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https://www.readbyqxmd.com/read/28322751/neuroprotective-effects-of-2-4-dinitrophenol-in-an-acute-model-of-parkinson-s-disease
#1
Yujeong Lee, Gwangbeom Heo, Kyung Moon Lee, Ah Hyun Kim, Ki Wung Chung, Eunok Im, Hae Young Chung, Jaewon Lee
Neurons depend on mitochondria for homeostasis and survival, and thus, mitochondrial dysfunction has been implicated in neurodegenerative diseases, including Parkinson's disease (PD). Increasing evidence indicates the mitochondrial uncoupler, 2,4-dinitrophenol (DNP), protects neurons against neurodegeneration and enhances neural plasticity. Here, the authors evaluated the protective effects of intraperitoneally (i.p.) administered low dose DNP in an acute mouse model of PD. Mice were administered DNP (1 or 5 mg/kg) for 12 consecutive days, and then on day 13, MPTP (20 mg/kg, i...
March 17, 2017: Brain Research
https://www.readbyqxmd.com/read/28315266/sigma-1-receptors-fine-tune-the-neuronal-networks
#2
Shang-Yi Anne Tsai, Tsung-Ping Su
The endoplasmic reticular (ER) protein sigma-1 receptor (Sig-1R) has been implicated in CNS disorders including but not limited to neurodegenerative diseases, depression , amnesia, and substance abuse. Sig-1Rs are particularly enriched in the specific domain where ER membranes make contacts with the mitochondria (MAM). Within that specific domain, Sig-1Rs play significant roles governing calcium signaling and reactive oxygen species homeostasis to maintain proper neuronal functions. Studies showed that the Sig-1R is pivotal to regulate neuroplasticity and neural survival via multiple aspects of mechanism...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28286181/amplifying-mitochondrial-function-rescues-adult-neurogenesis-in-a-mouse-model-of-alzheimer-s-disease
#3
Kevin Richetin, Manon Moulis, Aurélie Millet, Macarena S Arràzola, Trinovita Andraini, Jennifer Hua, Noélie Davezac, Laurent Roybon, Pascale Belenguer, Marie-Christine Miquel, Claire Rampon
Adult hippocampal neurogenesis is strongly impaired in Alzheimer's disease (AD). In several mouse models of AD, it was shown that adult-born neurons exhibit reduced survival and altered synaptic integration due to a severe lack of dendritic spines. In the present work, using the APPxPS1 mouse model of AD, we reveal that this reduced number of spines is concomitant of a marked deficit in their neuronal mitochondrial content. Remarkably, we show that targeting the overexpression of the pro-neural transcription factor Neurod1 into APPxPS1 adult-born neurons restores not only their dendritic spine density, but also their mitochondrial content and the proportion of spines associated with mitochondria...
March 10, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28283027/integrated-analysis-of-genetic-behavioral-and-biochemical-data-implicates-neural-stem-cell-induced-changes-in-immunity-neurotransmission-and-mitochondrial-function-in-dementia-with-lewy-body-mice
#4
Anita Lakatos, Natalie R S Goldberg, Mathew Blurton-Jones
We previously demonstrated that transplantation of murine neural stem cells (NSCs) can improve motor and cognitive function in a transgenic model of Dementia with Lewy Bodies (DLB). These benefits occurred without changes in human α-synuclein pathology and were mediated in part by stem cell-induced elevation of brain-derived neurotrophic factor (BDNF). However, instrastriatal NSC transplantation likely alters the brain microenvironment via multiple mechanisms that may synergize to promote cognitive and motor recovery...
March 10, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28250467/automated-synaptic-connectivity-inference-for-volume-electron-microscopy
#5
Sven Dorkenwald, Philipp J Schubert, Marius F Killinger, Gregor Urban, Shawn Mikula, Fabian Svara, Joergen Kornfeld
Teravoxel volume electron microscopy data sets from neural tissue can now be acquired in weeks, but data analysis requires years of manual labor. We developed the SyConn framework, which uses deep convolutional neural networks and random forest classifiers to infer a richly annotated synaptic connectivity matrix from manual neurite skeleton reconstructions by automatically identifying mitochondria, synapses and their types, axons, dendrites, spines, myelin, somata and cell types. We tested our approach on serial block-face electron microscopy data sets from zebrafish, mouse and zebra finch, and computed the synaptic wiring of songbird basal ganglia...
February 27, 2017: Nature Methods
https://www.readbyqxmd.com/read/28224980/alpha-synuclein-prevents-the-formation-of-spherical-mitochondria-and-apoptosis-under-oxidative-stress
#6
Stefanie Menges, Georgia Minakaki, Patrick M Schaefer, Holger Meixner, Iryna Prots, Ursula Schlötzer-Schrehardt, Kristina Friedland, Beate Winner, Tiago F Outeiro, Konstanze F Winklhofer, Christine A F von Arnim, Wei Xiang, Jürgen Winkler, Jochen Klucken
Oxidative stress (OS), mitochondrial dysfunction, and dysregulation of alpha-synuclein (aSyn) homeostasis are key pathogenic factors in Parkinson's disease. Nevertheless, the role of aSyn in mitochondrial physiology remains elusive. Thus, we addressed the impact of aSyn specifically on mitochondrial response to OS in neural cells. We characterize a distinct type of mitochondrial fragmentation, following H2O2 or 6-OHDA-induced OS, defined by spherically-shaped and hyperpolarized mitochondria, termed "mitospheres"...
February 22, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28223472/overexpression-of-sarcoendoplasmic-reticulum-calcium-atpase-2a-promotes-cardiac-sympathetic-neurotransmission-via-abnormal-endoplasmic-reticulum-and-mitochondria-ca-2-regulation
#7
Julia Shanks, Neil Herring, Errin Johnson, Kun Liu, Dan Li, David J Paterson
Reduced cardiomyocyte excitation-contraction coupling and downregulation of the SERCA2a (sarcoendoplasmic reticulum calcium ATPase 2a) is associated with heart failure. This has led to viral transgene upregulation of SERCA2a in cardiomyocytes as a treatment. We hypothesized that SERCA2a gene therapy expressed under a similar promiscuous cytomegalovirus promoter could also affect the cardiac sympathetic neural axis and promote sympathoexcitation. Stellate neurons were isolated from 90 to 120 g male, Sprague-Dawley, Wistar Kyoto, and spontaneously hypertensive rats...
April 2017: Hypertension
https://www.readbyqxmd.com/read/28188219/distinct-effects-of-mir-210-reduction-on-neurogenesis-increased-neuronal-survival-of-inflammation-but-reduced-proliferation-associated-with-mitochondrial-enhancement
#8
Ludmila A Voloboueva, Xiaoyun Sun, Lijun Xu, Yi-Bing Ouyang, Rona G Giffard
Neurogenesis is essential to brain development and plays a central role in the response to brain injury. Stroke and head trauma stimulate proliferation of endogenous neural stem cells (NSCs); however, the survival of young neurons is sharply reduced by postinjury inflammation. Cellular mitochondria are critical to successful neurogenesis and are a major target of inflammatory injury. Mitochondrial protection was shown to improve survival of young neurons. This study tested whether reducing cellular microRNA-210 (miR-210) would enhance mitochondrial function and improve survival of young murine neurons under inflammatory conditions...
March 15, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28164768/protective-effect-of-aspirin-against-oligomeric-a%C3%AE-42-induced-mitochondrial-alterations-and-neurotoxicity-in-differentiated-ec-p19-neuronal-cells
#9
Hamendra Singh Parmar, Zbynek Houdek, Martin Pesta, Vaclava Cerna, Pavel Dvorak, Jiri Hatina
Amyloid-beta (Aβ) induced mitochondrial dysfunction is one of the major causes of neuronal toxicity in Alzheimer's disease. Many recent reports suggest involvement of mitochondrial alterations through intracellular accumulation of oligomeric Aβ. These mitochondrial alterations include increased reactive oxygen species (ROS), mt-DNA depletion, decreased oxidative phosphorylation and ATP production, membrane depolarization, reduced number of mitochondria etc. These all defects cumulatively caused neural toxicity and alterations in cellular energy homeostasis...
February 2, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/28139935/systemic-activation-of-toll-like-receptor-2-suppresses-mitochondrial-respiration-and-exacerbates-hypoxic-ischemic-injury-in-the-developing-brain
#10
Amin Mottahedin, Pernilla Svedin, Syam Nair, Carl-Johan Mohn, Xiaoyang Wang, Henrik Hagberg, Joakim Ek, Carina Mallard
Infection and inflammation are known risk factors for neonatal brain injury. Mycoplasma and Gram-positive bacteria, for which Toll-like receptor 2 (TLR2) plays a key role in recognition and inflammatory response, are among the most common pathogens in the perinatal period. Here, we report that systemic activation of TLR2 by Pam3CSK4 (P3C) increases neural tissue loss and demyelination induced by subsequent hypoxia-ischemia (HI) in neonatal mice. High-resolution respirometry of brain isolated mitochondria revealed that P3C suppresses ADP-induced oxidative phosphorylation, the main pathway of cellular energy production...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/28118061/a-comparison-of-radiation-induced-mitochondrial-damage-between-neural-progenitor-stem-cells-and-differentiated-cells
#11
Tsutomu Shimura, Megumi Sasatani, Hidehiko Kawai, Kenji Kamiya, Junya Kobayashi, Kenshi Komatsu, Naoki Kunugita
Mitochondria play a key role in maintaining cellular homeostasis during stress responses, and mitochondrial dysfunction contributes to carcinogenesis, aging, and neurological disease. We here investigated ionizing radiation (IR)-induced mitochondrial damage in human neural progenitor stem cells (NSCs), their differentiated counterparts and human normal fibroblasts. Long-term fractionated radiation (FR) with low doses of X-rays for 31 days enhanced mitochondrial activity as evident by elevated mitochondrial membrane potential (ΔΨm) and mitochondrial complex IV (cytochrome c oxidase) activity to fill the energy demands for the chronic DNA damage response in differentiated cells...
January 24, 2017: Cell Cycle
https://www.readbyqxmd.com/read/28112198/chlorpyrifos-inhibits-neural-induction-via-mfn1-mediated-mitochondrial-dysfunction-in-human-induced-pluripotent-stem-cells
#12
Shigeru Yamada, Yusuke Kubo, Daiju Yamazaki, Yuko Sekino, Yasunari Kanda
Organophosphates, such as chlorpyrifos (CPF), are widely used as insecticides in agriculture. CPF is known to induce cytotoxicity, including neurodevelopmental toxicity. However, the molecular mechanisms of CPF toxicity at early fetal stage have not been fully elucidated. In this study, we examined the mechanisms of CPF-induced cytotoxicity using human induced pluripotent stem cells (iPSCs). We found that exposure to CPF at micromolar levels decreased intracellular ATP levels. As CPF suppressed energy production that is a critical function of the mitochondria, we focused on the effects of CPF on mitochondrial dynamics...
January 23, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28112032/spermidine-preconditioning-ameliorates-laurate-induced-brain-injury-by-maintaining-mitochondrial-stability
#13
Yi Zhang, Jie Yin, Lang Zhang, Chu-Chu Qi, Ze-Lin Ma, Li-Ping Gao, De-Gui Wang, Yu-Hong Jing
Ischemic precondition plays a protective effect during cerebral ischemia. This effect partly depends on the autophagic activity. However, whether the activity of autophagy can exert the protective effects after cerebral ischemia is unclear. In this study, rats were treated with spermidine, an activator of autophagy, and injected with sodium laurate via the internal carotid artery to stimulate cerebral small vessel disease (CSVD). The effects of the spermidine precondition on brain injury were evaluated by behavioural test, histology assay, ultrastructure observation, and autophagic-related signals...
March 2017: Neurological Research
https://www.readbyqxmd.com/read/28098577/mitochondria-initiate-and-regulate-sarcopenia
#14
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.
April 2017: Exercise and Sport Sciences Reviews
https://www.readbyqxmd.com/read/28095073/preclinical-and-potential-applications-of-common-western-herbal-supplements-as-complementary-treatment-in-parkinson-s-disease
#15
Luke A Morgan, Oliver Grundmann
Parkinson's disease (PD) is a neurological disorder with a complex pathological etiology, which is not fully understood. Progression of PD may be the result of a buildup of iron in the substantia nigra, microglia-mediated neuroinflammation, dysfunctional mitochondria, or abnormal protein handling. Dopamine is the main neurotransmitter affected, but as the disease progresses, a decrease in all the brain's biogenic amines occurs. Current medication used in the treatment of PD aims to prevent the breakdown of dopamine or increase dopaminergic neurotransmission in the central nervous system...
July 4, 2017: Journal of Dietary Supplements
https://www.readbyqxmd.com/read/28066829/the-multifaceted-role-of-nrf2-in-mitochondrial-function
#16
REVIEW
Kira M Holmström, Rumen V Kostov, Albena T Dinkova-Kostova
The transcription factor nuclear factor erythroid 2 p45-related factor 2 (Nrf2) is the master regulator of the cellular redox homeostasis. Nrf2 target genes comprise of a large network of antioxidant enzymes, proteins involved in xenobiotic detoxification, repair and removal of damaged proteins, inhibition of inflammation, as well as other transcription factors. In recent years it has emerged that as part of its role as a regulator of cytoprotective gene expression, Nrf2 impacts mitochondrial function. Increased Nrf2 activity defends against mitochondrial toxins...
December 2016: Curr Opin Toxicol
https://www.readbyqxmd.com/read/28065847/a-drosophila-model-of-gdap1-function-reveals-the-involvement-of-insulin-signalling-in-the-mitochondria-dependent-neuromuscular-degeneration
#17
Víctor López Del Amo, Martina Palomino-Schätzlein, Marta Seco-Cervera, José Luis García-Giménez, Federico Vicente Pallardó, Antonio Pineda-Lucena, Máximo Ibo Galindo
Charcot-Marie-Tooth disease is a rare peripheral neuropathy for which there is no specific treatment. Some forms of Charcot-Marie-Tooth are due to mutations in the GDAP1 gene. A striking feature of mutations in GDAP1 is that they have a variable clinical manifestation, according to disease onset and progression, histology and mode of inheritance. Studies in cellular and animal models have revealed a role of GDAP1 in mitochondrial morphology and distribution, calcium homeostasis and oxidative stress. To get a better understanding of the disease mechanism we have generated models of over-expression and RNA interference of the Drosophila Gdap1 gene...
January 6, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28057485/efficient-induction-of-dopaminergic-neuron-differentiation-from-induced-pluripotent-stem-cells-reveals-impaired-mitophagy-in-park2-neurons
#18
Sadafumi Suzuki, Wado Akamatsu, Fumihiko Kisa, Takefumi Sone, Kei-Ichi Ishikawa, Naoko Kuzumaki, Hiroyuki Katayama, Atsushi Miyawaki, Nobutaka Hattori, Hideyuki Okano
Patient-specific induced pluripotent stem cells (iPSCs) show promise for use as tools for in vitro modeling of Parkinson's disease. We sought to improve the efficiency of dopaminergic (DA) neuron induction from iPSCs by the using surface markers expressed in DA progenitors to increase the significance of the phenotypic analysis. By sorting for a CD184(high)/CD44(-) fraction during neural differentiation, we obtained a population of cells that were enriched in DA neuron precursor cells and achieved higher differentiation efficiencies than those obtained through the same protocol without sorting...
January 29, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28005071/rab8a-rab11a-regulate-intercellular-communications-between-neural-cells-via-tunneling-nanotubes
#19
Hui Zhu, Chengbin Xue, Xi Xu, Yibing Guo, Xiaohong Li, Jingjing Lu, Shaoqing Ju, Yongjun Wang, Zheng Cao, Xiaosong Gu
Tunneling nanotubes (TNTs) are F-actin-based membrane tubes, and can form between cultured cells and within vital tissues. TNTs mediate intercellular communications that range from electrical signaling to the transfer of organelles. Following peripheral nerve injury, the orchestrated intercellular communications among neural and non-neural cells are required for effective nerve regeneration. It remains unknown whether TNTs exist between neural cells in the peripheral nerve system and how TNTs affect neural regeneration...
December 22, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27941687/low-dose-methylmercury-induced-genes-regulate-mitochondrial-biogenesis-via-mir-25-in-immortalized-human-embryonic-neural-progenitor-cells
#20
Xinjin Wang, Mengling Yan, Lina Zhao, Qing Wu, Chunhua Wu, Xiuli Chang, Zhijun Zhou
Mitochondria are essential organelles and important targets for environmental pollutants. The detection of mitochondrial biogenesis and generation of reactive oxygen species (ROS) and p53 levels following low-dose methylmercury (MeHg) exposure could expand our understanding of underlying mechanisms. Here, the sensitivity of immortalized human neural progenitor cells (ihNPCs) upon exposure to MeHg was investigated. We found that MeHg altered cell viability and the number of 5-ethynyl-2'-deoxyuridine (EdU)-positive cells...
December 9, 2016: International Journal of Molecular Sciences
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