenergetics.
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Mechanism of age-dependent susceptibility and novel treatment strategy in glutaric acidemia type I.
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Oxidative Stress, Disrupted Energy Metabolism, and Altered Signaling Pathways in Glutaryl-CoA Dehydrogenase Knockout Mice: Potential Implications of Quinolinic Acid Toxicity in the Neuropathology of Glutaric Acidemia Type I.
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The role of oxidative damage in the neuropathology of organic acidurias: insights from animal studies.
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Biochemical, pathologic and behavioral analysis of a mouse model of glutaric acidemia type I.
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Altered Redox Homeostasis in Branched-Chain Amino Acid Disorders, Organic Acidurias, and Homocystinuria.
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Mitophagy and Alzheimer's Disease: Cellular and Molecular Mechanisms.
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Docking of axonal mitochondria by syntaphilin controls their mobility and affects short-term facilitation.
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Fundamentals of CNS energy metabolism and alterations in lysosomal storage diseases.
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Pleiotropic Mitochondria: The Influence of Mitochondria on Neuronal Development and Disease.
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Mitochondrial fusion/fission dynamics in neurodegeneration and neuronal plasticity.
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The multifaceted contributions of mitochondria to cellular metabolism.
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A proposed nosology of inborn errors of metabolism.
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Mitochondria as multifaceted regulators of cell death.
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SIRT1 regulation of apoptosis of human chondrocytes.
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Resveratrol Promotes Mitochondrial Biogenesis and Protects against Seizure-Induced Neuronal Cell Damage in the Hippocampus Following Status Epilepticus by Activation of the PGC-1α Signaling Pathway.
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Liara Rizzi, Matheus Roriz-Cruz. Neuropeptides 2018
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75-kd sirtuin 1 blocks tumor necrosis factor α-mediated apoptosis in human osteoarthritic chondrocytes.
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Epigallocatechin-3-gallate suppresses 1-methyl-4-phenyl-pyridine-induced oxidative stress in PC12 cells via the SIRT1/PGC-1α signaling pathway.
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The potential role of mitochondrial dysfunction in seizure-associated cell death in the hippocampus and epileptogenesis.
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Roles of oxidative stress, apoptosis, PGC-1α and mitochondrial biogenesis in cerebral ischemia.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.