Minocycline inhibits cytochrome c release and delays progression of amyotrophic lateral sclerosis in mice

By Shan Zhu, I. Stavrovskaya, M. Drozda, Betty Y. S. Kim, V. Ona, Mingwei Li, S. Sarang, Allen S. Liu, D. Hartley, D. Wu and 5 more. Nature, 2002

1,113 citations recorded by the source corpus.

Subfields: Neurology, Pharmacology

View Paper: https://www.semanticscholar.org/paper/3f48c90ecaf3866d3ab9b3dd3964ce1cb963b095

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Citations in the corpus

Inhibition of Microglial Activation Attenuates the Development but Not Existing Hypersensitivity in a Rat Model of Neuropathy (2003, background): “The selection of minocycline doses and the rationale for the dosing regime is within the range at which it was reported to be a neuroprotectant in rodents (Yrjanheikki et al., 1999; Wu et al., 2002; Zhu et al., 2002; Zhang et al., 2003).”
Pathophysiology and pharmacologic treatment of acute spinal cord injury. (2004, background): “Minocycline, a tetracycline antibiotic, has been shown to inhibit excitotoxicity [123] and provide neuroprotection in models of Parkinson disease [124], autoimmune encephalomyelitis [125], amyotrophic lateral sclerosis [126] and adult and neonatal brain ischemia [125,127,128], most likely through it”
Minocycline attenuates lipopolysaccharide (LPS)-induced neuroinflammation, sickness behavior, and anhedonia (2008, background): “This is relevant because minocycline attenuates neuroinflammation in several rodent models of disease including Amyotrophic Lateral Sclerosis [46], Experimental Autoimmune Encephalomyelitis (EAE) [45] and MPTP-induced Parkinson's disease [47].”
Molecular biology of amyotrophic lateral sclerosis: insights from genetics (2006, background): “Conversely, the disease is slowed by interventions that improve mitochondrial function — for example, creatine, which inhibits opening of the mitochondrial transition pore, and minocycline, which blocks the egress of cytochrome c”
Inflammation after Intracerebral Hemorrhage (2007, background): “These beneficial effects coincided with amelioration of microglial activation and downregulation of MMP-12 expression (Power et al, 2003), although other mechanisms, such as inhibition of cytochrome c release (Zhu et al, 2002), could also underlie the benefits.”
Tetracyclines: nonantibiotic properties and their clinical implications. (2006, background): “Minocycline may also have beneficial effects in chronic neurodegenerative diseases such as Huntington disease(29) and amyotrophic lateral sclerosis.(30)”
Minocycline attenuates mechanical allodynia and proinflammatory cytokine expression in rat models of pain facilitation (2005, background): “It has been shown to delay disease progression and mortality in models of Huntington’s disease and amyotrophic lateral sclerosis (Chen et al., 2000; Kriz et al., 2002; Zhu et al., 2002).”
Mitochondrial Calcium and the Permeability Transition in Cell Death (2009, background): “Cytoprotective mechanisms proposed for minocycline include inhibition of apoptotic pathways, decreased mitochondrial release of pro-apoptotic factors such as cytochrome c [55], up-regulation of antiapoptotic proteins [52], inhibition of caspase-1 and caspase-3 activation and suppression of cytochrom”
Evidence of widespread cerebral microglial activation in amyotrophic lateral sclerosis: an [11C](R)-PK11195 positron emission tomography study. (2004, background): “Moreover, drugs aimed at inflammatory pathways have beneficial effects on survival of transgenic mouse models of ALS (Drachman et al., 2002; Zhu et al., 2002).”
Contributions of Inflammatory Processes to the Development of the Early Stages of Diabetic Retinopathy (2007, background): “Minocycline has neuroprotective qualities in models of cerebral ischemia, traumatic brain injuries, ALS, Huntington’s, and Parkinson’s disease in mice [160–169].”