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https://www.readbyqxmd.com/read/28211874/datf4-regulation-of-mitochondrial-folate-mediated-one-carbon-metabolism-is-neuroprotective
#1
Ivana Celardo, Susann Lehmann, Ana C Costa, Samantha Hy Loh, L Miguel Martins
Neurons rely on mitochondria as their preferred source of energy. Mutations in PINK1 and PARKIN cause neuronal death in early-onset Parkinson's disease (PD), thought to be due to mitochondrial dysfunction. In Drosophila pink1 and parkin mutants, mitochondrial defects lead to the compensatory upregulation of the mitochondrial one-carbon cycle metabolism genes by an unknown mechanism. Here we uncover that this branch is triggered by the activating transcription factor 4 (ATF4). We show that ATF4 regulates the expression of one-carbon metabolism genes SHMT2 and NMDMC as a protective response to mitochondrial toxicity...
February 17, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28211814/are-major-dementias-triggered-by-poor-blood-flow-to-the-brain-theoretical-considerations
#2
Jack C de la Torre
There is growing evidence that chronic brain hypoperfusion plays a central role in the development of Alzheimer's disease (AD) long before dyscognitive symptoms or amyloid-β accumulation in the brain appear. This commentary proposes that dementia with Lewy bodies (DLB), frontotemporal dementia (FTD), and Creutzfeldt-Jakob disease (CJD) may also develop from chronic brain hypoperfusion following a similar but not identical neurometabolic breakdown as AD. The argument to support this conclusion is that chronic brain hypoperfusion, which is found at the early stages of the three dementias reviewed here, will reduce oxygen delivery and lower oxidative phosphorylation promoting a steady decline in the synthesis of the cell energy fuel adenosine triphosphate (ATP)...
February 15, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28210902/deletion-of-mammalian-sterile-20-like-kinase-1-attenuates-neuronal-loss-and-improves-locomotor-function-in-a-mouse-model-of-spinal-cord-trauma
#3
Pan-Feng Wang, Da-Yuan Xu, Yuntong Zhang, Xiao-Bin Liu, Yan Xia, Pan-Yu Zhou, Qing-Ge Fu, Shuo-Gui Xu
Neuronal cell death following spinal cord injury (SCI) is an important contributor to neurological deficits. The purpose of our work was to delineate the function of mammalian sterile 20-like kinase 1 (Mst1), a pro-apoptotic kinase and key mediator of apoptotic signaling, in the pathogenesis of an experimental mouse model of SCI. Male mice received a mid-thoracic spinal contusion injury, and it was found that phosphorylation of Mst1 at the injured site was enhanced significantly following SCI. Furthermore, when compared to the wild-type controls, Mst1-deficient mice displayed improved locomotor function by increased Basso mouse scale score...
February 16, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/28209644/mitochondrial-dysfunction-induces-dendritic-loss-via-eif2%C3%AE-phosphorylation
#4
Taiichi Tsuyama, Asako Tsubouchi, Tadao Usui, Hiromi Imamura, Tadashi Uemura
Mitochondria are key contributors to the etiology of diseases associated with neuromuscular defects or neurodegeneration. How changes in cellular metabolism specifically impact neuronal intracellular processes and cause neuropathological events is still unclear. We here dissect the molecular mechanism by which mitochondrial dysfunction induced by Prel aberrant function mediates selective dendritic loss in Drosophila melanogaster class IV dendritic arborization neurons. Using in vivo ATP imaging, we found that neuronal cellular ATP levels during development are not correlated with the progression of dendritic loss...
February 16, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28208702/the-glutamate-dehydrogenase-pathway-and-its-roles-in-cell-and-tissue-biology-in-health-and-disease
#5
REVIEW
Andreas Plaitakis, Ester Kalef-Ezra, Dimitra Kotzamani, Ioannis Zaganas, Cleanthe Spanaki
Glutamate dehydrogenase (GDH) is a hexameric enzyme that catalyzes the reversible conversion of glutamate to α-ketoglutarate and ammonia while reducing NAD(P)⁺ to NAD(P)H. It is found in all living organisms serving both catabolic and anabolic reactions. In mammalian tissues, oxidative deamination of glutamate via GDH generates α-ketoglutarate, which is metabolized by the Krebs cycle, leading to the synthesis of ATP. In addition, the GDH pathway is linked to diverse cellular processes, including ammonia metabolism, acid-base equilibrium, redox homeostasis (via formation of fumarate), lipid biosynthesis (via oxidative generation of citrate), and lactate production...
February 8, 2017: Biology
https://www.readbyqxmd.com/read/28202127/-role-of-mitophagy-in-neonatal-rats-with-hypoxic-ischemic-brain-damage
#6
Ming-Xi Li, Yi Qu, De-Zhi Mu
OBJECTIVE: To investigate mitophagy in an animal model of hypoxic-ischemic brain damage (HIBD) and its role in HIBD. METHODS: A total of 120 neonatal Sprague-Dawley rats aged 7 days were divided into three groups: sham-operation, HIBD, and autophagy inhibitor intervention (3MA group). The rats in the HIBD group were treated with right common carotid artery ligation and then put in a hypoxic chamber (8% oxygen and 92% nitrogen) for 2.5 hours. Those in the 3MA group were given ligation and hypoxic treatment at 30 minutes after intraperitoneal injection of 2 μL 3MA...
February 2017: Zhongguo Dang Dai Er Ke za Zhi, Chinese Journal of Contemporary Pediatrics
https://www.readbyqxmd.com/read/28198506/inhibition-of-mitochondrial-calcium-uptake-1-in-drosophila-neurons
#7
P G M'Angale, B E Staveley
The mitochondrial calcium uptake 1 (MICU1) is a regulatory subunit of the mitochondrial calcium uniporter that plays an important role in calcium sensing. It contains two EF-hand domains that are well conserved across diverse species from protozoa to plants and metazoans. The loss of MICU1 function in mammals is attributed to several neurological disorders that involve movement dysfunction. The CG4495 gene in Drosophila melanogaster was identified as a putative homolog of MICU1 in the HomoloGene database of the National Centre for Biotechnology Information (NCBI)...
February 8, 2017: Genetics and Molecular Research: GMR
https://www.readbyqxmd.com/read/28197093/ultrastructural-and-functional-properties-of-a-giant-synapse-driving-the-piriform-cortex-to-mediodorsal-thalamus-projection
#8
Patric Pelzer, Heinz Horstmann, Thomas Kuner
Neocortico-thalamo-cortical loops represent a common, yet poorly understood, circuit employing giant synapses also referred to as "class I", giant, or driver synapses. Here, we characterize a giant synapse formed by projection neurons of the paleocortical piriform cortex (PIR) onto neurons of the mediodorsal thalamus (MD). Three-dimensional (3D) ultrastructure of labeled PIR-MD terminals, obtained by using serial-section scanning electron microscopy (EM) combined with photooxidation-based detection of labeled terminals, revealed a large terminal engulfing multiple postsynaptic dendritic excrescences...
2017: Frontiers in Synaptic Neuroscience
https://www.readbyqxmd.com/read/28195557/biogenetic-and-morphofunctional-heterogeneity-of-mitochondria-the-case-of-synaptic-mitochondria
#9
Sergei V Fedorovich, Tatyana V Waseem, Ludmila V Puchkova
The mitochondria of different cells are different in their morphological and biochemical properties. These organelles generate free radicals during activity, leading inevitably to mitochondrial DNA damage. It is not clear how this problem is addressed in long-lived cells, such as neurons. We propose the hypothesis that mitochondria within the same cell also differ in lifespan and ability to divide. According to our suggestion, cells have a pool of 'stem' mitochondria with low metabolic activity and a pool of 'differentiated' mitochondria with significantly shorter lifespans and high metabolic activity...
February 14, 2017: Reviews in the Neurosciences
https://www.readbyqxmd.com/read/28193453/energy-and-the-alzheimer-brain
#10
REVIEW
Mortimer Mamelak
The high energy demands of the poorly myelinated long axon hippocampal and cortical neurons render these neurons selectively vulnerable to degeneration in Alzheimer's disease. However, pathology engages all of the major elements of the neurovascular unit of the mature Alzheimer brain, the neurons, glia and blood vessels. Neurons present with retrograde degeneration of the axodendritic tree, capillaries with string vessels and markedly reduced densities and glia with signs of inflammatory activation. The neurons, capillaries and astrocytes of the mature Alzheimer brain harbor structurally defective mitochondria...
February 10, 2017: Neuroscience and Biobehavioral Reviews
https://www.readbyqxmd.com/read/28191272/mitochondrial-ferritin-deletion-exacerbates-%C3%AE-amyloid-induced-neurotoxicity-in-mice
#11
Peina Wang, Qiong Wu, Wenyue Wu, Haiyan Li, Yuetong Guo, Peng Yu, Guofen Gao, Zhenhua Shi, Baolu Zhao, Yan-Zhong Chang
Mitochondrial ferritin (FtMt) is a mitochondrial iron storage protein which protects mitochondria from iron-induced oxidative damage. Our previous studies indicate that FtMt attenuates β-amyloid- and 6-hydroxydopamine-induced neurotoxicity in SH-SY5Y cells. To explore the protective effects of FtMt on β-amyloid-induced memory impairment and neuronal apoptosis and the mechanisms involved, 10-month-old wild-type and Ftmt knockout mice were infused intracerebroventricularly (ICV) with Aβ25-35 to establish an Alzheimer's disease model...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28190529/mitophagy-and-alzheimer-s-disease-cellular-and-molecular-mechanisms
#12
REVIEW
Jesse S Kerr, Bryan A Adriaanse, Nigel H Greig, Mark P Mattson, M Zameel Cader, Vilhelm A Bohr, Evandro F Fang
Neurons affected in Alzheimer's disease (AD) experience mitochondrial dysfunction and a bioenergetic deficit that occurs early and promotes the disease-defining amyloid beta peptide (Aβ) and Tau pathologies. Emerging findings suggest that the autophagy/lysosome pathway that removes damaged mitochondria (mitophagy) is also compromised in AD, resulting in the accumulation of dysfunctional mitochondria. Results in animal and cellular models of AD and in patients with sporadic late-onset AD suggest that impaired mitophagy contributes to synaptic dysfunction and cognitive deficits by triggering Aβ and Tau accumulation through increases in oxidative damage and cellular energy deficits; these, in turn, impair mitophagy...
February 9, 2017: Trends in Neurosciences
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
#13
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 (NSC). However, the survival of young neurons is sharply reduced by post-injury 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...
February 10, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28179130/mitochondrial-function-in-m%C3%A3-ller-cells-does-it-matter
#14
Anne Katrine Toft-Kehler, Dorte Marie Skytt, Alicia Svare, Evy Lefevere, Inge Van Hove, Lieve Moons, Helle S Waagepetersen, Miriam Kolko
Growing evidence suggests that mitochondrial dysfunction might play a key role in the pathogenesis of age-related neurodegenerative inner retinal diseases such as diabetic retinopathy and glaucoma. Therefore, the present review provides a perspective on the impact of functional mitochondria in the most predominant glial cells of the retina, the Müller cells. Müller cells span the entire thickness of the neuroretina and are in close proximity to retinal cells including the retinal neurons that provides visual signaling to the brain...
February 5, 2017: Mitochondrion
https://www.readbyqxmd.com/read/28178240/c-elegans-neurons-jettison-protein-aggregates-and-mitochondria-under-neurotoxic-stress
#15
Ilija Melentijevic, Marton L Toth, Meghan L Arnold, Ryan J Guasp, Girish Harinath, Ken C Nguyen, Daniel Taub, J Alex Parker, Christian Neri, Christopher V Gabel, David H Hall, Monica Driscoll
The toxicity of misfolded proteins and mitochondrial dysfunction are pivotal factors that promote age-associated functional neuronal decline and neurodegenerative disease. Accordingly, neurons invest considerable cellular resources in chaperones, protein degradation, autophagy and mitophagy to maintain proteostasis and mitochondrial quality. Complicating the challenges of neuroprotection, misfolded human disease proteins and mitochondria can move into neighbouring cells via unknown mechanisms, which may promote pathological spread...
February 8, 2017: Nature
https://www.readbyqxmd.com/read/28170536/astrocytes-in-the-optic-nerve-head-of-glaucomatous-mice-display-a-characteristic-reactive-phenotype
#16
Rui Wang, Philip Seifert, Tatjana C Jakobs
Purpose: Optic nerve head astrocytes, a subtype of white-matter astrocytes, become reactive early in the course of glaucoma. It was shown recently that in the DBA/2J mouse model of inherited glaucoma optic nerve astrocytes extend new longitudinal processes into the axon bundles before ganglion cell loss becomes apparent. The present study aims at testing whether this behavior of astrocytes is typical of early glaucomatous damage. Methods: Mice expressing green fluorescent protein in individual astrocytes were used to evaluate the early response of astrocytes in the glial lamina of the optic nerve head after increasing the IOP using the microbead occlusion method...
February 1, 2017: Investigative Ophthalmology & Visual Science
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
#17
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/28163681/app-deletion-accounts-for-age-dependent-changes-in-the-bioenergetic-metabolism-and-in-hyperphosphorylated-camkii-at-stimulated-hippocampal-presynaptic-active-zones
#18
Melanie Laßek, Jens Weingarten, Martin Wegner, Moritz Neupärtl, Tabiwang N Array, Eva Harde, Benedikt Beckert, Vahid Golghalyani, Jörg Ackermann, Ina Koch, Ulrike C Müller, Michael Karas, Amparo Acker-Palmer, Walter Volknandt
Synaptic release sites are characterized by exocytosis-competent synaptic vesicles tightly anchored to the presynaptic active zone (PAZ) whose proteome orchestrates the fast signaling events involved in synaptic vesicle cycle and plasticity. Allocation of the amyloid precursor protein (APP) to the PAZ proteome implicated a functional impact of APP in neuronal communication. In this study, we combined state-of-the-art proteomics, electrophysiology and bioinformatics to address protein abundance and functional changes at the native hippocampal PAZ in young and old APP-KO mice...
2017: Frontiers in Synaptic Neuroscience
https://www.readbyqxmd.com/read/28163159/mitochondrial-ferritin-protects-sh-sy5y-cells-against-h2o2-induced-oxidative-stress-and-modulates-%C3%AE-synuclein-expression
#19
Hongpeng Guan, Hongkuan Yang, Mingchun Yang, Daijiro Yanagisawa, Jean-Pierre Bellier, Masaki Mori, Shogo Takahata, Takashi Nonaka, Shiguang Zhao, Ikuo Tooyama
Mitochondrial ferritin (FtMt) is a type of ferritin that sequesters iron. Previous studies have shown that FtMt is expressed by dopaminergic neurons in the substantia nigra and that it may be involved in the pathology of Parkinson's disease. However, the functional roles of FtMt in dopaminergic neurons remain unclear. In this study, we investigated the function of FtMt in α-synuclein regulation and its antioxidant roles in dopaminergic cells using human dopaminergic neuroblastoma cells, SH-SY5Y. In physiological conditions, FtMt knockdown increased α-synuclein expression at the protein level but not at the mRNA level...
February 3, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28163115/jia-jian-di-huang-yin-zi-decoction-reduces-apoptosis-induced-by-both-mitochondrial-and-endoplasmic-reticulum-caspase12-pathways-in-the-mouse-model-of-parkinson-s-disease
#20
Jingsi Zhang, Zhennian Zhang, Jie Bao, Zhonghai Yu, Min Cai, Xiangting Li, Ting Wu, Jun Xiang, Dingfang Cai
ETHNOPHARMACOLOGICAL RELEVANCE: As a classical prescription of traditional Chinese medicine (TCM), Jia-Jian-Di-Huang-Yin-Zi decoction (JJDHYZ) has been used to treat the symptoms of neurological disorders with a long history. AIM OF THE STUDY: To evaluate the effects and possible mechanisms of JJDHYZ on a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced subacute mouse model of Parkinson's disease. MATERIALS AND METHODS: Adult male C57BL/6 mice were randomly divided into five groups: control, MPTP, JJDHYZ low dosage (JJDHYZ-L, 8...
February 2, 2017: Journal of Ethnopharmacology
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