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Molecular Neurobiology

Thein Than Htike, Sachin Mishra, Sundramurthy Kumar, Parasuraman Padmanabhan, Balázs Gulyás
Neurological disorders are found to be influencing the peripheral tissues outside CNS. Recent developments in biomarkers for CNS have emerged with various diagnostic and therapeutic shortcomings. The role of central biomarkers including CSF-based and molecular imaging-based probes are still unclear for early diagnosis of major neurological diseases. Current trends show that early detection of neurodegenerative diseases with non-invasive methods is a major focus of researchers, and the development of biomarkers aiming peripheral tissues is in demand...
July 14, 2018: Molecular Neurobiology
Plamena R Angelova, Darya Vinogradova, Margarita E Neganova, Tatiana P Serkova, Vladimir V Sokolov, Sergey O Bachurin, Elena F Shevtsova, Andrey Y Abramov
Neuronal excitotoxicity which is induced by exposure to excessive extracellular glutamate is shown to be involved in neuronal cell death in acute brain injury and a number of neurological diseases. High concentration of glutamate induces calcium deregulation which results in mitochondrial calcium overload and mitochondrial depolarization that triggers the mechanism of cell death. Inhibition of mitochondrial calcium uptake could be potentially neuroprotective but complete inhibition of mitochondrial calcium uniporter could result in the loss of some physiological processes linked to Ca2+ in mitochondria...
July 14, 2018: Molecular Neurobiology
Dong-Dong Shi, Yu-Hua Huang, Cora Sau Wan Lai, Celia M Dong, Leon C Ho, Ed X Wu, Qi Li, Xiao-Min Wang, Sookja Kim Chung, Pak Chung Sham, Zhang-Jin Zhang
Chemotherapy-induced cognitive impairment, often referred to as "chemobrain," is a common side effect. In this study, mice received three intraperitoneal injections of a combination of docetaxel, adriamycin, and cyclophosphamide (DAC) at 2-day intervals. A water maze test was used to examine cognitive performance, and manganese-enhanced magnetic resonance imaging (MEMRI) was used to examine hippocampal neuronal activity. The whole brain, prefrontal cortex, hippocampus, and blood samples were then collected for cytokine measurement...
July 14, 2018: Molecular Neurobiology
Hui-Fang Chiu, Michael W Y Chan, Chiung-Yin Cheng, Jian-Liang Chou, Jora Meng-Ju Lin, Yi-Ling Yang, Kwok-Tung Lu
Previous studies showed that neonatal dexamethasone treatment (NDT) transiently impaired hippocampal function in male rats. Hippocampal estrogen receptors (ERs) participate in avoidance learning. As previous studies focused on males only, this study was aimed to investigate the NDT effects on the hippocampal function of female rats. Newborn Wistar female rats were subjected to a tapering dose of dexamethasone (0.5 mg, 0.3 mg, and 0.1 mg/kg, subcutaneously) from postnatal days 1 to 3 and were subjected to experiments at the age of 6 weeks (adolescence)...
July 13, 2018: Molecular Neurobiology
Sarah Schemmert, Elena Schartmann, Christian Zafiu, Bettina Kass, Sonja Hartwig, Stefan Lehr, Oliver Bannach, Karl-Josef Langen, Nadim Joni Shah, Janine Kutzsche, Antje Willuweit, Dieter Willbold
Oligomers of the amyloid-β (Aβ) protein are suspected to be responsible for the development and progression of Alzheimer's disease. Thus, the development of compounds that are able to eliminate already formed toxic Aβ oligomers is very desirable. Here, we describe the in vivo efficacy of the compound RD2, which was developed to directly and specifically eliminate toxic Aβ oligomers. In a truly therapeutic, rather than a preventive study, oral treatment with RD2 was able to reverse cognitive deficits and significantly reduce Aβ pathology in old-aged transgenic Alzheimer's Disease mice with full-blown pathology and behavioral deficits...
July 12, 2018: Molecular Neurobiology
Filipa I Baptista, Helena Pinheiro, Catarina A Gomes, António F Ambrósio
Diabetes mellitus is a chronic disease with numerous complications that severely impact on the quality of life of patients. Different neuropathies may arise as complications associated with the nervous system, both peripherally and at the central level. The mechanisms behind these neuronal complications are far from being clarified, but axonal transport impairment, a vital process for neuronal physiology, has been described in the context of experimental diabetes. Alterations in neuronal cytoskeleton and motor proteins, deficits in ATP supply or neuroinflammation, as processes that disturb the effective transport of cargoes along the axon, were reported as putative causes of axonal impairment, ultimately leading to axonal degeneration...
July 12, 2018: Molecular Neurobiology
Hui Zhao, Nur-Ezan Mohamed, Su Jing Chan, Chong Teik Tan, Ran Tao, Victor C Yu, Peter T-H Wong
Modulator of apoptosis 1 (MOAP-1) is a Bcl-2-associated X Protein (BAX)-associating protein that plays an important role in regulating apoptosis. It is highly enriched in the brain but its function in this organ remains unknown. Studies on BAX-/- mice suggested that disruption of programmed cell death may lead to abnormal emotional states. We thus hypothesize that MOAP-1-/- mice may also display stress-related behavioral differences and perhaps involved in stress responses in the brain and investigated if a depression-like trait exists in MOAP-1-/- mice, and if so, whether it is age related, and how it relates to central serotonergic stress response in the dorsal raphe nucleus...
July 12, 2018: Molecular Neurobiology
Marcos Roberto de Oliveira, Flávia de Bittencourt Brasil, Cristina Ribas Fürstenau
Mitochondria are double-membrane organelles involved in the transduction of energy from different metabolic substrates into adenosine triphosphate (ATP) in mammalian cells. The oxidative phosphorylation system is comprised by the activity of the respiratory chain and the complex V (ATP synthase/ATPase). This system is dependent on oxygen gas (O2 ) in order to maintain a flux of electrons in the respiratory chain, since O2 is the final acceptor of these electrons. Electron leakage from this complex system leads to the continuous generation of reactive species in the cells...
July 11, 2018: Molecular Neurobiology
Théo Z Hirsch, Séverine Martin-Lannerée, Fabienne Reine, Julia Hernandez-Rapp, Laetitia Herzog, Michel Dron, Nicolas Privat, Bruno Passet, Sophie Halliez, Ana Villa-Diaz, Caroline Lacroux, Victor Klein, Stéphane Haïk, Olivier Andréoletti, Juan-Maria Torres, Jean-Luc Vilotte, Vincent Béringue, Sophie Mouillet-Richard
Among the ever-growing number of self-replicating proteins involved in neurodegenerative diseases, the prion protein PrP remains the most infamous for its central role in transmissible spongiform encephalopathies (TSEs). In these diseases, pathogenic prions propagate through a seeding mechanism, where normal PrPC molecules are converted into abnormally folded scrapie isoforms termed PrPSc . Since its discovery over 30 years ago, much advance has contributed to define the host-encoded cellular prion protein PrPC as a critical relay of prion-induced neuronal cell demise...
July 11, 2018: Molecular Neurobiology
Cátia Gomes, Carolina Cunha, Filipe Nascimento, Joaquim A Ribeiro, Ana Rita Vaz, Dora Brites
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by motor neuron (MN) loss. Recent evidences highlight astrocytes as important players in MN death, but the mechanism-based neurotoxicity is still unknown. It is also unclear whether activation of astrocytes in ALS occurs differently in the cerebral cortex and spinal cord. We investigated glial and neuronal alterations in the cortex of SOD1G93A (mSOD1) mice in pre-symptomatic and symptomatic stages. We also characterized astrocytes isolated from the cortex of 7-day-old mSOD1 mice for their aberrancy and MN-induced degenerative effects...
July 11, 2018: Molecular Neurobiology
Jing Ye, Sabyasachi Das, Adhiraj Roy, Wenzhong Wei, Huachen Huang, Joshua Michael Lorenz-Guertin, Qian Xu, Tija C Jacob, Bing Wang, Dandan Sun, Qiming Jane Wang
Ca2+ /calmodulin-dependent protein kinase II (CaMKII) has long been implicated in neuronal injury caused by acute ischemia/reperfusion (I/R). However, its precise role and regulatory mechanisms remain obscure. Here, we investigated the role of the CaMKII family in neuronal survival during I/R. Our data indicated that CAMK2D/CaMKIIδ and CAMK2G/CaMKIIγ were selectively upregulated in a time-dependent manner at both transcriptional and protein levels after acute ischemia. Overexpression of CaMKIIδ promoted neuronal survival, while their depletion exacerbated ischemic neuronal death...
July 11, 2018: Molecular Neurobiology
Zoë P Van Acker, Evi Luyckx, Sylvia Dewilde
After its discovery in 2000, the notion grew that neuroglobin, a neuronal specific heme protein, is involved in cytoprotection. To date, neuroglobin levels have been positively correlated with a beneficial outcome in a plethora of neurotoxic insults, e.g., ischemic and traumatic brain injuries and Alzheimer's disease. The first part of this review goes further into these changes of neuroglobin expression upon different neuronal insults as well as the underlying regulation. In the second part, we shed light on the mechanisms by which neuroglobin contributes to neuroprotection, being (i) the scavenging and detoxification of reactive oxygen/nitrogen species, (ii) the augmentation of the threshold for apoptosis initiation, (iii) its contribution to an anti-inflammatory milieu, and (iv) tissue regeneration...
July 10, 2018: Molecular Neurobiology
Núria Martín-Flores, Rubén Fernández-Santiago, Francesa Antonelli, Catalina Cerquera, Verónica Moreno, Maria Josep Martí, Mario Ezquerra, Cristina Malagelada
Dyskinesia induced by L-DOPA administration (LID) is one of the most invalidating adverse effects of the gold standard treatment restoring dopamine transmission in Parkinson's disease (PD). However, LID manifestation in parkinsonian patients is variable and heterogeneous. Here, we performed a candidate genetic pathway analysis of the mTOR signaling cascade to elucidate a potential genetic contribution to LID susceptibility, since mTOR inhibition ameliorates LID in PD animal models. We screened 64 single nucleotide polymorphisms (SNPs) mapping to 57 genes of the mTOR pathway in a retrospective cohort of 401 PD cases treated with L-DOPA (70 PD with moderate/severe LID and 331 with no/mild LID)...
July 10, 2018: Molecular Neurobiology
Joanna E Pankiewicz, Sandrine Sanchez, Kent Kirshenbaum, Regina B Kascsak, Richard J Kascsak, Martin J Sadowski
PrPSc is an infectious and disease-specific conformer of the prion protein, which accumulation in the CNS underlies the pathology of prion diseases. PrPSc replicates by binding to the cellular conformer of the prion protein (PrPC ) expressed by host cells and rendering its secondary structure a likeness of itself. PrPC is a plasma membrane anchored protein, which constitutively recirculates between the cell surface and the endocytic compartment. Since PrPSc engages PrPC along this trafficking pathway, its replication process is often referred to as "recycling propagation...
July 9, 2018: Molecular Neurobiology
Fanny Gaudel, Delphine Stephan, Véréna Landel, Gilles Sicard, François Féron, Gaëlle Guiraudie-Capraz
A growing number of studies report the expression of olfactory receptors (ORs) in many non-chemosensory tissues and organs. However, within the brain, very few ectopic ORs are exhaustively documented. Their kinetic expression, cellular localization, and functions remain elusive. Using cDNA microarrays, quantitative PCR, and immunohistochemistry, we studied the cellular and sub-cellular localization of Olfr110/111 and Olfr544 and their timely expression in various brain areas of wild-type and transgenic Alzheimer's disease-like (5xFAD) mice...
July 8, 2018: Molecular Neurobiology
Yasuo Uchida, Tomohito Sumiya, Masanori Tachikawa, Tatsuya Yamakawa, Sho Murata, Yuta Yagi, Kazuki Sato, Alice Stephan, Katsuaki Ito, Sumio Ohtsuki, Pierre-Olivier Couraud, Takashi Suzuki, Tetsuya Terasaki
It is important to understand the molecular mechanisms of barrier disruption in the central nervous system (CNS) of patients with multiple sclerosis (MS). The purpose of the present study was to clarify whether claudin-11 is involved in the disruption of two endothelial barriers (blood-brain barrier (BBB) and blood-spinal cord barrier (BSCB)) and two epithelial barriers (blood-arachnoid barrier (BAB) and blood-CSF barrier (BCSFB)) in the CNS in MS. Immunohistochemical analysis revealed that, in both normal human and mouse, claudin-11 is co-localized with claudin-5 in the brain and spinal cord capillaries...
July 8, 2018: Molecular Neurobiology
Ricardo Cabezas, Eliana Baez-Jurado, Oscar Hidalgo-Lanussa, Valentina Echeverria, Ghulam Md Ashrad, Amirhossein Sahebkar, George E Barreto
Neurodegenerative diseases, such as Parkinson and Alzheimer, are among the main public health issues in the world due to their effects on life quality and high mortality rates. Although neuronal death is the main cause of disruption in the central nervous system (CNS) elicited by these pathologies, other cells such as astrocytes are also affected. There is no treatment for preventing the cellular death during neurodegenerative processes, and current drug therapy is focused on decreasing the associated motor symptoms...
July 7, 2018: Molecular Neurobiology
Caroline Peres Klein, Juliana Bender Hoppe, André Brum Saccomori, Bernardo Gindri Dos Santos, João Pedro Sagini, Mariana Scortegagna Crestani, Pauline Maciel August, Régis Mateus Hözer, Mateus Grings, Belisa Parmeggiani, Guilhian Leipnitz, Plácido Navas, Christianne Gazzana Salbego, Cristiane Matté
Alzheimer's disease (AD) is the main aging-associated neurodegenerative disorder and is characterized by mitochondrial dysfunction, oxidative stress, synaptic failure, and cognitive decline. It has been a challenge to find disease course-modifying treatments. However, several studies demonstrated that regular physical activity and exercise are capable of promoting brain health by improving the cognitive function. Maternal lifestyle, including regular exercise during pregnancy, has also been shown to influence fetal development and disease susceptibility in adulthood through fetal metabolism programming...
July 7, 2018: Molecular Neurobiology
Gye Sun Jeon, Yu-Mi Shim, Do-Yeon Lee, Jun-Soon Kim, MinJin Kang, So Hyun Ahn, Je-Young Shin, Dongho Geum, Yoon Ho Hong, Jung-Joon Sung
Amyotrophic lateral sclerosis (ALS) is a fatal, adult-onset, progressive neurodegenerative disorder with no known cure. Cu/Zn-superoxide dismutase (SOD1) was the first identified protein associated with familial ALS (fALS). Recently, TAR DNA-binding protein 43 (TDP-43) has been found to be a principal component of ubiquitinated cytoplasmic inclusions in neurons and glia in ALS. However, it remains unclear whether these ALS-linked proteins partly have a shared pathogenesis. Here, we determine the association between mutant SOD1 and the modification of TDP-43 and the relationship of pathologic TDP-43 to neuronal cytotoxicity in SOD1 ALS...
July 7, 2018: Molecular Neurobiology
T Peeyush Kumar, Devin W McBride, Pramod K Dash, Kanako Matsumura, Alba Rubi, Spiros L Blackburn
In the brain, vascular endothelial cells conserve blood viscosity, control blood flow, and form the interface between central nervous system and circulating blood. Clinical outcome after aneurysmal subarachnoid hemorrhage is linked to early brain injury, cerebral vasospasm, and other causes of delayed cerebral ischemia. The cerebral vasculature remains a unique target for therapies since it becomes rapidly disrupted after subarachnoid hemorrhage, and damage to the blood vessels continues into the delayed injury phase...
July 7, 2018: Molecular Neurobiology
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