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https://www.readbyqxmd.com/read/29760952/downregulation-of-the-psychiatric-susceptibility-gene-cacna1c-promotes-mitochondrial-resilience-to-oxidative-stress-in-neuronal-cells
#1
Susanne Michels, Goutham K Ganjam, Helena Martins, Gerhard M Schratt, Markus Wöhr, Rainer K W Schwarting, Carsten Culmsee
Affective disorders such as major depression and bipolar disorder are among the most prevalent forms of mental illness and their etiologies involve complex interactions between genetic and environmental risk factors. Over the past ten years, several genome wide association studies (GWAS) have identified CACNA1C as one of the strongest genetic risk factors for the development of affective disorders. However, its role in disease pathogenesis is still largely unknown. Vulnerability to affective disorders also involves diverse environmental risk factors such as perinatal insults, childhood maltreatment, and other adverse pathophysiological or psychosocial life events...
2018: Cell Death Discovery
https://www.readbyqxmd.com/read/29742940/the-role-of-oxidative-stress-in-anxiety-disorder-cause-or-consequence
#2
Alessandra das Graças Fedoce, Frederico Ferreira, Robert G Bota, Vicent Bonet-Costa, Patrick Y Sun, Kelvin J A Davies
Anxiety disorders are the most common mental illness in the USA affecting 18% of the population. The cause(s) of anxiety disorders is/are not completely clear, and research in the neurobiology of anxiety at the molecular level is still rather limited. Although mounting clinical and preclinical evidence now indicates that oxidative stress may be a major component of anxiety pathology, whether oxidative stress is the cause or consequence remains elusive. Studies conducted over the past few years suggest that anxiety disorders may be characterized by lowered antioxidant defenses and increased oxidative damage to proteins, lipids and nucleic acids...
May 9, 2018: Free Radical Research
https://www.readbyqxmd.com/read/29628042/a-comprehensive-analysis-of-nuclear-encoded-mitochondrial-genes-in-schizophrenia
#3
Vanessa F Gonçalves, Carolina Cappi, Christian M Hagen, Adolfo Sequeira, Marquis P Vawter, Andriy Derkach, Clement C Zai, Paula L Hedley, Jonas Bybjerg-Grauholm, Jennie G Pouget, Ari B Cuperfain, Patrick F Sullivan, Michael Christiansen, James L Kennedy, Lei Sun
BACKGROUND: The genetic risk factors of schizophrenia (SCZ), a severe psychiatric disorder, are not yet fully understood. Multiple lines of evidence suggest that mitochondrial dysfunction may play a role in SCZ, but comprehensive association studies are lacking. We hypothesized that variants in nuclear-encoded mitochondrial genes influence susceptibility to SCZ. METHODS: We conducted gene-based and gene-set analyses using summary association results from the Psychiatric Genomics Consortium Schizophrenia Phase 2 (PGC-SCZ2) genome-wide association study comprising 35,476 cases and 46,839 control subjects...
May 1, 2018: Biological Psychiatry
https://www.readbyqxmd.com/read/29594645/the-role-of-suboptimal-mitochondrial-function-in-vulnerability-to-post-traumatic-stress-disorder
#4
REVIEW
Graeme Preston, Faisal Kirdar, Tamas Kozicz
Post-traumatic stress disorder remains the most significant psychiatric condition associated with exposure to a traumatic event, though rates of traumatic event exposure far outstrip incidence of PTSD. Mitochondrial dysfunction and suboptimal mitochondrial function have been increasingly implicated in several psychopathologies, and recent genetic studies have similarly suggested a pathogenic role of mitochondria in PTSD. Mitochondria play a central role in several physiologic processes underlying PTSD symptomatology, including abnormal fear learning, brain network activation, synaptic plasticity, steroidogenesis, and inflammation...
March 28, 2018: Journal of Inherited Metabolic Disease
https://www.readbyqxmd.com/read/29560378/phenotypic-heterogeneity-in-m-3243a-g-mitochondrial-disease-the-role-of-nuclear-factors
#5
Sarah J Pickett, John P Grady, Yi Shiau Ng, Gráinne S Gorman, Andrew M Schaefer, Ian J Wilson, Heather J Cordell, Doug M Turnbull, Robert W Taylor, Robert McFarland
Objective: The pathogenic mitochondrial DNA m.3243A>G mutation is associated with a wide range of clinical features, making disease prognosis extremely difficult to predict. We aimed to understand the cause of this heterogeneity. Methods: We examined the phenotypic profile of 238 adult m.3243A>G carriers (patients and asymptomatic carriers) from the UK MRC Mitochondrial Disease Patient Cohort using the Newcastle Mitochondrial Disease Adult Scale. We modeled the role of risk factors for the development of specific phenotypes using proportional odds logistic regression...
March 2018: Annals of Clinical and Translational Neurology
https://www.readbyqxmd.com/read/29530757/neuromuscular-synapse-degeneration-without-muscle-function-loss-in-the-diaphragm-of-a-murine-model-for-huntington-s-disease
#6
Priscila A C Valadão, Matheus P S M Gomes, Bárbara C Aragão, Hermann A Rodrigues, Jéssica N Andrade, Rubens Garcias, Julliane V Joviano-Santos, Murilo A Luiz, Wallace L Camargo, Lígia A Naves, Christopher Kushmerick, Walter L G Cavalcante, Márcia Gallacci, Itamar C G de Jesus, Silvia Guatimosim, Cristina Guatimosim
Huntington's disease (HD) is an autosomal dominant neurodegenerative disease characterized by chorea, incoordination, and psychiatric and behavioral symptoms. The leading cause of death in HD patients is aspiration pneumonia, associated with respiratory dysfunction, decreased respiratory muscle strength and dysphagia. Although most of the motor symptoms are derived from alterations in the central nervous system, some might be associated with changes in the components of motor units (MU). To explore this hypothesis, we evaluated morphofunctional aspects of the diaphragm muscle in a mouse model of HD (BACHD)...
March 9, 2018: Neurochemistry International
https://www.readbyqxmd.com/read/29523295/molecular-hypotheses-to-explain-the-shared-pathways-and-underlying-pathobiological-causes-in-catatonia-and-in-catatonic-presentations-in-neuropsychiatric-disorders
#7
E M Peter-Ross
The pathobiological causes, the shared cellular and molecular pathways in catatonia and in catatonic presentation in neuropsychiatric disorders are yet to be determined. The hypotheses in this paper have been deduced from the latest scientific research findings and clinical observations of patients with genetic disorders, behavioral phenotypes and other family members suffering mental disorders. The first hypothesis postulates that catatonia and the heterogeneity of catatonic signs and symptoms involve nucleolar dysfunction arising from abnormalities of the brain-specific, non-coding micro-RNA, SNORD115 genes (either duplications or deletions) which result in pathobiological dysfunction of various combinations in the downstream pathways (possibly along with other genes in these shared pathways)...
April 2018: Medical Hypotheses
https://www.readbyqxmd.com/read/29486891/dynamic-changes-of-the-mitochondria-in-psychiatric-illnesses-new-mechanistic-insights-from-human-neuronal-models
#8
REVIEW
Rupali Srivastava, Travis Faust, Adriana Ramos, Koko Ishizuka, Akira Sawa
Mitochondria play a crucial role in neuronal function, especially in energy production, the generation of reactive oxygen species, and calcium signaling. Multiple lines of evidence have suggested the possible involvement of mitochondrial deficits in major psychiatric disorders, such as schizophrenia and bipolar disorder. This review will outline the current understanding of the physiological role of mitochondria and their dysfunction under pathological conditions, particularly in psychiatric disorders. The current knowledge about mitochondrial deficits in these disorders is somewhat limited because of the lack of effective methods to dissect dynamic changes in functional deficits that are directly associated with psychiatric conditions...
May 1, 2018: Biological Psychiatry
https://www.readbyqxmd.com/read/29477041/mitochondrial-proteomics-investigation-of-frontal-cortex-in-an-animal-model-of-depression-focus-on-chronic-antidepressant-drugs-treatment
#9
Katarzyna Głombik, Aneta Stachowicz, Ewa Trojan, Joanna Ślusarczyk, Maciej Suski, Katarzyna Chamera, Katarzyna Kotarska, Rafał Olszanecki, Agnieszka Basta-Kaim
BACKGROUND: Alteration in the brain mitochondrial functions have been suggested to participate, as a relevant factor, in the development of mental disorders. Therefore, the brain mitochondria may be a crucial therapeutic target in the course of depression. METHODS: Our goal was to find out the impact of two antidepressant drugs with various mechanisms of action - imipramine and fluoxetine, on the frontal cortex mitochondria-enriched fraction in an animal model of depression based on the prenatal stress procedure...
April 2018: Pharmacological Reports: PR
https://www.readbyqxmd.com/read/29458125/pluripotent-stem-cells-for-uncovering-the-role-of-mitochondria-in-human-brain-function-and-dysfunction
#10
REVIEW
Annika Zink, Josef Priller, Alessandro Prigione
Mitochondrial dysfunctions are a known pathogenetic mechanism of a number of neurological and psychiatric disorders. At the same time, mutations in genes encoding for components of the mitochondrial respiratory chain cause mitochondrial diseases, which commonly exhibit neurological symptoms. Mitochondria are therefore critical for the functionality of the human nervous system. The importance of mitochondria stems from their key roles in cellular metabolism, calcium handling, redox and protein homeostasis, and overall cellular homeostasis through their dynamic network...
March 30, 2018: Journal of Molecular Biology
https://www.readbyqxmd.com/read/29411264/understanding-miro-gtpases-implications-in-the-treatment-of-neurodegenerative-disorders
#11
REVIEW
Laura Kay, Ilse S Pienaar, Ruwini Cooray, Gary Black, Meera Soundararajan
The Miro GTPases represent an unusual subgroup of the Ras superfamily and have recently emerged as important mediators of mitochondrial dynamics and for maintaining neuronal health. It is now well-established that these enzymes act as essential components of a Ca2+ -sensitive motor complex, facilitating the transport of mitochondria along microtubules in several cell types, including dopaminergic neurons. The Miros appear to be critical for both anterograde and retrograde mitochondrial transport in axons and dendrites, both of which are considered essential for neuronal health...
February 6, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29289598/why-should-neuroscientists-worry-about-iron-the-emerging-role-of-ferroptosis-in-the-pathophysiology-of-neuroprogressive-diseases
#12
REVIEW
Gerwyn Morris, Michael Berk, André F Carvalho, Michael Maes, Adam J Walker, Basant K Puri
Ferroptosis is a unique form of programmed death, characterised by cytosolic accumulation of iron, lipid hydroperoxides and their metabolites, and effected by the fatal peroxidation of polyunsaturated fatty acids in the plasma membrane. It is a major driver of cell death in neurodegenerative neurological diseases. Moreover, cascades underpinning ferroptosis could be active drivers of neuropathology in major psychiatric disorders. Oxidative and nitrosative stress can adversely affect mechanisms and proteins governing cellular iron homeostasis, such as the iron regulatory protein/iron response element system, and can ultimately be a source of abnormally high levels of iron and a source of lethal levels of lipid membrane peroxidation...
April 2, 2018: Behavioural Brain Research
https://www.readbyqxmd.com/read/28831049/treating-the-placenta-to-prevent-adverse-effects-of-gestational-hypoxia-on-fetal-brain-development
#13
Tom J Phillips, Hannah Scott, David A Menassa, Ashleigh L Bignell, Aman Sood, Jude S Morton, Takami Akagi, Koki Azuma, Mark F Rogers, Catherine E Gilmore, Gareth J Inman, Simon Grant, Yealin Chung, Mais M Aljunaidy, Christy-Lynn Cooke, Bruno R Steinkraus, Andrew Pocklington, Angela Logan, Gavin P Collett, Helena Kemp, Peter A Holmans, Michael P Murphy, Tudor A Fulga, Andrew M Coney, Mitsuru Akashi, Sandra T Davidge, C Patrick Case
Some neuropsychiatric disease, including schizophrenia, may originate during prenatal development, following periods of gestational hypoxia and placental oxidative stress. Here we investigated if gestational hypoxia promotes damaging secretions from the placenta that affect fetal development and whether a mitochondria-targeted antioxidant MitoQ might prevent this. Gestational hypoxia caused low birth-weight and changes in young adult offspring brain, mimicking those in human neuropsychiatric disease. Exposure of cultured neurons to fetal plasma or to secretions from the placenta or from model trophoblast barriers that had been exposed to altered oxygenation caused similar morphological changes...
August 22, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28793231/association-of-mitochondrial-dna-10398-a-g-polymorphism-with-attention-deficit-and-hyperactivity-disorder-in-korean-children
#14
In Wook Hwang, Jun Ho Hong, Bit Na Kwon, Hyung Jun Kim, Noo Ri Lee, Myung Ho Lim, Ho Jang Kwon, Han Jun Jin
Mitochondria are subcellular organelles that contribute to aerobic ATP generation by oxidative phosphorylation (OXPHOS). Previous studies reported that mitochondrial dysfunction and deficiency caused by mitochondrial DNA polymorphisms is associated with various diseases. Especially, mitochondrial DNA 10398 A/G polymorphism is known to affect the regulation of mitochondrial calcium levels related to energy production, and its association with psychiatric disorders such as schizophrenia and bipolar disorder has been reported...
September 30, 2017: Gene
https://www.readbyqxmd.com/read/28639241/huntington-s-disease-and-mitochondria
#15
REVIEW
Mohammad Jodeiri Farshbaf, Kamran Ghaedi
Huntington's disease (HD) as an inherited neurodegenerative disorder leads to neuronal loss in striatum. Progressive motor dysfunction, cognitive decline, and psychiatric disturbance are the main clinical symptoms of the HD. This disease is caused by expansion of the CAG repeats in exon 1 of the huntingtin which encodes Huntingtin protein (Htt). Various cellular and molecular events play role in the pathology of HD. Mitochondria as important organelles play crucial roles in the most of neurodegenerative disorders like HD...
October 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28534301/effects-of-acetyl-l-carnitine-in-diabetic-neuropathy-and-other-geriatric-disorders
#16
REVIEW
G Sergi, S Pizzato, F Piovesan, C Trevisan, N Veronese, E Manzato
A long history of diabetes mellitus and increasing age are associated with the onset of diabetic neuropathy, a painful and highly disabling complication with a prevalence peaking at 50% among elderly diabetic patients. Acetyl-L-carnitine (ALC) is a molecule derived from the acetylation of carnitine in the mitochondria that has an essential role in energy production. It has recently been proposed as a therapy to improve the symptoms of diabetic neuropathy. ALC is widely distributed in mammalian tissues, including the brain, blood-brain barrier, brain neurons, and astrocytes...
February 2018: Aging Clinical and Experimental Research
https://www.readbyqxmd.com/read/28488129/loss-of-the-association-between-telomere-length-and-mitochondrial-dna-copy-number-contribute-to-colorectal-carcinogenesis
#17
Hyunsu Lee, Ji-Hyoung Cho, Won-Jin Park, Soo-Jung Jung, In-Jang Choi, Jae-Ho Lee
Positive association between telomere length and mitochondrial DNA (mtDNA) copy number were introduced in healthy and patients with psychiatric disorder. Based on frequent genetic changes of telomere and mitochondria in colorectal carcinomas (CRC), we studied their clinical characteristics and their association in colorectal carcinogenesis. DNA was extracted from 109 CRCs, 64 colorectal tubular adenomas (TAs), and 28 serrated polyps (SPs), and then, telomere length and mtDNA copy number were analyzed in these legions by using a real-time PCR assay...
May 9, 2017: Pathology Oncology Research: POR
https://www.readbyqxmd.com/read/28469467/interactions-of-tryptophan-and-its-catabolites-with-melatonin-and-the-alpha-7-nicotinic-receptor-in-central-nervous-system-and-psychiatric-disorders-role-of-the-aryl-hydrocarbon-receptor-and-direct-mitochondria-regulation
#18
REVIEW
George Anderson, Michael Maes
Recent work indicates an intimate interaction of the tryptophan catabolite (TRYCAT) pathways with the melatonergic pathways, primarily via TRYCAT pathway induction taking tryptophan away from the production of serotonin, which is a necessary precursor for the melatonergic pathways. The alpha 7 nicotinic receptor may be significantly modulated by this interaction, given its inactivation by the TRYCAT, kynurenic acid, and its induction by melatonin. Similarly, the aryl hydrocarbon receptor is activated by both kynurenic acid and kynurenine, leading to CYP1A2 and melatonin metabolism, whereas melatonin may act to inhibit the aryl hydrocarbon receptor...
2017: International Journal of Tryptophan Research: IJTR
https://www.readbyqxmd.com/read/28279571/sex-dependent-mental-illnesses-and-mitochondria
#19
REVIEW
Akiko Shimamoto, Virginie Rappeneau
The prevalence of some mental illnesses, including major depression, anxiety-, trauma-, and stress-related disorders, some substance use disorders, and later onset of schizophrenia, is higher in women than men. While the higher prevalence in women could simply be explained by socioeconomic determinants, such as income, social status, or cultural background, extensive studies show sex differences in biological, pharmacokinetic, and pharmacological factors contribute to females' vulnerability to these mental illnesses...
September 2017: Schizophrenia Research
https://www.readbyqxmd.com/read/28087269/mitochondrial-roles-of-the-psychiatric-disease-risk-factor-disc1
#20
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...
September 2017: Schizophrenia Research
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