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https://www.readbyqxmd.com/read/28807675/substantial-protection-against-mptp-associated-parkinson-s-neurotoxicity-in-vitro-and-in-vivo-by-anti-cancer-agent-su4312-via-activation-of-mef2d-and-inhibition-of-mao-b
#1
Baojian Guo, Shengquan Hu, Chengyou Zheng, Hongyu Wang, Fangcheng Luo, Haitao Li, Wei Cui, Xifei Yang, Guozhen Cui, Shinghung Mak, Tony Chung-Lit Choi, Edmond Dik-Lung Ma, Yuqiang Wang, Simon Ming Yuen Lee, Zaijun Zhang, Yifan Han
We have previously demonstrated the unexpected neuroprotection of the anti-cancer agent SU4312 in cellular models associated with Parkinson's disease (PD). However, the precise mechanisms underlying its neuroprotection are still unknown, and the effects of SU4312 on rodent models of PD have not been characterized. In the current study, we found that the protection of SU4312 against 1-methyl-4-phenylpyridinium ion (MPP(+))-induced neurotoxicity in PC12 cells was achieved through the activation of transcription factor myocyte enhancer factor 2D (MEF2D), as evidenced by the fact that SU4312 stimulated myocyte enhancer factor 2 (MEF2) transcriptional activity and prevented the inhibition of MEF2D protein expression caused by MPP(+), and that short hairpin RNA (ShRNA)-mediated knockdown of MEF2D significantly abolished the neuroprotection of SU4312...
August 11, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28806787/antagonism-of-proteasome-inhibitor-induced-heme-oxygenase-1-expression-by-pink1-mutation
#2
Xiang-Jun Sheng, Hunag-Ju Tu, Wei-Lin Chien, Kai-Hsiang Kang, Dai-Hua Lu, Horng-Huei Liou, Ming-Jen Lee, Wen-Mei Fu
PTEN-induced putative kinase 1 (PINK1) is an integral protein in the mitochondrial membrane and maintains mitochondrial fidelity. Pathogenic mutations in PINK1 have been identified as a cause of early-onset autosomal recessive familial Parkinson's disease (PD). The ubiquitin proteasome pathway is associated with neurodegenerative diseases. In this study, we investigated whether mutations of PINK1 affects the cellular stress response following proteasome inhibition. Administration of MG132, a peptide aldehyde proteasome inhibitor, significantly increased the expression of heme oxygenase-1 (HO-1) in rat dopaminergic neurons in the substantia nigra and in the SH-SY5Y neuronal cell line...
2017: PloS One
https://www.readbyqxmd.com/read/28806519/pluronic-p85-f68-micelles-of-baicalein-could-interfere-with-mitochondria-to-overcome-mrp2-mediated-efflux-and-offer-improved-anti-parkinsonian-activity
#3
Tongkai Chen, Ye Li, Chuwen Li, Xiang Yi, Ruibing Wang, Simon Ming Yuen Lee, Ying Zheng
Overexpression of the drug efflux transporter multidrug resistance-associated protein 2 (MRP2) in the gastrointestinal tract and blood-brain barrier compromises the oral delivery of drugs to the circulation system and brain in the treatment of Parkinson's disease (PD). In this study, we aim to develop small-sized Pluronic P85/F68 micelles loaded with baicalein (B-MCs) to overcome MRP2-mediated efflux and to investigate related mechanism, as well as the anti-Parkinsonian efficacy. Spherical and sustained-release B-MCs have a mean particle size of 40...
August 14, 2017: Molecular Pharmaceutics
https://www.readbyqxmd.com/read/28803490/parkin-pink1-and-dj1-as-possible-modulators-of-mtor-pathway-in-ganglioglioma
#4
Katarzyna Drapalo, Jaroslaw Jozwiak
Ganglioglioma (GG) is a non-malignant tumor classified as G1 by the WHO. Although we currently know that the neoplasm may result from the hyperactivity of protein kinase B (PKB or Akt) or extracellular-regulated kinase (Erk), which upregulates mammalian target of rapamycin kinase (mTOR) and leads to translation of proteins responsible for cell cycle regulation, there are still many questions to be answered. In the current paper we try to analyze the link between GG formation and activity of three proteins known to play a role in neuroprotection...
August 14, 2017: International Journal of Neuroscience
https://www.readbyqxmd.com/read/28801915/manganese-and-1-methyl-4-phenylpyridinium-mpp-induced-neurotoxicity-indicate-differences-in-morphological-electrophysiological-and-genome-wide-alterations-implications-for-idiopathic-parkinson-s-disease
#5
Rajeswara Babu Mythri, Narayana Reddy Raghunath, Santosh Chandrakant Narwade, Mirazkar DasharathaRao Pandareesh, Kollarkandi Rajesh Sabitha, Mohamad Aiyaz, Bipin Chand, Manas Sule, Krittika Ghosh, Senthil Kumar, Bhagyalakshmi Shankarappa, Soundarya Soundararajan, Phalguni Anand Alladi, Meera Purushottam, Narayanappa Gayathri, Deepti Dileep Deobagkar, Thenkanidiyoor Rao Laxmi, Srinivas Bharath Muchukunte Mukunda
Idiopathic Parkinson's disease (iPD) and manganese-induced atypical Parkinsonism are characterized by movement disorder and nigrostriatal pathology. Although clinical features, brain region involved and responsiveness to levodopa distinguish both, differences at the neuronal level are largely unknown. We studied the morphological, neurophysiological and molecular differences in dopaminergic neurons exposed to the PD toxin 1-methyl-4-phenylpyridinium ion (MPP(+) ) and manganese (Mn) followed by validation in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and Mn mouse models...
August 12, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28800639/mitochondrial-impairment-and-melatonin-protection-in-parkinsonian-mice-do-not-depend-of-inducible-or-neuronal-nitric-oxide-synthases
#6
Ana López, Francisco Ortiz, Carolina Doerrier, Carmen Venegas, Marisol Fernández-Ortiz, Paula Aranda, María E Díaz-Casado, Beatriz Fernández-Gil, Eliana Barriocanal-Casado, Germaine Escames, Luis C López, Darío Acuña-Castroviejo
MPTP-mouse model constitutes a well-known model of neuroinflammation and mitochondrial failure occurring in Parkinson's disease (PD). Although it has been extensively reported that nitric oxide (NO●) plays a key role in the pathogenesis of PD, the relative roles of nitric oxide synthase isoforms iNOS and nNOS in the nigrostriatal pathway remains, however, unclear. Here, the participation of iNOS/nNOS isoforms in the mitochondrial dysfunction was analyzed in iNOS and nNOS deficient mice. Our results showed that MPTP increased iNOS activity in substantia nigra and striatum, whereas it sharply reduced complex I activity and mitochondrial bioenergetics in all strains...
2017: PloS One
https://www.readbyqxmd.com/read/28800113/biomarker-research-in-parkinson-s-disease-using-metabolite-profiling
#7
REVIEW
Jesper F Havelund, Niels H H Heegaard, Nils J K Færgeman, Jan Bert Gramsbergen
Biomarker research in Parkinson's disease (PD) has long been dominated by measuring dopamine metabolites or alpha-synuclein in cerebrospinal fluid. However, these markers do not allow early detection, precise prognosis or monitoring of disease progression. Moreover, PD is now considered a multifactorial disease, which requires a more precise diagnosis and personalized medication to obtain optimal outcome. In recent years, advanced metabolite profiling of body fluids like serum/plasma, CSF or urine, known as "metabolomics", has become a powerful and promising tool to identify novel biomarkers or "metabolic fingerprints" characteristic for PD at various stages of disease...
August 11, 2017: Metabolites
https://www.readbyqxmd.com/read/28799502/mitochondrial-dynamics-and-proteins-related-to-neurodegenerative-diseases
#8
Athanasios Alexiou, Bilal Nizami, Faez Iqbal Khan, Georgia Soursou, Charalampos Vairaktarakis, Stylianos Chatzichronis, Vasilis Tsiamis, Vasileios Manztavinos, Nagendra Sastry Yarla, Ghulam Md Ashraf
Disruptions in the regulation of mitochondrial dynamics and the occurrence of proteins misfolding lead to neuronal death, resulting in Age-related Dementia and Neurodegenerative diseases as well as Frailty. Functional, neurophysiologic and biochemical alterations within the mitochondrial populations can reveal deficits in brain energy metabolism resulting in Mild Cognitive Impairment, abnormal neural development, autonomic dysfunction and other mitochondrial disorders. Additionally, in cases of Alzheimer's disease or Parkinson's disease, a significant number of proteins seems to form unordered and problematic structures, leading through unknown mechanisms to pathological conditions...
August 10, 2017: Current Protein & Peptide Science
https://www.readbyqxmd.com/read/28798236/the-unintended-mitochondrial-uncoupling-effects-of-the-fda-approved-anti-helminth-drug-nitazoxanide-mitigates-experimental-parkinsonism-in-mice
#9
Niharika Amireddy, Srinivas N Puttapaka, Ravali L Vinnakota, Halley G Ravuri, Swaroop Thonda, Shasi V Kalivendi
Mitochondria plays a primary role in the pathophysiology of Parkinson's disease (PD) and small molecules that counteract the initial stages of disease may offer therapeutic benefit. In this regard, we have examined whether the off-target effects of the FDA approved anti-helminth drug, nitazoxanide (NTZ) on mitochondrial respiration could possess any therapeutic potential for PD. Results indicate that MPP(+) induced loss in oxygen consumption rate (OCR) and ATP production by mitochondria were ameliorated by NTZ in real-time by virtue of its mild-uncoupling effect...
August 10, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28797885/mitophagy-in-neurodegenerative-diseases
#10
REVIEW
Carlo Rodolfo, Silvia Campello, Francesco Cecconi
Neurodegenerative diseases, such as Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), and Amyotrophic Lateral Sclerosis (ALS), are a complex "family" of pathologies, characterised by the progressive loss of neurons and/or neuronal functions, leading to severe physical and cognitive inabilities in affected patients. These syndromes, despite differences in the causative events, the onset, and the progression of the disease, share as common features the presence of aggregate-prone neuro-toxic proteins, in the form of aggresomes and/or inclusion bodies, perturbing cellular homeostasis and neuronal function (Popovic et al...
August 7, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28794205/the-human-serum-metabolome-of-vitamin-b-12-deficiency-and-repletion-and-associations-with-neurological-function-in-elderly-adults
#11
Alex Brito, Dmitry Grapov, Johannes Fahrmann, Danielle Harvey, Ralph Green, Joshua W Miller, Sergey N Fedosov, Setareh Shahab-Ferdows, Daniela Hampel, Theresa L Pedersen, Oliver Fiehn, John W Newman, Ricardo Uauy, Lindsay H Allen
Background: The specific metabolomic perturbations that occur in vitamin B-12 deficiency, and their associations with neurological function, are not well characterized.Objective: We sought to characterize the human serum metabolome in subclinical vitamin B-12 deficiency and repletion.Methods: A before-and-after treatment study provided 1 injection of 10 mg vitamin B-12 (with 100 mg pyridoxine and 100 mg thiamin) to 27 community-dwelling elderly Chileans (∼74 y old) with vitamin B-12 deficiency, as evaluated with serum vitamin B-12, total plasma homocysteine (tHcy), methylmalonic acid (MMA), and holotranscobalamin...
August 9, 2017: Journal of Nutrition
https://www.readbyqxmd.com/read/28791420/melatonin-as-a-mitochondrial-protector-in-neurodegenerative-diseases
#12
REVIEW
Pawaris Wongprayoon, Piyarat Govitrapong
Mitochondria are crucial organelles as their role in cellular energy production of eukaryotes. Because the brain cells demand high energy for maintaining their normal activities, disturbances in mitochondrial physiology may lead to neuropathological events underlying neurodegenerative conditions such as Alzheimer's disease, Parkinson's disease and Huntington's disease. Melatonin is an endogenous compound with a variety of physiological roles. In addition, it possesses potent antioxidant properties which effectively play protective roles in several pathological conditions...
August 8, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28790323/mitochondrial-division-inhibitor-1-is-neuroprotective-in-the-a53t-%C3%AE-synuclein-rat-model-of-parkinson-s-disease
#13
Simone Bido, Federico N Soria, Rebecca Z Fan, Erwan Bezard, Kim Tieu
Alpha-synuclein (α-syn) is involved in both familial and sporadic Parkinson's disease (PD). One of the proposed pathogenic mechanisms of α-syn mutations is mitochondrial dysfunction. However, it is not entirely clear the impact of impaired mitochondrial dynamics induced by α-syn on neurodegeneration and whether targeting this pathway has therapeutic potential. In this study we evaluated whether inhibition of mitochondrial fission is neuroprotective against α-syn overexpression in vivo. To accomplish this goal, we overexpressed human A53T-α- synuclein (hA53T-α-syn) in the rat nigrostriatal pathway, with or without treatment using the small molecule Mitochondrial Division Inhibitor-1 (mdivi-1), a putative inhibitor of the mitochondrial fission Dynamin-Related Protein-1 (Drp1)...
August 8, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28790012/mdivi-1-ameliorates-early-brain-injury-after-subarachnoid-hemorrhage-via-the-suppression-of-inflammation-related-blood-brain-barrier-disruption-and-endoplasmic-reticulum-stress-based-apoptosis
#14
Lin-Feng Fan, Ping-You He, Yu-Cong Peng, Qing-Hua Du, Yi-Jun Ma, Jian-Xiang Jin, Hang-Zhe Xu, Jian-Ru Li, Zhi-Jiang Wang, Sheng-Long Cao, Tao Li, Feng Yan, Chi Gu, Lin Wang, Gao Chen
Aberrant modulation of mitochondrial dynamic network, which shifts the balance of fusion and fission towards fission, is involved in brain damage of various neurodegenerative diseases including Parkinson's disease, Huntington's disease and Alzheimer's disease. A recent research has shown that the inhibition of mitochondrial fission alleviates early brain injury after experimental subarachnoid hemorrhage, however, the underlying molecular mechanisms have remained to be elucidated. This study was undertaken to characterize the effects of the inhibition of dynamin-related protein-1 (Drp1, a dominator of mitochondrial fission) on blood-brain barrier (BBB) disruption and neuronal apoptosis following SAH and the potential mechanisms...
August 5, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28782874/in-vivo-imaging-reveals-mitophagy-independence-in-the-maintenance-of-axonal-mitochondria-during-normal-aging
#15
Xu Cao, Haiqiong Wang, Zhao Wang, Qingyao Wang, Shuang Zhang, Yuanping Deng, Yanshan Fang
Mitophagy is thought to be a critical mitochondrial quality control mechanism in neurons and has been extensively studied in neurological disorders such as Parkinson's disease. However, little is known about how mitochondria are maintained in the lengthy neuronal axons in the context of physiological aging. Here, we utilized the unique Drosophila wing nerve model and in vivo imaging to rigorously profile changes in axonal mitochondria during aging. We revealed that mitochondria became fragmented and accumulated in aged axons...
August 7, 2017: Aging Cell
https://www.readbyqxmd.com/read/28782591/mitochondrial-dysfunction-in-the-neuro-degenerative-and-cardio-degenerative-disease-friedreich-s-ataxia
#16
Shannon Chiang, Danuta S Kalinowski, Patric J Jansson, Des R Richardson, Michael L-H Huang
Mitochondrial homeostasis is essential for maintaining healthy cellular function and survival. The detrimental involvement of mitochondrial dysfunction in neuro-degenerative diseases has recently been highlighted in human conditions, such as Parkinson's, Alzheimer's and Huntington's disease. Friedreich's ataxia (FA) is another neuro-degenerative, but also cardio-degenerative condition, where mitochondrial dysfunction plays a crucial role in disease progression. Deficient expression of the mitochondrial protein, frataxin, is the primary cause of FA, which leads to adverse alterations in whole cell and mitochondrial iron metabolism...
August 4, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28782414/protective-effect-of-neuropeptide-apelin-13-on-6-hydroxydopamine-induced-neurotoxicity-in-sh-sy5y-dopaminergic-cells-involvement-of-its-antioxidant-and-antiapoptotic-properties
#17
Elham Pooresmaeili-Babaki, Saeed Esmaeili-Mahani, Mehdi Abbasnejad, Hadi Ravan
Parkinson's disease (PD) is a severe neurodegenerative disorder characterized by the loss of brain dopaminergic neurons. Beside pharmacologic and symptomatic treatment of PD the neuroprotective therapy has recently attracted more attention. Apelin, a novel neuropeptide, and its receptors have numerous reported roles in regulating brain functions. In addition, this peptide has potent neuroprotective effects in some neurodegenerative situations. Here, the effects of apelin-13 were investigated in a cell model of PD...
August 7, 2017: Rejuvenation Research
https://www.readbyqxmd.com/read/28780195/calcium-mitochondrial-dysfunction-and-slowing-the-progression-of-parkinson-s-disease
#18
REVIEW
D James Surmeier, Glenda M Halliday, Tanya Simuni
Parkinson's disease is characterized by progressively distributed Lewy pathology and neurodegeneration. The motor symptoms of cPD are unequivocally linked to the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc). Several features of these neurons appear to make them selectively vulnerable to factors thought to cause cPD, like aging, genetic mutations and environmental toxins. Among these features, Ca(2+) entry through Cav1 channels is particularly amenable to pharmacotherapy in early stage cPD patients...
August 2, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28780078/atp-maintenance-via-two-types-of-atp-regulators-mitigates-pathological-phenotypes-in-mouse-models-of-parkinson-s-disease
#19
Masaki Nakano, Hiromi Imamura, Norio Sasaoka, Masamichi Yamamoto, Norihito Uemura, Toshiyuki Shudo, Tomohiro Fuchigami, Ryosuke Takahashi, Akira Kakizuka
Parkinson's disease is assumed to be caused by mitochondrial dysfunction in the affected dopaminergic neurons in the brain. We have recently created small chemicals, KUSs (Kyoto University Substances), which can reduce cellular ATP consumption. By contrast, agonistic ligands of ERRs (estrogen receptor-related receptors) are expected to raise cellular ATP levels via enhancing ATP production. Here, we show that esculetin functions as an ERR agonist, and its addition to culture media enhances glycolysis and mitochondrial respiration, leading to elevated cellular ATP levels...
August 2017: EBioMedicine
https://www.readbyqxmd.com/read/28780002/sex-specific-gene-expression-and-life-span-regulation
#20
REVIEW
John Tower
Aging-related diseases show a marked sex bias. For example, women live longer than men yet have more Alzheimer's disease and osteoporosis, whereas men have more cancer and Parkinson's disease. Understanding the role of sex will be important in designing interventions and in understanding basic aging mechanisms. Aging also shows sex differences in model organisms. Dietary restriction (DR), reduced insulin/IGF1-like signaling (IIS), and reduced TOR signaling each increase life span preferentially in females in both flies and mice...
August 2, 2017: Trends in Endocrinology and Metabolism: TEM
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