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https://www.readbyqxmd.com/read/28103389/the-use-of-antioxidants-in-the-treatment-of-traumatic-brain-injury
#1
Whitney Venegoni, Qiuhua Shen, Amanda R Thimmesch, Meredith Bell, John B Hiebert, Janet D Pierce
AIMS: To discuss secondary traumatic brain injury, the mitochondria and the use of antioxidants as a treatment. BACKGROUND: One of the leading causes of death in young adults internationally is traumatic brain injury, affecting individuals in all demographics. Traumatic brain injury is produced by an external blunt force or penetration resulting in alterations in brain function or pathology. Often, with a traumatic brain injury, secondary injury causes additional damage to the brain tissue that can have further impact on recovery and the quality of life...
January 19, 2017: Journal of Advanced Nursing
https://www.readbyqxmd.com/read/28103118/park2-dependent-mitophagy-induced-by-acidic-postconditioning-protects-against-focal-cerebral-ischemia-and-extends-the-reperfusion-window
#2
Zhe Shen, Yanrong Zheng, Jiaying Wu, Ying Chen, Xiaoli Wu, Yiting Zhou, Yang Yuan, Shousheng Lu, Lei Jiang, Zhenghong Qin, Zhong Chen, Weiwei Hu, Xiangnan Zhang
Prompt reperfusion after cerebral ischemia is critical for neuronal survival. Any strategies that extend the limited reperfusion window will be of great importance. Acidic postconditioning (APC) is a mild acidosis treatment that involves inhaling CO2 during reperfusion following ischemia. APC attenuates ischemic brain injury although the underlying mechanisms have not been elucidated. Here we report that APC reinforces ischemia-reperfusion-induced mitophagy in middle cortical artery occlusion (MCAO)-treated mice, and in oxygen-glucose deprivation (OGD)-treated brain slices and neurons...
January 19, 2017: Autophagy
https://www.readbyqxmd.com/read/28100752/differential-vulnerability-of-ca1-versus-ca3-pyramidal-neurons-after-ischemia-possible-relationship-to-sources-of-zn2-accumulation-and-its-entry-into-and-prolonged-effects-on-mitochondria
#3
Yuliya V Medvedeva, Sung G Ji, Hong Z Yin, John H Weiss
: Excitotoxic mechanisms contribute to the degeneration of hippocampal pyramidal neurons after recurrent seizures and brain ischemia. However, susceptibility differs, with CA1 neurons degenerating preferentially after global ischemia and CA3 neurons after limbic seizures. Whereas most studies address contributions of excitotoxic Ca(2+) entry, it is apparent that Zn(2+) also contributes, reflecting accumulation in neurons either after synaptic release and entry through postsynaptic channels or upon mobilization from intracellular Zn(2+)-binding proteins such as metallothionein-III (MT-III)...
January 18, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28098577/mitochondria-initiate-and-regulate-sarcopenia
#4
Stephen E Alway, Junaith S Mohamed, Matthew J Myers
We present the hypothesis that an accumulation of dysfunctional mitochondria initiates a signaling cascade leading to motor neuron and muscle fiber death and culminating in sarcopenia. Interactions between neural and muscle cells that contain dysfunctional mitochondria exacerbate sarcopenia. Preventing sarcopenia will require identifying mitochondrial sources of dysfunction that are reversible.
January 16, 2017: Exercise and Sport Sciences Reviews
https://www.readbyqxmd.com/read/28098219/combined-lrrk2-mutation-aging-and-chronic-low-dose-oral-rotenone-as-a-model-of-parkinson-s-disease
#5
Hui-Fang Liu, Philip Wing-Lok Ho, Gideon Chi-Ting Leung, Colin Siu-Chi Lam, Shirley Yin-Yu Pang, Lingfei Li, Michelle Hiu-Wai Kung, David Boyer Ramsden, Shu-Leong Ho
Aging, genetics and environmental toxicity are important etiological factors in Parkinson's disease (PD). However, its pathogenesis remains unclear. A major obstacle is the lack of an appropriate experimental model which incorporates genetic susceptibility, aging and prolonged environmental toxicity. Here, we explored the interplay amongst these factors using mutant LRRK2(R1441G) (leucine-rich-repeat-kinase-2) knockin mice. We found that mutant primary cortical and mesencephalic dopaminergic neurons were more susceptible to rotenone-induced ATP deficiency and cell death...
January 18, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28093214/the-upr-reduces-glucose-metabolism-via-ire1-signaling
#6
Judith M van der Harg, Jessica C van Heest, Fabian N Bangel, Sanne Patiwael, Jan R T van Weering, Wiep Scheper
Neurons are highly dependent on glucose. A disturbance in glucose homeostasis therefore poses a severe risk that is counteracted by activation of stress responses to limit damage and restore the energy balance. A major stress response that is activated under conditions of glucose deprivation is the unfolded protein response (UPR) that is aimed to restore proteostasis in the endoplasmic reticulum. The key signaling of the UPR involves the transient activation of a transcriptional program and an overall reduction of protein synthesis...
January 13, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28091556/vegf-b-promotes-recovery-of-corneal-innervations-and-trophic-functions-in-diabetic-mice
#7
Guohu Di, Xiaowen Zhao, Xia Qi, Songmei Zhang, Lu Feng, Weiyun Shi, Qingjun Zhou
Vascular endothelial growth factor (VEGF)-B possesses the capacity of promoting injured peripheral nerve regeneration and restore their sensory and trophic functions. However, the contribution and mechanism of VEGF-B in diabetic peripheral neuropathy remains unclear. In the present study, we investigated the expression and role of VEGF-B in diabetic corneal neuropathy by using type 1 diabetic mice and cultured trigeminal ganglion (TG) neurons. Hyperglycemia attenuated the endogenous expression of VEGF-B in regenerated diabetic corneal epithelium, but not that of VEGF receptors in diabetic TG neurons and axons...
January 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28087734/increased-mitophagy-in-the-skeletal-muscle-of-spinal-and-bulbar-muscular-atrophy-patients
#8
Doriana Borgia, Adriana Malena, Marco Spinazzi, Maria Andrea Desbats, Leonardo Salviati, Aaron P Russell, Giovanni Miotto, Laura Tosatto, Elena Pegoraro, Gianni Sorarù, Maria Pennuto, Lodovica Vergani
Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disorder caused by polyglutamine expansion in the androgen receptor (AR) and characterized by the loss of lower motor neurons. Here we investigated pathological processes occurring in muscle biopsy specimens derived from SBMA patients and, as controls, age-matched healthy subjects and patients suffering from amyotrophic lateral sclerosis (ALS) and neurogenic atrophy. We detected atrophic fibers in the muscle of SBMA, ALS and neurogenic atrophy patients...
January 13, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28087269/mitochondrial-roles-of-the-psychiatric-disease-risk-factor-disc1
#9
REVIEW
R Norkett, S Modi, J T Kittler
Ion transport during neuronal signalling utilizes the majority of the brain's energy supply. Mitochondria are key sites for energy provision through ATP synthesis and play other important roles including calcium buffering. Thus, tightly regulated distribution and function of these organelles throughout the intricate architecture of the neuron is essential for normal synaptic communication. Therefore, delineating mechanisms coordinating mitochondrial transport and function is essential for understanding nervous system physiology and pathology...
January 10, 2017: Schizophrenia Research
https://www.readbyqxmd.com/read/28077713/reversible-disruption-of-neuronal-mitochondria-by-ischemic-and-traumatic-injury-revealed-by-quantitative-two-photon-imaging-in-the-neocortex-of-anesthetized-mice
#10
Mikhail Kislin, Jeremy Sword, Ioulia V Fomitcheva, Deborah Croom, Evgeny Pryazhnikov, Eero Lihavainen, Dmytro Toptunov, Heikki Rauvala, Andre S Ribeiro, Leonard Khiroug, Sergei A Kirov
: Mitochondria play a variety of functional roles in cortical neurons, from metabolic support and neuroprotection to the release of cytokines that trigger apoptosis. In dendrites, mitochondrial structure is closely linked to their function, and fragmentation (fission) of the normally elongated mitochondria indicates loss of their function under pathological conditions, such as stroke and brain trauma. Using in vivo two-photon microscopy in mouse brain, we quantified mitochondrial fragmentation in a full spectrum of cortical injuries, ranging from severe to mild...
January 11, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28076767/-s-pot-on-mitochondria-cannabinoids-disrupt-cellular-respiration-to-limit-neuronal-activity
#11
Tibor Harkany, Tamas L Horvath
Classical views posit G protein-coupled cannabinoid receptor 1s (CB1Rs) at the cell surface with cytosolic Giα-mediated signal transduction. Hebert-Chatelain et al. (2016) instead place CB1Rs at mitochondria limiting neuronal respiration by soluble adenylyl cyclase-dependent modulation of complex I activity. Thus, neuronal bioenergetics link to synaptic plasticity and, globally, learning and memory.
January 10, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28076378/p62-pathology-model-in-the-rat-substantia-nigra-with-filamentous-inclusions-and-progressive-neurodegeneration
#12
Kasey L Jackson, Wen-Lang Lin, Sumitra Miriyala, Robert D Dayton, Manikandan Panchatcharam, Kevin J McCarthy, Monica Castanedes-Casey, Dennis W Dickson, Ronald L Klein
One of the proteins most frequently found in neuropathological lesions is the ubiquitin binding protein p62 (sequestosome 1). Post-mortem analysis of p62 is a defining diagnostic marker in several neurodegenerative diseases including amyotrophic lateral sclerosis and inclusion body myositis. Since p62 functions in protein degradation pathways including autophagy, the build-up of p62-positive inclusions suggests defects in protein clearance. p62 was expressed unilaterally in the rat substantia nigra with an adeno-associated virus vector (AAV9) in order to study p62 neuropathology...
2017: PloS One
https://www.readbyqxmd.com/read/28075229/altered-mitochondrial-dynamics-as-a-consequence-of-venezuelan-equine-encephalitis-virus-infection
#13
Forrest Keck, Taryn Brooks-Faulconer, Tyler Lark, Pavitra Ravishankar, Charles Bailey, Carolina Salvador-Morales, Aarthi Narayanan
Mitochondria are sentinel organelles that are impacted by various forms of cellular stress, including viral infections. While signaling events associated with mitochondria, including those activated by pathogen associated molecular patterns (PAMPs), are widely studied, alterations in mitochondrial distribution and changes in mitochondrial dynamics are also beginning to be associated with cellular insult. Cells of neuronal origin have been demonstrated to display remarkable alterations in several instances, including neurodegenerative disorders...
January 11, 2017: Virulence
https://www.readbyqxmd.com/read/28069436/streptozotocin-causes-neurotoxic-effect-in-cultured-cerebellar-granule-neurons
#14
Elisaveta E Genrikhs, Elena V Stelmashook, Sergey A Golyshev, Olga P Aleksandrova, Nickolay K Isaev
Streptozotocin (STZ) is a glucosamine-nitrosourea compound used for experimental simulation of sporadic Alzheimer's disease at intracerebroventricular administration in vivo. The studies of STZ influence on neurons of central nervous system performed on the primary cultures are practically absent. We have shown the application of STZ (1-5mM) in primary culture for 48h induced strong dose-dependent death in cultured cerebellar granule neurons. This toxic effect was decreased by pyruvate, insulin partially. Using the indicator Fluo-4 AM for measurements of intracellular calcium ions and tetramethylrhodamine ethyl ester (TMRE) for detection of changes of mitochondrial membrane potential in live cells we have shown that 5 h-exposure to STZ induced intensive increase of Fluo-4 and decrease TMRE fluorescence in neurons...
January 6, 2017: Brain Research Bulletin
https://www.readbyqxmd.com/read/28063983/loss-of-laforin-or-malin-results-in-increased-drp1-level-and-concomitant-mitochondrial-fragmentation-in-lafora-disease-mouse-models
#15
Mamta Upadhyay, Saloni Agarwal, Pratibha Bhadauriya, Subramaniam Ganesh
Lafora disease (LD) is an autosomal recessive form of a fatal disorder characterized by the myoclonus epilepsy, ataxia, psychosis, dementia, and dysarthria. A hallmark of LD is the presence of abnormal glycogen inclusions called Lafora bodies in the affected tissues including the neurons. LD can be caused by defects either in the laforin phosphatase coded by the EPM2A gene or in the malin E3 ubiquitin ligase coded by the NHLRC1 gene. The mouse models of LD, created by the targeted disruption of the LD genes, display several neurodegenerative changes...
January 4, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28063266/antibiotics-may-trigger-mitochondrial-dysfunction-inducing-psychiatric-disorders
#16
George B Stefano, Joshua Samuel, Richard M Kream
Clinical usage of several classes of antibiotics is associated with moderate to severe side effects due to the promotion of mitochondrial dysfunction. We contend that this may be due to perturbation of unique evolutionary relationships that link selective biochemical and molecular aspects of mitochondrial biology to conserved enzymatic processes derived from bacterial progenitors. Operationally, stereo-selective conformational matching between mitochondrial respiratory complexes, cytosolic and nuclear signaling complexes appears to support the conservation of a critically important set of chemical messengers required for existential regulation of homeostatic cellular processes...
January 7, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/28062185/allicin-protects-auditory-hair-cells-and-spiral-ganglion-neurons-from-cisplatin-induced-apoptosis
#17
Xianmin Wu, Xiaofei Li, Yongdong Song, He Li, Xiaohui Bai, Wenwen Liu, Yuechen Han, Lei Xu, Jianfeng Li, Daogong Zhang, Haibo Wang, Zhaomin Fan
Cisplatin is a broad-spectrum anticancer drug that is commonly used in the clinic. Ototoxicity is one of the major side effects of this drug, which caused irreversible sensorineural hearing loss. Allicin, the main biologically active compound derived from garlic, has been shown to exert various anti-apoptotic and anti-oxidative activities in vitro and in vivo studies. We took advantage of C57 mice intraperitoneally injected with cisplatin alone or with cisplatin and allicin combined, to investigate whether allicin plays a protective role in vivo against cisplatin ototoxicity...
January 3, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28061689/mitochondrial-mechanisms-of-neuronal-cell-death-potential-therapeutics
#18
Ted M Dawson, Valina L Dawson
Mitochondria lie at the crossroads of neuronal survival and cell death. They play important roles in cellular bioenergetics, control intracellular Ca(2+) homeostasis, and participate in key metabolic pathways. Mutations in genes involved in mitochondrial quality control cause a myriad of neurodegenerative diseases. Mitochondria have evolved strategies to kill cells when they are not able to continue their vital functions. This review provides an overview of the role of mitochondria in neurologic disease and the cell death pathways that are mediated through mitochondria, including their role in accidental cell death, the regulated cell death pathways of apoptosis and parthanatos, and programmed cell death...
January 6, 2017: Annual Review of Pharmacology and Toxicology
https://www.readbyqxmd.com/read/28060833/wnt-signaling-prevents-the-a%C3%AE-oligomer-induced-mitochondrial-permeability-transition-pore-opening-preserving-mitochondrial-structure-in-hippocampal-neurons
#19
Macarena S Arrázola, Eva Ramos-Fernández, Pedro Cisternas, Daniela Ordenes, Nibaldo C Inestrosa
Alzheimer's disease (AD) is a neurodegenerative disorder mainly known for synaptic impairment and neuronal cell loss, affecting memory processes. Beside these damages, mitochondria have been implicated in the pathogenesis of AD through the induction of the mitochondrial permeability transition pore (mPTP). The mPTP is a non-selective pore that is formed under apoptotic conditions, disturbing mitochondrial structure and thus, neuronal viability. In AD, Aβ oligomers (Aβos) favor the opening of the pore, activating mitochondria-dependent neuronal cell death cascades...
2017: PloS One
https://www.readbyqxmd.com/read/28060357/the-optical-detection-of-retinal-ganglion-cell-damage
#20
J E Morgan, J Tribble, J Fergusson, N White, I Erchova
We provide an overview of developments in the use optical coherence tomography (OCT) imaging for the detection of retinal ganglion cell (RGC) damage in vivo that avoid use of any exogenous ligands to label cells. The method employs high-resolution OCT using broad spectral light sources to deliver axial resolution of under 5 μm. The resolution approximates that of cellular organelles, which undergo degenerative changes that progress to apoptosis as a result of axon damage. These degenerative changes are manifest as the loss of RGC dendrites and fragmentation of the subcellular network of organelles, in particular, the mitochondria that support dendritic structure...
January 6, 2017: Eye
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