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https://www.readbyqxmd.com/read/28917665/improving-mitochondrial-function-significantly-reduces-metabolic-visual-motor-and-cognitive-decline-in-aged-drosophila-melanogaster
#1
Tobias W Weinrich, Ariathney Coyne, Thomas E Salt, Christopher Hogg, Glen Jeffery
Mitochondria play a major role in aging. Over time, mutations accumulate in mitochondrial DNA leading to reduced adenosine triphosphate (ATP) production and increased production of damaging reactive oxygen species. If cells fail to cope, they die. Reduced ATP will result in declining cellular membrane potentials leading to reduced central nervous system function. However, aged mitochondrial function is improved by long wavelength light (670 nm) absorbed by cytochrome c oxidase in mitochondrial respiration...
August 30, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/28917260/roles-of-sigma-1-receptors-on-mitochondrial-functions-relevant-to-neurodegenerative-diseases
#2
REVIEW
Tzu-Yu Weng, Shang-Yi Anne Tsai, Tsung-Ping Su
The sigma-1 receptor (Sig-1R) is a chaperone that resides mainly at the mitochondrion-associated endoplasmic reticulum (ER) membrane (called the MAMs) and acts as a dynamic pluripotent modulator in living systems. At the MAM, the Sig-1R is known to play a role in regulating the Ca(2+) signaling between ER and mitochondria and in maintaining the structural integrity of the MAM. The MAM serves as bridges between ER and mitochondria regulating multiple functions such as Ca(2+) transfer, energy exchange, lipid synthesis and transports, and protein folding that are pivotal to cell survival and defense...
September 16, 2017: Journal of Biomedical Science
https://www.readbyqxmd.com/read/28915325/brown-and-beige-adipose-tissues-in-health-and-disease
#3
Liangyou Rui
Brown and beige adipocytes arise from distinct developmental origins. Brown adipose tissue (BAT) develops embryonically from precursors that also give to skeletal muscle. Beige fat develops postnatally and is highly inducible. Beige fat recruitment is mediated by multiple mechanisms, including de novo beige adipogenesis and white-to-brown adipocyte transdifferentiaiton. Beige precursors reside around vasculatures, and proliferate and differentiate into beige adipocytes. PDGFRα+Ebf2+ precursors are restricted to beige lineage cells, while another PDGFRα+ subset gives rise to beige adipocytes, white adipocytes, or fibrogenic cells...
September 12, 2017: Comprehensive Physiology
https://www.readbyqxmd.com/read/28913661/discovery-of-non-peptidic-small-molecule-inhibitors-of-cyclophilin-d-as-neuroprotective-agents-in-a%C3%AE-induced-mitochondrial-dysfunction
#4
Insun Park, Ashwini M Londhe, Ji Woong Lim, Beoung-Geon Park, Seo Yun Jung, Jae Yeol Lee, Sang Min Lim, Kyoung Tai No, Jiyoun Lee, Ae Nim Pae
Cyclophilin D (CypD) is a mitochondria-specific cyclophilin that is known to play a pivotal role in the formation of the mitochondrial permeability transition pore (mPTP).The formation and opening of the mPTP disrupt mitochondrial homeostasis, cause mitochondrial dysfunction and eventually lead to cell death. Several recent studies have found that CypD promotes the formation of the mPTP upon binding to β amyloid (Aβ) peptides inside brain mitochondria, suggesting that neuronal CypD has a potential to be a promising therapeutic target for Alzheimer's disease (AD)...
September 14, 2017: Journal of Computer-aided Molecular Design
https://www.readbyqxmd.com/read/28912677/reversible-axonal-dystrophy-by-calcium-modulation-in-frataxin-deficient-sensory-neurons-of-yg8r-mice
#5
Belén Mollá, Diana C Muñoz-Lasso, Fátima Riveiro, Arantxa Bolinches-Amorós, Federico V Pallardó, Angel Fernandez-Vilata, María de la Iglesia-Vaya, Francesc Palau, Pilar Gonzalez-Cabo
Friedreich's ataxia (FRDA) is a peripheral neuropathy involving a loss of proprioceptive sensory neurons. Studies of biopsies from patients suggest that axonal dysfunction precedes the death of proprioceptive neurons in a dying-back process. We observed that the deficiency of frataxin in sensory neurons of dorsal root ganglia (DRG) of the YG8R mouse model causes the formation of axonal spheroids which retain dysfunctional mitochondria, shows alterations in the cytoskeleton and it produces impairment of axonal transport and autophagic flux...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28904018/dyslipidemia-impairs-mitochondrial-trafficking-and-function-in-sensory-neurons
#6
Amy E Rumora, Stephen I Lentz, Lucy M Hinder, Samuel W Jackson, Andrew Valesano, Gideon E Levinson, Eva L Feldman
Mitochondrial trafficking plays a central role in dorsal root ganglion (DRG) neuronal cell survival and neurotransmission by transporting mitochondria from the neuronal cell body throughout the bundles of DRG axons. In type 2 diabetes (T2DM), dyslipidemia and hyperglycemia damage DRG neurons and induce mitochondrial dysfunction; however, the impact of free fatty acids and glucose on mitochondrial trafficking in DRG neurons remains unknown. To evaluate the impact of free fatty acids compared to hyperglycemia on mitochondrial transport, primary adult mouse DRG neuron cultures were treated with physiologic concentrations of palmitate and glucose and assessed for alterations in mitochondrial trafficking, mitochondrial membrane potential, and mitochondrial bioenergetics...
September 13, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28903499/the-long-lasting-rodenticide-brodifacoum-induces-neuropathology-in-adult-male-rats
#7
Sergey Kalinin, Natalia Marangoni, Katarzyna Kowal, Arunangsu Dey, Kinga Lis, Sergey Brodsky, Richard van Breemen, Zane Hauck, Richard Ripper, Israel Rubinstein, Guy Weinberg, Douglas L Feinstein
Superwarfarins are very long-lasting rodenticides effective in warfarin-resistant rodents at extremely low doses. The consequences of chronic superwarfarin levels in tissues, due to biological half-lives on the order of 20 days, have not been examined. We now characterized the neurological effects of brodifacoum (BDF), one of the most widely used superwarfarins, in adult male Sprague Dawley rats. Dosing curves established the acute oral lethal dose for BDF as 221 ± 14 μg/kg. Measurement of tissue BDF levels showed accumulation throughout the body, including the central nervous system, with levels diminishing over several days...
September 1, 2017: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/28903070/role-of-the-ampk-pathway-in-promoting-autophagic-flux-via-modulating-mitochondrial-dynamics-in-neurodegenerative-diseases-insight-into-prion-diseases
#8
REVIEW
Syed Zahid Ali Shah, Deming Zhao, Tariq Hussain, Lifeng Yang
Neurons are highly energy demanding cells dependent on the mitochondrial oxidative phosphorylation system. Mitochondria generate energy via respiratory complexes that constitute the electron transport chain. Adenosine triphosphate depletion or glucose starvation act as a trigger for the activation of adenosine monophosphate-activated protein kinase (AMPK). AMPK is an evolutionarily conserved protein that plays an important role in cell survival and organismal longevity through modulation of energy homeostasis and autophagy...
September 10, 2017: Ageing Research Reviews
https://www.readbyqxmd.com/read/28902452/mgrn1-mediated-ubiquitination-of-%C3%AE-tubulin-regulates-microtubule-dynamics-and-intracellular-transport
#9
Rukmini Mukherjee, Priyanka Majumder, Oishee Chakrabarti
MGRN1 mediated ubiquitination of α-tubulin regulates microtubule stability and mitotic spindle positioning in mitotic cells. This study elucidates the effect of MGRN1 mediated ubiquitination of α-tubulin in interphase cells. Here, we show that MGRN1 mediated ubiquitination regulates dynamics of EB1 labelled plus ends of microtubules. Intracellular transport of mitochondria and endosomes are affected in cultured cells where functional MGRN1 is depleted. Defects in microtubule-dependent organellar transport are evident in cells where noncanonical K6 mediated ubiquitination of α-tubulin by MGRN1 is compromised...
September 13, 2017: Traffic
https://www.readbyqxmd.com/read/28891994/mdivi-1-protects-adult-rat-hippocampal-neural-stem-cells-against-palmitate-induced-oxidative-stress-and-apoptosis
#10
Sehee Kim, Chanyang Kim, Seungjoon Park
Palmitate concentrations in type 2 diabetic patients are higher than in healthy subjects. The prolonged elevation of plasma palmitate levels induces oxidative stress and mitochondrial dysfunction in neuronal cells. In this study, we examined the role of mdivi-1, a selective inhibitor of mitochondrial fission protein dynamin-regulated protein 1 (Drp1), on the survival of cultured hippocampal neural stem cells (NSCs) exposed to high palmitate. Treatment of hippocampal NSCs with mdivi-1 attenuated palmitate-induced increase in cell death and apoptosis...
September 11, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28891816/syntaphilin-controls-a-mitochondrial-rheostat-for-proliferation-motility-decisions-in-cancer
#11
M Cecilia Caino, Jae Ho Seo, Yuan Wang, Dayana B Rivadeneira, Dmitry I Gabrilovich, Eui Tae Kim, Ashani T Weeraratna, Lucia R Languino, Dario C Altieri
Tumors adapt to an unfavorable microenvironment by controlling the balance between cell proliferation and cell motility, but the regulators of this process are largely unknown. Here, we show that an alternatively spliced isoform of syntaphilin (SNPH), a cytoskeletal regulator of mitochondrial movements in neurons, is directed to mitochondria of tumor cells. Mitochondrial SNPH buffers oxidative stress and maintains complex II-dependent bioenergetics, sustaining local tumor growth while restricting mitochondrial redistribution to the cortical cytoskeleton and tumor cell motility...
September 11, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28890689/integration-between-glycolysis-and-glutamate-glutamine-cycle-flux-may-explain-preferential-glycolytic-increase-during-brain-activation-requiring-glutamate
#12
REVIEW
Leif Hertz, Ye Chen
The 1988 observation by Fox et al. (1988) that brief intense brain activation increases glycolysis (pyruvate formation from glucose) much more than oxidative metabolism has been abundantly confirmed. Specifically glycolytic increase was unexpected because the amount of ATP it generates is much smaller than that formed by subsequent oxidative metabolism of pyruvate. The present article shows that preferential glycolysis can be explained by metabolic processes associated with activation of the glutamate-glutamine cycle...
2017: Frontiers in Integrative Neuroscience
https://www.readbyqxmd.com/read/28890682/impaired-mitophagy-plays-a-role-in-denervation-of-neuromuscular-junctions-in-als-mice
#13
Robert S Rogers, Sudheer Tungtur, Tomohiro Tanaka, Lisa L Nadeau, Yomna Badawi, Hua Wang, Hong-Min Ni, Wen-Xing Ding, Hiroshi Nishimune
Motor neurons in amyotrophic lateral sclerosis (ALS) patients and animal models show degeneration from the nerve terminal, known as dying-back neuropathy. To investigate the mechanism underlying this neuropathy, we analyzed the neuromuscular junctions (NMJs) and motor neuron cell bodies in SOD1(G93A) mice using electron microscopy. NMJs of SOD1(G93A) mice exhibited significantly higher numbers of autophagosomes and degenerated mitochondria compared to wild-type controls. Mitophagosomes were identified in the NMJ presynaptic terminals of wild-type mice and SOD1(G93A) mice...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28883788/loss-of-mitochondrial-ndufs4-in-striatal-medium-spiny-neurons-mediates-progressive-motor-impairment-in-a-mouse-model-of-leigh-syndrome
#14
Byron Chen, Jessica Hui, Kelsey S Montgomery, Alejandro Gella, Irene Bolea, Elisenda Sanz, Richard D Palmiter, Albert Quintana
Inability of mitochondria to generate energy leads to severe and often fatal myoencephalopathies. Among these, Leigh syndrome (LS) is one of the most common childhood mitochondrial diseases; it is characterized by hypotonia, failure to thrive, respiratory insufficiency and progressive mental and motor dysfunction, leading to early death. Basal ganglia nuclei, including the striatum, are affected in LS patients. However, neither the identity of the affected cell types in the striatum nor their contribution to the disease has been established...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28882593/real-time-subpixel-accuracy-tracking-of-single-mitochondria-in-neurons-reveals-heterogeneous-mitochondrial-motion
#15
Adolfo Alsina, Wu Ming Lai, Wai Kin Wong, Xianan Qin, Min Zhang, Hyokeun Park
Mitochondria are essential for cellular survival and function. In neurons, mitochondria are transported to various subcellular regions as needed. Thus, defects in the axonal transport of mitochondria are related to the pathogenesis of neurodegenerative diseases, and the movement of mitochondria has been the subject of intense research. However, the inability to accurately track mitochondria with subpixel accuracy has hindered this research. Here, we report an automated method for tracking mitochondria based on the center of fluorescence...
September 4, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28877995/a-neuroprotective-agent-that-inactivates-prodegenerative-trka-and-preserves-mitochondria
#16
Konstantin Feinberg, Adelaida Kolaj, Chen Wu, Natalie Grinshtein, Jonathan R Krieger, Michael F Moran, Lee L Rubin, Freda D Miller, David R Kaplan
Axon degeneration is an early event and pathological in neurodegenerative conditions and nerve injuries. To discover agents that suppress neuronal death and axonal degeneration, we performed drug screens on primary rodent neurons and identified the pan-kinase inhibitor foretinib, which potently rescued sympathetic, sensory, and motor wt and SOD1 mutant neurons from trophic factor withdrawal-induced degeneration. By using primary sympathetic neurons grown in mass cultures and Campenot chambers, we show that foretinib protected neurons by suppressing both known degenerative pathways and a new pathway involving unliganded TrkA and transcriptional regulation of the proapoptotic BH3 family members BimEL, Harakiri,and Puma, culminating in preservation of mitochondria in the degenerative setting...
September 6, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28877835/pathological-changes-in-app-ps-1-transgenic-mouse-models-of-alzheimer-s-disease-treated-with-ganoderma-lucidum-preparation
#17
Chuan Qin, Shan-Qiu Wu, Bao-Sheng Chen, Xiao-Xian Wu, Kun-Yao Qu, Jun-Min Liu, Gui-Fang Zhang, Yan-Feng Xu, Shunli Shu, Lihua Sun, Yan-Yong Li, Hua Zhu, Lan Huang, Chun-Mei Ma, Yu-Huan Xu, Yun-Lin Han, Yao-Zeng Lu
Objective To explore the efficacy of ganoderma lucidum preparation(Ling Zhi) in treating APP/PS-1 transgenic mouse models of Alzheimer's disease(AD).Methods APP/PS-1 transgenic mice of 4 months were randomly divided into model group,ganoderma lucidum treatment groups,including high [2250 mg/(kg·d)] and middle [750 mg/(kg·d)] dose groups,i.e.LZ-H and LZ-M groups,and the positive control group(treated with donepezil hydrochloride [2 mg/(kg·d)]).In addition,C57BL/6J wild mice were selected as normal group.The animals were administered for 4 months...
August 20, 2017: Zhongguo Yi Xue Ke Xue Yuan Xue Bao. Acta Academiae Medicinae Sinicae
https://www.readbyqxmd.com/read/28877447/limiting-oxidative-stress-following-neurotrauma-with-a-combination-of-ion-channel-inhibitors
#18
Hannah R Milbourn, Lillian M Toomey, Nikolas Gavriel, Chloe G G Gray, Alexander H Gough, Marcus K Giacci, Melinda Fitzgerald
Following injury to the central nervous system, secondary degeneration is mediated by Ca2+ imbalances and overproduction of reactive oxygen species from mitochondria, and is associated with myelin deficits and loss of function. Preventing intracellular Ca2+ influx at the acute phase of injury is a potential strategy for limiting these deficits and preserving function. The use of single ion channel inhibitors has had little success in attenuating morphological and functional deficits, potentially due to the many pathways by which calcium can traverse the cell membrane...
June 2017: Discovery Medicine
https://www.readbyqxmd.com/read/28877029/impairments-in-age-dependent-ubiquitin-proteostasis-and-structural-integrity-of-selective-neurons-by-uncoupling-ran-gtpase-from-the-ran-binding-domain-3-of-ranbp2-and-identification-of-novel-mitochondrial-isoforms-of-ubiquitin-conjugating-enzyme-e2i-ubc9-and
#19
Hemangi Patil, Dosuk Yoon, Reshma Bhowmick, Yunfei Cai, Kyoung-In Cho, Paulo A Ferreira
The Ran-binding protein 2 (Ranbp2/Nup358) is a cytoplasmic and peripheral nucleoporin comprised of four Ran-GTP-binding domains (RBDs) that are interspersed among diverse structural domains with multifunctional activities. Our prior studies found that the RBD2 and RBD3 of Ranbp2 control mitochondrial motility independently of Ran-GTP-binding in cultured cells, whereas loss of Ran-GTP-binding to RBD2 and RBD3 are essential to support cone photoreceptor development and the survival of mature retinal pigment epithelium (RPE) in mice...
September 6, 2017: Small GTPases
https://www.readbyqxmd.com/read/28874589/dual-role-of-mitochondria-in-producing-melatonin-and-driving-gpcr-signaling-to-block-cytochrome-c-release
#20
Yalikun Suofu, Wei Li, Frédéric G Jean-Alphonse, Jiaoying Jia, Nicolas K Khattar, Jiatong Li, Sergei V Baranov, Daniela Leronni, Amanda C Mihalik, Yanqing He, Erika Cecon, Vanessa L Wehbi, JinHo Kim, Brianna E Heath, Oxana V Baranova, Xiaomin Wang, Matthew J Gable, Eric S Kretz, Giulietta Di Benedetto, Timothy R Lezon, Lisa M Ferrando, Timothy M Larkin, Mara Sullivan, Svitlana Yablonska, Jingjing Wang, M Beth Minnigh, Gérald Guillaumet, Franck Suzenet, R Mark Richardson, Samuel M Poloyac, Donna B Stolz, Ralf Jockers, Paula A Witt-Enderby, Diane L Carlisle, Jean-Pierre Vilardaga, Robert M Friedlander
G protein-coupled receptors (GPCRs) are classically characterized as cell-surface receptors transmitting extracellular signals into cells. Here we show that central components of a GPCR signaling system comprised of the melatonin type 1 receptor (MT1), its associated G protein, and β-arrestins are on and within neuronal mitochondria. We discovered that the ligand melatonin is exclusively synthesized in the mitochondrial matrix and released by the organelle activating the mitochondrial MT1 signal-transduction pathway inhibiting stress-mediated cytochrome c release and caspase activation...
September 5, 2017: Proceedings of the National Academy of Sciences of the United States of America
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