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https://www.readbyqxmd.com/read/28324489/monitoring-mitochondrial-changes-by-alteration-of-the-pink1-parkin-signaling-in-drosophila
#1
Tsuyoshi Inoshita, Kahori Shiba-Fukushima, Hongrui Meng, Nobutaka Hattori, Yuzuru Imai
Mitochondrial quality control is a key process in tissues with high energy demands, such as the brain and muscles. Recent studies using Drosophila have revealed that the genes responsible for familial forms of juvenile Parkinson's disease (PD), PINK1 and Parkin regulate mitochondrial function and motility. Cell biological analysis using mammalian cultured cells suggests that the dysregulation of mitophagy by PINK1 and Parkin leads to neurodegeneration in PD. In this chapter, we describe the methods to monitor mitochondrial morphology in the indirect flight muscles of adult Drosophila and Drosophila primary cultured neurons and the methods to analyze the motility of mitochondria in the axonal transport of living larval motor neurons...
March 22, 2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28323427/kinetin-riboside-and-its-protides-activate-the-parkinson-s-disease-associated-pten-induced-putative-kinase-1-pink1-independent-of-mitochondrial-depolarisation
#2
Laura Osgerby, Yu-Chiang Lai, Peter J Thornton, Joseph Amalfitano, Cécile S Le Duff, Iqra Jabeen, Hachemi Kadri, Ageo Miccoli, James H R Tucker, Miratul M K Muqit, Youcef Mehellou
Since loss of function mutations of PINK1 lead to early-onset Parkinson's disease, there has been growing interest in the discovery of small molecules that amplify the kinase activity of PINK1. We herein report the design, synthesis, serum stability and hydrolysis of four kinetin riboside ProTides. These ProTides, along with kinetin riboside, activated PINK1 in cells independent of mitochondrial depolarization. This highlights the potential of modified nucleosides and their phosphate prodrugs as treatments for neurodegenerative diseases...
March 21, 2017: Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/28319892/mitochondrial-hyperpolarization-in-ipsc-derived-neurons-from-patients-of-ftdp-17-with-10-16-mapt-mutation-leads-to-oxidative-stress-and-neurodegeneration
#3
Noemí Esteras, Jonathan D Rohrer, John Hardy, Selina Wray, Andrey Y Abramov
Tau protein inclusions are a frequent hallmark of a variety of neurodegenerative disorders. The 10+16 intronic mutation in MAPT gene, encoding tau, causes frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), by altering the splicing of the gene and inducing an increase in the production of 4R tau isoforms, which are more prone to aggregation. However, the molecular mechanisms linking increased 4R tau to neurodegeneration are not well understood. Here, we have used iPSC-derived neurons from patients of FTDP-17 carrying the 10+16 mutation to study the molecular mechanisms underlying neurodegeneration...
March 10, 2017: Redox Biology
https://www.readbyqxmd.com/read/28315271/role-of-sigma-1-receptor-in-cocaine-abuse-and-neurodegenerative-disease
#4
Yu Cai, Lu Yang, Fang Niu, Ke Liao, Shilpa Buch
Sigma-1 receptors (Sig-1R) are recognized as a unique class of non-G protein-coupled intracellular protein. Sig-1R binds to its ligand such as cocaine , resulting in dissociation of Sig-1R from mitochondrion-associated ER membrane (MAM) to the endoplasmic reticulum (ER), plasma membrane, and nuclear membrane, regulating function of various proteins. Sig-1R has diverse roles in both physiological as well as in pathogenic processes. The disruption of Sig-1R pathways has been implicated as causative mechanism(s) in the development of both neurodegenerative disorders such as Alzheimer disease (AD ), Parkinson disease (PD ), amyotrophic lateral sclerosis (ALS ) and Huntington Disease (HD ) ...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28306509/the-pten-parkin-axis-at-the-nexus-of-cancer-and-neurodegeneration
#5
Nathan T Ihle, Robert T Abraham
The PARK2 gene encodes an ubiquitin E3 ligase that is involved in mitochondrial homeostasis and linked to Parkinson's disease. In this issue, Gupta et al. (2017) demonstrate that PARK2 expression is frequently reduced in human cancers and that this alteration leads to dysregulated PI3K signaling.
March 16, 2017: Molecular Cell
https://www.readbyqxmd.com/read/28291352/understanding-the-molecular-determinant-of-reversible-human-monoamine-oxidase-b-inhibitors-containing-2h-chromen-2-one-core-structure-based-and-ligand-based-derived-3-d-qsar-predictive-models
#6
Milan Mladenovic, Alexandros Patsilinakos, Adele Pirolli, Manuela Sabatino, Rino Ragno
Monoamine oxidase B (MAO B) catalyzes the oxidative deamination of aryalkylamines neurotransmitters with concomitant reduction of oxygen to hydrogen peroxide. Consequently, the enzyme's malfunction can induce oxidative damage to mitochondrial DNA and mediates development of Parkinson's disease. Thus, MAO B emerges as a promising target for developing pharmaceuticals potentially useful to treat this vicious neurodegenerative condition. Aiming to contribute to the development of drugs with the reversible mechanism of MAO B inhibition only, herein, an extended in silico-in vitro procedure for the selection of novel MAO B inhibitors is demonstrated, including: (1) definition of optimized and validated structure-based (SB) 3-D QSAR models derived from available co-crystallized inhibitor-MAO B complexes; (2) elaboration of structure-activity relationships (SAR) features for either irreversible or reversible MAO B inhibitors to characterize and improve coumarin-based inhibitor activity (Protein Data Bank ID: 2V61) as the most potent reversible lead compound; (3) definition of structure-based (SB) and ligand-based (LB) alignment rules assessments by which virtually any untested potential MAO B inhibitor might be evaluated; (4) predictive ability validation of the best 3-D QSAR model through SB/LB modeling of four coumarin-based external test sets (267 compounds); (5) design and SB/LB alignment of novel coumarin-based scaffolds experimentally validated through synthesis and biological evaluation in vitro...
March 14, 2017: Journal of Chemical Information and Modeling
https://www.readbyqxmd.com/read/28290146/cyclooxygenase-2-directs-microglial-activation-mediated-inflammation-and-oxidative-stress-leading-to-intrinsic-apoptosis-in-zn-induced-parkinsonism
#7
Amit Kumar Chauhan, Namrata Mittra, Devendra Kumar Patel, Chetna Singh
Inflammation is decisive in zinc (Zn)-induced nigrostriatal dopaminergic neurodegeneration; however, the contribution of cyclooxygenase-2 (COX-2) is not yet known. The present study aimed to explore the role of COX-2 in Zn-induced Parkinsonism and its association with the microglial activation. Male Wistar rats were treated intraperitoneally (i.p.) with Zn as zinc sulphate (20 mg/kg) along with respective controls for 2-12 weeks. In a few sets, animals were also treated with/without celecoxcib (CXB, 20 mg/kg, i...
March 13, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28289790/-new-therapy-approaches-for-parkinson-s-disease
#8
K Brockmann, D Berg
Over the last years major advances have been made in the identification of specific pathways underlying the pathophysiology of subgroups of patients with Parkinson' disease. These pathways include mitochondrial and lysosomal dysfunction as well as inflammatory patterns and represent the basis for new causative and disease-modifying treatment strategies, possibly not only for the respective subgroups of patients but hopefully also for the majority of patients with idiopathic Parkinson's disease. This article highlights the main treatment strategies focusing on causative and disease course-modifying strategies as well as quality of life...
March 13, 2017: Der Nervenarzt
https://www.readbyqxmd.com/read/28281653/nix-restores-mitophagy-and-mitochondrial-function-to-protect-against-pink1-parkin-related-parkinson-s-disease
#9
Brianada Koentjoro, Jin-Sung Park, Carolyn M Sue
Therapeutic targets are needed to develop neuroprotective treatments for Parkinson's disease (PD). Mitophagy, the selective autophagic elimination of dysfunctional mitochondria, is essential for the maintenance of mitochondrial integrity and is predominantly regulated by the PINK1/Parkin-mediated pathway. Loss of function mutations in Parkin and PINK1 cause an accumulation of dysfunctional mitochondria, leading to nigral neurodegeneration and early-onset PD with a high penetrance rate. We previously identified an asymptomatic homozygous Parkin mutation carrier who had not developed PD by her eighth decade despite the loss of functional Parkin...
March 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28280525/the-short-isoform-of-dnajb6-protects-against-1-methyl-4-phenylpridinium-ion-induced-apoptosis-in-ln18-cells-via-inhibiting-both-ros-formation-and-mitochondrial-membrane-potential-loss
#10
Yeon-Mi Hong, Yohan Hong, Yeong-Gon Choi, Sujung Yeo, Soo Hee Jin, Sae-Won Lee, Backil Sung, Sook-Hyun Lee, Hyejin Jung, Sabina Lim
In a previous study, we found that the short isoform of DNAJB6 (DNAJB6(S)) had been decreased in the striatum of a mouse model of Parkinson's disease (PD) induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). DNAJB6, one of the heat shock proteins, has been implicated in the pathogenesis of PD. In this study, we explored the cytoprotective effect of DNAJB6(S) against 1-methyl-4-phenylpyridinium ion- (MPP(+)-) induced apoptosis and the underlying molecular mechanisms in cultured LN18 cells from astrocytic tumors...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28275647/inappropriate-trafficking-of-damaged-mitochondria-in-parkinson-s-disease
#11
EDITORIAL
Chi-Jing Choong, Hideki Mochizuki
No abstract text is available yet for this article.
2017: Stem Cell Investigation
https://www.readbyqxmd.com/read/28273839/parkinson-s-disease-from-pathogenesis-to-pharmacogenomics
#12
REVIEW
Ramón Cacabelos
Parkinson's disease (PD) is the second most important age-related neurodegenerative disorder in developed societies, after Alzheimer's disease, with a prevalence ranging from 41 per 100,000 in the fourth decade of life to over 1900 per 100,000 in people over 80 years of age. As a movement disorder, the PD phenotype is characterized by rigidity, resting tremor, and bradykinesia. Parkinson's disease -related neurodegeneration is likely to occur several decades before the onset of the motor symptoms. Potential risk factors include environmental toxins, drugs, pesticides, brain microtrauma, focal cerebrovascular damage, and genomic defects...
March 4, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28273718/mechanisms-of-parkinson-s-disease-related-proteins-in-mediating-secondary-brain-damage-after-cerebral-ischemia
#13
TaeHee Kim, Raghu Vemuganti
Both Parkinson's disease (PD) and stroke are debilitating conditions that result in neuronal death and loss of neurological functions. These two conditions predominantly affect aging populations with the deterioration of the quality of life for the patients themselves and a tremendous burden to families. While the neurodegeneration and symptomology of PD develop chronically over the years, post-stroke neuronal death and dysfunction develop rapidly in days. Despite the discrepancy in the pathophysiological time frame and severity, both conditions share common molecular mechanisms that include oxidative stress, mitochondrial dysfunction, inflammation, endoplasmic reticulum stress, and activation of various cell death pathways (apoptosis/necrosis/autophagy) that synergistically modulate the neuronal death...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/28256436/parkinsonian-pyramidal-syndromes-a-systematic-review
#14
REVIEW
Christine Tranchant, Meriam Koob, Mathieu Anheim
INTRODUCTION: Parkinsonian-Pyramidal syndrome (PPS), defined as the combination of both pyramidal and parkinsonian signs is a concept that recently emerged. PPS may manifest itself in numerous neurodegenerative diseases, many of these being inherited. Their diagnosis is a major challenge for the clinical management, for the prognosis, for genetic counselling and, in a few cases, which should not be neglected, for specific treatment. OBJECTIVE: Our objective is to provide a review of PPS and an algorithm in order to guide their diagnosis in clinical practice...
February 22, 2017: Parkinsonism & related Disorders
https://www.readbyqxmd.com/read/28254618/parkin-promotes-proteasomal-degradation-of-synaptotagmin-iv-by-accelerating-polyubiquitination
#15
Hiroyuki Kabayama, Naoko Tokushige, Makoto Takeuchi, Miyuki Kabayama, Mitsunori Fukuda, Katsuhiko Mikoshiba
Parkin is an E3 ubiquitin ligase whose mutations cause autosomal recessive juvenile Parkinson's disease (PD). Unlike the human phenotype, parkin knockout (KO) mice show no apparent dopamine neuron degeneration, although they demonstrate reduced expression and activity of striatal mitochondrial proteins believed to be necessary for neuronal survival. Instead, parkin-KO mice show reduced striatal evoked dopamine release, abnormal synaptic plasticity, and non-motor symptoms, all of which appear to mimic the preclinical features of Parkinson's disease...
February 22, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28253983/micrornas-aging-cellular-senescence-and-alzheimer-s-disease
#16
P H Reddy, J Williams, F Smith, J S Bhatti, S Kumar, M Vijayan, R Kandimalla, C S Kuruva, R Wang, M Manczak, X Yin, A P Reddy
Aging is a normal process of living being. It has been reported that multiple cellular changes, including oxidative damage/mitochondrial dysfunction, telomere shortening, inflammation, may accelerate the aging process, leading to cellular senescence. These cellular changes induce age-related human diseases, including Alzheimer's, Parkinson's, multiple sclerosis, amyotrophic lateral sclerosis, cardiovascular, cancer, and skin diseases. Changes in somatic and germ-line DNA and epigenetics are reported to play large roles in accelerating the onset of human diseases...
2017: Progress in Molecular Biology and Translational Science
https://www.readbyqxmd.com/read/28251677/mitochondrial-dna-and-primary-mitochondrial-dysfunction-in-parkinson-s-disease
#17
REVIEW
Maria Pia Giannoccaro, Chiara La Morgia, Giovanni Rizzo, Valerio Carelli
In 1979, it was observed that parkinsonism could be induced by a toxin inhibiting mitochondrial respiratory complex I. This initiated the long-standing hypothesis that mitochondrial dysfunction may play a key role in the pathogenesis of Parkinson's disease (PD). This hypothesis evolved, with accumulating evidence pointing to complex I dysfunction, which could be caused by environmental or genetic factors. Attention was focused on the mitochondrial DNA, considering the occurrence of mutations, polymorphic haplogroup-specific variants, and defective mitochondrial DNA maintenance with the accumulation of multiple deletions and a reduction of copy number...
March 2, 2017: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/28250973/mpp-induces-necrostatin-1-and-ferrostatin-1-sensitive-necrotic-death-of-neuronal-sh-sy5y-cells
#18
Keisuke Ito, Yutaka Eguchi, Yusuke Imagawa, Shuji Akai, Hideki Mochizuki, Yoshihide Tsujimoto
Regulation of cell death is potentially a powerful treatment modality for intractable diseases such as neurodegenerative diseases. Although there have been many reports about the possible involvement of various types of cell death in neurodegenerative diseases, it is still unclear exactly how neurons die in patients with these diseases, thus treatment strategies based on cell death regulation have not been established yet. To obtain some insight into the mechanisms of cell death involved in neurodegenerative diseases, we studied the effect of 1-methyl-4-phenylpyridinium (MPP+) on the human neuroblastoma cell line SH-SY5Y (a widely used model of Parkinson's disease)...
2017: Cell Death Discovery
https://www.readbyqxmd.com/read/28242362/intravenous-administration-of-mitochondria-for-treating-experimental-parkinson-s-disease
#19
Xianxun Shi, Ming Zhao, Chen Fu, Ailing Fu
Mitochondrial dysfunction is associated with a large number of human diseases, including neurological and muscular degeneration, cardiovascular disorders, obesity, diabetes, aging and rare mitochondrial diseases. Replacement of dysfunctional mitochondria with functional exogenous mitochondria is proposed as a general principle to treat these diseases. Here we found that mitochondria isolated from human hepatoma cell could naturally enter human neuroblastoma SH-SY5Y cell line, and when the mitochondria were intravenously injected into mice, all of the mice were survived and no obvious abnormality appeared...
February 24, 2017: Mitochondrion
https://www.readbyqxmd.com/read/28242245/inhibition-of-neuronal-mitochondrial-complex-i-or-lysosomal-glucocerebrosidase-is-associated-with-increased-dopamine-and-serotonin-turnover
#20
Carmen de la Fuente, Derek Burke, Simon Eaton, Simon J Heales
Parkinson's disease (PD) is a neurodegenerative disorder caused by loss of dopaminergic and serotoninergic signalling. A number of pathogenic mechanisms have been implicated including loss of mitochondrial function at the level of complex I, and lysosomal metabolism at the level of lysosomal glucocerebrosidase (GBA1). In order to investigate further the potential involvement of complex I and GBA1 in PD, we assessed the impact of loss of respective enzyme activities upon dopamine and serotonin turnover. Using SH-SY5Y cells, complex I deficiency was modelled by using rotenone whilst GBA1 deficiency was modelled by the use of conduritol B epoxide (CBE)...
February 24, 2017: Neurochemistry International
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