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Experimental Neurology

Bin Wang, Qiong Wu, Lei Lei, Hailun Sun, Ntim Michael, Xuan Zhang, Ying Wang, Yue Zhang, Biying Ge, Yi Xin, Jie Zhao, Shao Li
Social isolation in adolescence leads to lasting deficits in hippocampal-dependent tasks. The reported effects of isolation on learning and memory in the Morris water maze and synaptic-related proteins have been inconsistent. Moreover, the autophagy level and its effect on cognition in the isolation model are also not clear. In the present study, we did an extended isolation period up to six months to establish a stable and appropriate isolation model to investigate the cognitive changes associated with it...
September 13, 2018: Experimental Neurology
Jin-Liang Chen, Cheng Luo, Die Pu, Guo-Qiang Zhang, Yu-Xing Zhao, Yue Sun, Ke-Xiang Zhao, Zhi-Yin Liao, An-Kang Lv, Shi-Yu Zhu, Jing-Zhou, Qian Xiao
Diabetes mellitus (DM) can increase the risk of Alzheimer's disease (AD) in patients. However, no effective approaches are available to prevent its progression and development. Recently, autophagy dysfunction was identified to be involved in the pathogenesis of neurodegenerative diseases. This study was designed to investigate the effect of metformin on hyperphosphorylated tau proteins in diabetic encephalopathy (DE) by regulating autophagy clearance. db/db mice were randomly divided into four groups, db/+ mice were used as control group...
September 13, 2018: Experimental Neurology
Xiaodi Chen, Jiyong Zhang, Boram Kim, Siddhant Jaitpal, Steven S Meng, Kwame Adjepong, Sayumi Imamura, Hidenori Wake, Masahiro Nishibori, Edward G Stopa, Barbara S Stonestreet
Inflammation contributes to neonatal brain injury. Pro-inflammatory cytokines represent key inflammatory meditators in neonatal hypoxic-ischemic (HI) brain injury. The high mobility group box-1 (HMGB1) protein is a nuclear protein with pro-inflammatory cytokine properties when it is translocated from the nucleus and released extracellularly after stroke in adult rodents. We have previously shown that HMGB1 is translocated from the nucleus to cytosolic compartment after ischemic brain injury in fetal sheep. In the current study, we utilized the Rice-Vannucci model to investigate the time course of HMGB1 translocation and release after HI injury in neonatal rats...
September 11, 2018: Experimental Neurology
Jianbang Han, Zhiming Feng, Yu Xie, Feng Li, Bingke Lv, Tian Hua, Zhongfei Zhang, Chengmei Sun, Dazhuang Su, Qian Ouyang, Yingqian Cai, Yuxi Zou, Yanping Tang, Haitao Sun, Xiaodan Jiang
Bone marrow-derived mesenchymal stem cells (BMSCs) exhibit potential regenerative effects on the injured brain. However, these effects are constrained by their limited ability to migrate to the injured site. Oncostatin M (OSM) has been shown to affect the proliferation and migration of mesenchymal stem cells. Therefore, in the present study, we explored whether OSM improves BMSC migration and secretion of growth factors and cytokines in a rat middle cerebral artery occlusion (MCAO) stroke model. The effect of OSM on the proliferation and apoptosis of rat BMSCs was first assessed in vitro, and the gene and secretion levels of factors related to cell nutrition and migration, such as SDF-1 and VEGF, were detected...
September 10, 2018: Experimental Neurology
Mulan He, Xia Shi, Miao Yang, Ting Yang, Tingyu Li, Jie Chen
Mesenchymal stem cells (MSCs) treatment is an effective strategy for the functional repair of central nervous system (CNS) insults through the production of bioactive molecules. We have previously demonstrated that the interleukin-6 (IL-6) secreted by MSCs plays an anti-apoptotic role in injured astrocytes and partly promotes functional recovery in neonatal rats with hypoxic-ischemic brain damage (HIBD). However, the mechanisms of IL-6 underlying the proliferation of injured astrocytes have not been fully elucidated...
September 10, 2018: Experimental Neurology
Bianca Backofen-Wehrhahn, Laura Gey, Sonja Bröer, Björn Petersen, Miriam Schiff, Annelie Handreck, Nancy Stanslowsky, Jessica Scharrenbroich, Michael Weißing, Selma Staege, Florian Wegner, Heiner Niemann, Wolfgang Löscher, Manuela Gernert
Cell transplantation based therapy is a promising strategy for treating intractable epilepsies. Inhibition of the subthalamic nucleus (STN) or substantia nigra pars reticulata (SNr) is a powerful experimental approach for remote control of different partial seizure types, when targeting the seizure focus is not amenable. Here, we tested the hypothesis that grafting of embryonic/fetal neural precursor cells (NPCs) from various species (rat, human, pig) into STN or SNr of adult rats induces anticonvulsant effects...
September 8, 2018: Experimental Neurology
Su-Su Tang, Yi Ren, Xiao-Qian Ren, Jing-Ran Cao, Hao Hong, Hui Ji, Qing-Hua Hu
Estrogen receptors (ERs) are thought to be associated with the onset and progression of neurodegenerative injuries and diseases, but the relationship and mechanisms underlying between ERs and cognition in type 2 diabetes remain elusive. In the current study, we investigated the effects of ERα and ERβ on the cognition, neurogenesis and apoptosis in high-fat diet and streptozocin-induced diabetic mice. We found that ERα and/or ERβ activation using their agonists (0.5 mg/kg E2, PPT or DPN) ameliorate memory impairment in the Morris water maze and Y-maze tests, increase hippocampal neurogenesis and prevent hippocampal apoptotic responses...
September 7, 2018: Experimental Neurology
Na Zhang, Jiah Shin Chin, Sing Yian Chew
Axons damaged by traumatic injuries are often unable to spontaneously regenerate in the adult central nervous system (CNS). Although the peripheral nervous system (PNS) has some regenerative capacity, its ability to regrow remains limited across large lesion gaps due to scar tissue formation. Nucleic acid therapy holds the potential of improving regeneration by enhancing the intrinsic growth ability of neurons and overcoming the inhibitory environment that prevents neurite outgrowth. Nucleic acids modulate gene expression by over-expression of neuronal growth factor or silencing growth-inhibitory molecules...
September 6, 2018: Experimental Neurology
Jason F Cooper, Katie K Spielbauer, Megan M Senchuk, Saravanapriah Nadarajan, Monica P Colaiácovo, Jeremy M Van Raamsdonk
Parkinson's disease (PD) is the second most common neurodegenerative disease and is characterized by the formation of α-synuclein-containing protein aggregates called Lewy bodies within the brain. A crucial role for α-synuclein in the pathogenesis of PD is also suggested by the fact that point mutations, increased copy number, or polymorphisms in the α-synuclein gene SNCA all cause or contribute to the development of PD. In addition to SNCA, an increasing number of other genes have been implicated in PD...
September 5, 2018: Experimental Neurology
Kasra Tajdaran, Katelyn Chan, Tessa Gordon, Gregory H Borschel
Local application of exogenous agents with neurotrophic properties enhances the regenerative capacity of injured neurons, especially following reconstructions of long nerve gaps and delayed nerve repairs. Recent advances in biomaterials and biomedical engineering have provided options for the sustained and controlled release of macromolecules to the peripheral nerve. Here, we review five methods for delivering macromolecules to the peripheral nerve including mini-osmotic pumps, hydrogel-based delivery systems, nerve guidance conduits, electrospun fibers, and nerve wraps...
August 31, 2018: Experimental Neurology
Svitlana Garbuzova-Davis, Edward Haller, Stephanie Navarro, Tony E Besong, Kayla J Boccio, Surafuale Hailu, Mohammed Khatib, Paul R Sanberg, Stanley H Appel, Cesario V Borlongan
Accumulating evidence shows alterations in the blood-brain barrier (BBB) and blood-spinal cord barrier (BSCB) in ALS patients and in animal models of disease, mainly by endothelial cell (EC) damage. Repair of the altered barrier in the CNS by replacement of ECs via cell transplantation may be a new therapeutic approach for ALS. Recently, we demonstrated positive effects towards BSCB repair by intravenous administration of unmodified human bone marrow CD34+ (hBM34+ ) cells at different doses into symptomatic ALS mice...
August 30, 2018: Experimental Neurology
Baruh Polis, Hava Gil-Henn
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is the most common cause of dementia and the 6th leading cause of death. Although research has revealed significant information about AD, much is yet to be discovered about the precise biological changes that cause AD and how the disease could be prevented, slowed, or stopped. Accumulating evidence suggests the involvement of the non-receptor proline-rich tyrosine kinase 2 (Pyk2) in AD, but the downstream signaling events triggered by this protein and their implications on the pathology of the disease were unclear until recently...
August 29, 2018: Experimental Neurology
Xiuli Yang, Jing Sun, Tae Jung Kim, Young-Ju Kim, Sang-Bae Ko, Chi Kyung Kim, Xiaofeng Jia, Byung-Woo Yoon
Nucleotide-binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, which is composed of an NLRP3 domain, the adaptor molecule apoptosis-associated speck-like protein containing a CARD (ASC) domain, and procaspase-1, plays an important role in the immune pathophysiology of the secondary damage induced by intracerebral hemorrhage (ICH). This study aims to investigate whether pre-stroke treatment with fimasartan, an angiotensin II receptor blocker, has anti-inflammatory effects on ICH by inhibiting the activation of the NLRP3 inflammasome...
August 29, 2018: Experimental Neurology
Janowska Justyna, Gargas Justyna, Ziemka-Nalecz Malgorzata, Zalewska Teresa, Buzanska Leonora, Sypecka Joanna
Glial cells which are indispensable for the central nervous system development and functioning, are proven to be vulnerable to a harmful influence of pathological cues and tissue misbalance. However, they are also highly sensitive to both in vitro and in vivo modulation of their commitment, differentiation, activity and even the fate-switch by different types of bioactive molecules. Since glial cells (comprising macroglia and microglia) are an abundant and heterogeneous population of neural cells, which are almost uniformly distributed in the brain and the spinal cord parenchyma, they all create a natural endogenous reservoir of cells for potential neurogenerative processes required to be initiated in response to pathophysiological cues present in the local tissue microenvironment...
August 29, 2018: Experimental Neurology
Yuuka Muraoka, Aya Nakamura, Ryo Tanaka, Kojiro Suda, Yumiko Azuma, Yukie Kushimura, Luca Lo Piccolo, Hideki Yoshida, Ikuko Mizuta, Takahiko Tokuda, Toshiki Mizuno, Masanori Nakagawa, Masamitsu Yamaguchi
Neuron-specific knockdown of the dFIG4 gene, a Drosophila homologue of human FIG4 and one of the causative genes for Charcot-Marie-Tooth disease (CMT), reduces the locomotive abilities of adult flies, as well as causing defects at neuromuscular junctions, such as reduced synaptic branch length in presynaptic terminals of the motor neurons in third instar larvae. Eye imaginal disc-specific knockdown of dFIG4 induces abnormal morphology of the adult compound eye, the rough eye phenotype. In this study, we carried out modifier screening of the dFIG4 knockdown-induced rough eye phenotype using a set of chromosomal deficiency lines on the second chromosome...
August 28, 2018: Experimental Neurology
Juan Ramón Perea, Jesús Ávila, Marta Bolós
Tauopathies are a broad set of neurodegenerative dementias characterized by the aggregation of Tau protein. Activated microglia and elevated levels of pro-inflammatory molecules are also pathological hallmarks of tauopathies. In these diseases, intracellular Tau is secreted to the extracellular space, where it interacts with other cells, such as neurons and glia, promoting inflammation. However, the mechanism through which extracellular Tau triggers pro-inflammatory responses in microglia remains unknown. Primary microglia cultures were treated with extracellular Tau in its hyperphosphorylated, dephosphorylated or non-phosphorylated form...
August 20, 2018: Experimental Neurology
Maurine C Braun, Alexandra Castillo-Ruiz, Premananda Indic, Dae Young Jung, Jason K Kim, Robert H Brown, Steven J Swoap, William J Schwartz
Current understanding of the pathogenesis of the familial form of amyotrophic lateral sclerosis has been aided by the study of transgenic mice that over-express mutated forms of the human CuZn-superoxide dismutase (SOD1) gene. While mutant SOD1 in motor neurons determines disease onset, other non-cell autonomous factors are critical for disease progression, and altered energy metabolism has been implicated as a contributing factor. Since most energy expended by laboratory mice is utilized to defend body temperature (Tb ), we analyzed thermoregulation in transgenic mice carrying the G93A mutation of the human SOD1 gene, using implantable temperature data loggers to continuously record Tb for up to 85 days...
July 18, 2018: Experimental Neurology
Lorraine Siebold, Andre Obenaus, Ravi Goyal
Traumatic brain injury (TBI) is a major health concern in the United States resulting in a substantial number of hospitalizations and in a broad spectrum of symptoms and disabilities. In the clinical setting, neurological responsiveness and structural imaging are used to classify mild, moderate and severe TBI. To evaluate the complex secondary and severity-specific injury response, investigators have relied on pre-clinical rodent models. The controlled cortical impact (CCI) model in mice is a widely used to study TBI...
July 12, 2018: Experimental Neurology
Michelle D Rudman, James S Choi, Ha Eun Lee, Sze Kiat Tan, Nagi G Ayad, Jae K Lee
Inflammation is a major contributor to the secondary damage that occurs after spinal cord injury (SCI). The inflammatory response is coordinated by many different signaling modalities including the epigenetic modification of promoters and enhancers. Bromodomain and extraterminal domain-containing proteins (BETs; Brd2, Brd3, Brd4, BrdT) are epigenetic readers that bind acetylated histones to promote transcription of pro-inflammatory genes. BET inhibition is anti-inflammatory in animal models of cancer, rheumatoid arthritis, and coronary artery disease...
November 2018: Experimental Neurology
Kallol Dutta, Priyanka Patel, Jean-Pierre Julien
Withania somnifera (WS; commonly known as Ashwagandha or Indian ginseng) is a medicinal plant whose extracts have been in use for centuries in various regions of the world as a rejuvenator. There is now a growing body of evidence documenting neuroprotective functions of the plant extracts or its purified compounds in several models of neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). Based on the extract's beneficial effect in a mouse model of ALS with TDP-43 proteinopathy, the current study was designed to test its efficacy in another model of familial ALS...
November 2018: Experimental Neurology
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