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Neuromolecular Medicine

Megan A Evans, Hyun Ah Kim, Yeong Hann Ling, Sandy Uong, Antony Vinh, T Michael De Silva, Thiruma V Arumugam, Andrew N Clarkson, Graeme R Zosky, Grant R Drummond, Brad R S Broughton, Christopher G Sobey
Acute inflammation can exacerbate brain injury after ischemic stroke. Beyond its well-characterized role in calcium metabolism, it is becoming increasingly appreciated that the active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25-VitD3 ), has potent immunomodulatory properties. Here, we aimed to determine whether 1,25-VitD3 supplementation could reduce subsequent brain injury and associated inflammation after ischemic stroke. Male C57Bl6 mice were randomly assigned to be administered either 1,25-VitD3 (100 ng/kg/day) or vehicle i...
February 23, 2018: Neuromolecular Medicine
Sheikh F Ahmad, Mushtaq A Ansari, Ahmed Nadeem, Mohammad Z Alzahrani, Saleh A Bakheet, Sabry M Attia
Autism is a neurodevelopmental disorder characterized by deficits in qualitative impairments in communication, repetitive and social interaction, restricted, and stereotyped patterns of behavior. Resveratrol has been extensively studied pharmacologically and biologically and has anti-inflammatory, antioxidant, and neuroprotective effects on neuronal damage in neurodegenerative disorders. The BTBR T+ Itpr3tf /J (BTBR) autistic mouse model has been explored for treatment of autism, which shows low reciprocal social interactions, impaired juvenile play, and decreased social approach...
February 21, 2018: Neuromolecular Medicine
Elizabeth S Chan, Christopher Chen, Tuck Wah Soong, Boon-Seng Wong
Apolipoprotein E4 (ApoE4) is the strongest genetic risk factor for sporadic Alzheimer's disease (AD), where inheritance of this isoform predisposes development of AD in a gene dose-dependent manner. Although the mode of action of ApoE4 on AD onset and progression remains unknown, we have previously shown that ApoE4, and not ApoE3 expression, resulted in insulin signaling deficits in the presence of amyloid beta (Aβ). However, these reports were not conducted with clinical samples that more accurately reflect human disease...
February 15, 2018: Neuromolecular Medicine
Karolina Pierzynowska, Lidia Gaffke, Aleksandra Hać, Jagoda Mantej, Natalia Niedziałek, Joanna Brokowska, Grzegorz Węgrzyn
Huntington's disease (HD) is a monogenic disorder, caused by mutations in the HTT gene which result in expansion of CAG triplets. The product of the mutated gene is misfolded huntingtin protein that forms aggregates leading to impairment of neuronal function, neurodegeneration, motor abnormalities and cognitive deficits. No effective cure is currently available for HD. Here we studied effects of genistein (trihydroxyisoflavone) on a HD cellular model consisting of HEK-293 cells transfected with a plasmid bearing mutated HTT gene...
February 12, 2018: Neuromolecular Medicine
Zohara Sternberg
The high prevalence of osteoporosis, observed in multiple sclerosis (MS) patients, has been attributed to reduced mobility and or the use of disease-modifying drugs. However, MS-impaired cardiovascular autonomic nervous system (ANS) function has the potential of reducing bone mass density (BMD) by altering the expression and/or function of the neuronal, systemic, and local mediators of bone remodeling. This review describes the complex regulation of bone homeostasis with a focus on MS, providing evidence that ANS dysfunction and low BMD are intertwined with MS inflammatory and neurodegenerative processes, and with other MS-related morbidities, including depression, fatigue, and migraine...
February 10, 2018: Neuromolecular Medicine
Shobi Veleri, Pradeep Punnakkal, Gary L Dunbar, Panchanan Maiti
In eukaryotes, the cellular functions are segregated to membrane-bound organelles. This inherently requires sorting of metabolites to membrane-limited locations. Sorting the metabolites from ribosomes to various organelles along the intracellular trafficking pathways involves several integral cellular processes, including an energy-dependent step, in which the sorting of metabolites between organelles is catalyzed by membrane-anchoring protein Rab-GTPases (Rab). They contribute to relaying the switching of the secretory proteins between hydrophobic and hydrophilic environments...
February 8, 2018: Neuromolecular Medicine
Gaoxiao Zhang, Tao Zhang, Liangmiao Wu, Xinhua Zhou, Jianbo Gu, Cuimei Li, Wei Liu, Cheng Long, Xifei Yang, Luchen Shan, Lipeng Xu, Yuqiang Wang, Yewei Sun, Zaijun Zhang
Our previous studies demonstrated that the multifunctional agent TBN, a derivative of tetramethylpyrazine armed with a nitrone moiety, displayed high therapeutic efficacy in experimental ischemic stroke models. However, its molecular mechanisms of action underlying the neuroprotective effect need further exploration. In the present study, we found that TBN had significant activities scavenging free radicals such as ·OH, O 2·- and ONOO-, inhibiting Ca2+ overload, maintaining mitochondrial function and preventing neuronal damage in primary cortical cultures...
February 6, 2018: Neuromolecular Medicine
Pradeep Punnakkal, Deity Dominic
NMDA receptors (NMDARs) play a key role in synaptic plasticity and excitotoxicity. Subtype-specific role of NMDAR in neural disorders is an emerging area. Recent studies have revealed that mutations in NMDARs are a cause for epilepsy. Hippocampus is a known focal point for epilepsy. In hippocampus, expression of the NMDAR subtypes GluN1/GluN2A and GluN1/GluN2B is temporally regulated. However, the pharmacological significance of these subtypes is not well understood in epileptic context/models. To investigate this, epilepsy was induced in hippocampal slices by the application of artificial cerebrospinal fluid that contained high potassium but no magnesium...
January 15, 2018: Neuromolecular Medicine
Alice Laschuk Herlinger, Agihane Rodrigues Almeida, Sarah Martins Presti-Silva, Evaldo Vitor Pereira, Filipe Andrich, Rita Gomes Wanderley Pires, Cristina Martins-Silva
The neurotoxin MPTP has long been used to create a mouse model of Parkinson's disease (PD). Indeed, several MPTP analogues have been developed, including 2'-CH3-MPTP, which was shown to induce nigrostriatal DA neuronal depletion more potently than MPTP. However, no study on behavioral and molecular alterations in response to 2'-CH3-MPTP has been carried out so far. In the present work, 2'-CH3-MPTP was administered to mice (2.5, 5.0 and 10 mg/kg per injection, once a day, 5 days) and histological, biochemical, molecular and behavioral alterations were evaluated...
January 13, 2018: Neuromolecular Medicine
Amrendra Pratap Singh, Teena Bajaj, Divya Gupta, Sundararajan Baskar Singh, Avinash Chakrawarty, Vinay Goyal, Aparajit B Dey, Sharmistha Dey
Mortalin, a mitochondrial chaperone, plays a crucial role in reducing toxicity of Lewy bodies. Earlier studies had reported that Mortalin level gets downregulated in astrocytes and other brain tissue samples in Parkinson's disease (PD). This study aims to estimate the Mortalin concentration in serum and correlate with α-synuclein (α-Syn) in PD. The concentration of Mortalin and α-Syn in serum samples of 38 PD patients and 33 control group (CG) individuals was quantified by surface plasmon resonance. The receiver operating characteristic curves were plotted to develop it as blood-based protein marker...
January 6, 2018: Neuromolecular Medicine
Cristina Politi, Cinzia Ciccacci, Giuseppe Novelli, Paola Borgiani
Parkinson's disease (PD) is a complex neurodegenerative disorder characterized by a progressive loss of dopamine neurons of the central nervous system. The disease determines a significant disability due to a combination of motor symptoms such as bradykinesia, rigidity and rest tremor and non-motor symptoms such as sleep disorders, hallucinations, psychosis and compulsive behaviors. The current therapies consist in combination of drugs acting to control only the symptoms of the illness by the replacement of the dopamine lost...
January 5, 2018: Neuromolecular Medicine
Xinzhi Chen, Thiruma V Arumugam, Yi-Lin Cheng, Jong-Hwan Lee, Srinivasulu Chigurupati, Mark P Mattson, Milan Basta
Acute ischemic stroke causes a high rate of deaths and permanent neurological deficits in survivors. Current interventional treatment, in the form of enzymatic thrombolysis, benefits only a small percentage of patients. Brain ischemia triggers mobilization of innate immunity, specifically the complement system and Toll-like receptors (TLRs), ultimately leading to an exaggerated inflammatory response. Here we demonstrate that intravenous immunoglobulin (IVIG), a scavenger of potentially harmful complement fragments, and C1-esterase inhibitor (C1-INH), an inhibitor of complement activation, exert a beneficial effect on the outcome of experimental brain ischemia (I) and reperfusion (R) injury induced by transient occlusion of middle cerebral artery in mice...
January 3, 2018: Neuromolecular Medicine
Jingjing Zhang, Changlei Cui, Yanhui Li, Haiyang Xu
Clinical application of anesthetic reagent, ketamine (Keta), may induce irreversible neurotoxicity in central nervous system. In this work, we utilized an in vitro model of neural stem cells-derived neurons (nSCNs) to evaluate the role of GSK-3 signaling pathway in Keta-induced neurotoxicity. Embryonic mouse-brain neural stem cells were differentiated into neurons in vitro. Keta (50 μM)-induced neurotoxicity in cultured nSCNs was monitored by apoptosis, immunohistochemical and western blot assays, respectively...
March 2018: Neuromolecular Medicine
Sung-Chun Tang, Kai-Chien Yang, Chaur-Jong Hu, Hung-Yi Chiou, Chau Chung Wu, Jiann-Shing Jeng
The receptor for advanced glycation end products (RAGE) and its downstream pathways are involved in various inflammatory and immune responses. Importantly, there is soluble RAGE (sRAGE) that forms either by alternative splicing of RAGE messenger ribonucleic acid as the endogenous soluble form of RAGE (esRAGE) or by proteolytic cleavage of full-length RAGE protein. This study aimed to investigate the associations of the plasma levels of sRAGE and esRAGE in ischemic stroke (IS) patients with and without dementia...
December 2017: Neuromolecular Medicine
Ji Yeon Choi, Chul Ju Hwang, Do Yeon Lee, Sun Mi Gu, Hee Pom Lee, Dong Young Choi, Ki Wan Oh, Sang-Bae Han, Jin Tae Hong
Alzheimer's disease (AD) is pathologically characterized by an excessive accumulation of amyloid-beta (Aβ) fibrils within the brain. We tested the anti-inflammatory and anti-amyloidogenic effects of (E)-2-methoxy-4-(3-(4-methoxyphenyl) prop-1-en-1-yl) phenol (MMPP), a selective signal transducer and activator of transcription 3 (STAT3) inhibitor. We examined whether MMPP (5 mg/kg in drinking water for 1 month) prevents amyloidogenesis and cognitive impairment on AD model mice induced by intraperitoneal LPS (250 μg/kg daily 7 times) injections...
December 2017: Neuromolecular Medicine
I Díaz-Maroto Cicuéndez, E Fernández-Díaz, J García-García, J Jordán, I Fernández-Cadenas, J Montaner, G Serrano-Heras, T Segura
Recent studies based on experimental animal models of stroke have suggested that uncoupling protein 2 (UCP2), an inner mitochondrial membrane protein that is thought to regulate energy metabolism and reduce reactive oxygen species generation, provides protection against reperfusion damage. We aimed to investigate whether -866G/A polymorphism in the promoter of the UCP2 gene, which enhances its transcriptional activity, is associated with functional prognosis in patients with embolic ischemic stroke after early recanalization...
December 2017: Neuromolecular Medicine
Slawomir Michalak, Alicja Kalinowska-Lyszczarz, Danuta Wegrzyn, Anna Thielemann, Krystyna Osztynowicz, Wojciech Kozubski
Migraine has been reported as a risk factor for ischemic stroke or cardiovascular events, and dysfunction of endothelial cells has been evidenced in migraine patients. Proangiogenic factors are potential endothelial stimulators, and their disturbances can link abnormalities of endothelium with increased risk of vascular disorders. The aim of this study was to evaluate the levels of circulating proangiogenic factors in sera of migraineurs during interictal period. Fifty-two patients aged 37.9 ± 9.6 years, fulfilling International Headache Society criteria for migraine, were included in this observational case-control study...
December 2017: Neuromolecular Medicine
Tan Li, Yong-Mei Zhang, Dong Han, Rong Hua, Bing-Nan Guo, Shu-Qun Hu, Xian-Liang Yan, Tie Xu
The pro-inflammatory activity of interleukin 17, which is produced by the IL-23/IL-17 axis, has been associated with the pathogenesis of traumatic brain injury (TBI). The study investigated the potential role of IL-17 in secondary brain injury of TBI in a rat model. Our data showed that the levels of IL-17 increased from 6 h to 7 days and peaked at 3 days, in both the CNS and serum, which were consistent with the severity of secondary brain injury. The IL-23 inhibitor suberoylanilide hydroxamic acid (SAHA) treatment markedly decreased the expressions of IL-17 and apoptosis-associated proteins cleaved caspase-3 and increased the protein ratio of Bcl-2 (B cell lymphoma/leukemia-2)/Bax (Bcl-2-associated X protein)...
December 2017: Neuromolecular Medicine
Giovana B Bampi, Rafael Bisso-Machado, Tábita Hünemeier, Tailise C Gheno, Gabriel V Furtado, Diego Veliz-Otani, Mario Cornejo-Olivas, Pillar Mazzeti, Maria Cátira Bortolini, Laura B Jardim, Maria Luiza Saraiva-Pereira
Spinocerebellar ataxia type 10 (SCA10) is an autosomal dominant neurodegenerative disorder characterized by progressive cerebellar ataxia and epilepsy. The disease is caused by a pentanucleotide ATTCT expansion in intron 9 of the ATXN10 gene on chromosome 22q13.3. SCA10 has shown a geographical distribution throughout America with a likely degree of Amerindian ancestry from different countries so far. Currently available data suggest that SCA10 mutation might have spread out early during the peopling of the Americas...
December 2017: Neuromolecular Medicine
Pratibha Chanana, Gayatri Padhy, Kalpana Bhargava, Ranjana Arya
GNE myopathy is a rare neuromuscular genetic disorder characterized by early adult onset and muscle weakness due to mutation in sialic acid biosynthetic enzyme, UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE). More than 180 different GNE mutations are known all over the world with unclear pathomechanism. Although hyposialylation of glycoproteins is speculated to be the major cause, but cellular mechanism leading to loss of muscle mass has not yet been deciphered. Besides sialic acid biosynthesis, GNE affects other cellular functions such as cell adhesion and apoptosis...
December 2017: Neuromolecular Medicine
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