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Neurobiology of Disease

Limor Raz, Kiran Bhaskar, John Weaver, Sandro Marini, Quanguang Zhang, Jeffery F Thompson, Candice Espinoza, Sulaiman Iqbal, Nicole M Maphis, Lea Weston, Laurel O Sillerud, Arvind Caprihan, John C Pesko, Erik B Erhardt, Gary A Rosenberg
BACKGROUND: Hypertension-induced microvascular brain injury is a major vascular contributor to cognitive impairment and dementia. We hypothesized that chronic hypoxia promotes the hyperphosphorylation of tau and cell death in an accelerated spontaneously hypertensive stroke prone rat model of vascular cognitive impairment. METHODS: Hypertensive male rats (n = 13) were fed a high salt, low protein Japanese permissive diet and were compared to Wistar Kyoto control rats (n = 5)...
July 12, 2018: Neurobiology of Disease
Nonneman Annelies, Criem Nathan, A Lewandowski Sebastian, Nuyts Rik, R Thal Dietmar, W Pfrieger Frank, Ravits John, Van Damme Philip, Zwijsen An, Van Den Bosch Ludo, Robberecht Wim
Amyotrophic lateral sclerosis (ALS) is a late-onset devastating degenerative disease mainly affecting motor neurons. Motor neuron degeneration is accompanied and aggravated by oligodendroglial pathology and the presence of reactive astrocytes and microglia. We studied the role of the Notch signaling pathway in ALS, as it is implicated in several processes that may contribute to this disease, including axonal retraction, microgliosis, astrocytosis, oligodendrocyte precursor cell proliferation and differentiation, and cell death...
July 12, 2018: Neurobiology of Disease
Pampa Saha, Rajaneesh Gupta, Tanusree Sen, Nilkantha Sen
Cell cycle activation has been associated with varying types of neurological disorders including brain injury. Cyclin D1 is a critical modulator of cell cycle activation and upregulation of Cyclin D1 in neurons contributes to the pathology associated with traumatic brain injury (TBI). Mitochondrial mass is a critical factor to maintain the mitochondrial function, and it can be regulated by different signaling cascades and transcription factors including NRF1. However, the underlying mechanism of how TBI leads to impairment of mitochondrial mass following TBI remains obscure...
July 12, 2018: Neurobiology of Disease
Jonatan Sanchez-Garcia, Pedro Fernandez-Funez
Prion diseases are fatal neurodegenerative diseases caused by misfolding of the prion protein (PrP). These conditions affect humans and animals, including endemic forms in sheep and deer. Bovine, rodents, and many zoo mammals also developed prion diseases during the "mad-cow" epidemic in the 1980's. Interestingly, rabbits, horses, and dogs show unusual resistance to prion diseases, suggesting that specific sequence changes in the corresponding endogenous PrP prevents the accumulation of pathogenic conformations...
July 12, 2018: Neurobiology of Disease
Mingyue Xu, Michael M Wang, Yanqin Gao, Richard F Keep, Yejie Shi
White matter injury is a crucial component of human stroke, but it has often been neglected in preclinical studies. Most human stroke is associated with one or more comorbidities, including aging, hypertension, diabetes and metabolic syndrome including hyperlipidemia. The purpose of this review is to examine how age and hypertension impact stroke-induced white matter injury as well as white matter repair in both human stroke and preclinical models. It is essential that comorbidities be examined in preclinical trials as they may impact translatability to the clinic...
July 11, 2018: Neurobiology of Disease
Antonella Tramutola, Francesca Triani, Fabio Di Domenico, Eugenio Barone, Jun Cai, Jon B Klein, Marzia Perluigi, D Allan Butterfield
Alzheimer disease (AD) is a neurodegenerative disorder characterized by progressive loss of memory, reasoning and other cognitive functions. Pathologically, patients with AD are characterized by deposition of senile plaques (SPs), formed by β-amyloid (Aβ), and neurofibrillary tangles (NTFs) that consist of aggregated hyperphosphorylated tau protein. The accumulation of insoluble protein aggregates in AD brain can be associated with an impairment of degradative systems. This current study investigated if the disturbance of protein polyubiquitination is associated with AD neurodegeneration...
July 9, 2018: Neurobiology of Disease
Scherazad Kootar, Marie-Lise Frandemiche, Gihen Dhib, Xavier Mouska, Thomas Lorivel, Gwenola Poupon-Silvestre, Hazel Hunt, François Tronche, Ingrid Bethus, Jacques Barik, Hélène Marie
Amyloid-β is a peptide released by synapses in physiological conditions and its pathological accumulation in brain structures necessary for memory processing represents a key toxic hallmark underlying Alzheimer's disease. The oligomeric form of Amyloid-β (Aβο) is now believed to represent the main Amyloid-β species affecting synapse function. Yet, the exact molecular mechanism by which Aβο modifies synapse function remains to be fully elucidated. There is accumulating evidence that glucocorticoid receptors (GRs) might participate in Aβο generation and activity in the brain...
July 9, 2018: Neurobiology of Disease
Eung Chang Kim, Jiaren Zhang, Weilun Pang, Shuwei Wang, Kwan Young Lee, John P Cavaretta, Jennifer Walters, Erik Procko, Nien-Pei Tsai, Hee Jung Chung
Neuronal Kv 7/KCNQ channels are voltage-gated potassium channels composed of Kv 7.2/KCNQ2 and Kv 7.3/KCNQ3 subunits. Enriched at the axonal membrane, they potently suppress neuronal excitability. De novo and inherited dominant mutations in Kv 7.2 cause early onset epileptic encephalopathy characterized by drug resistant seizures and profound psychomotor delay. However, their precise pathogenic mechanisms remain elusive. Here, we investigated selected epileptic encephalopathy causing mutations in calmodulin (CaM)-binding helices A and B of Kv 7...
July 6, 2018: Neurobiology of Disease
Chandan Sona, Ajeet Kumar, Shalini Dogra, Boda Arun Kumar, Deepmala Umrao, Prem N Yadav
GPR40 (Free fatty acid receptor 1) has emerged as an important therapeutic target for diabetes. Several studies have demonstrated the association of comorbid psychiatric conditions with decreased n-3 polyunsaturated fatty acids, which may act as an agonist for GPR40. In this study, we for the first time provide evidence of reduced GPR40 signaling in the hippocampus and cortex which may be a critical underlying mechanism mediating cognitive deficits in diabesity (diabetes and obesity together). Specifically, we showed decreased GPR40 and brain-derived neurotrophic factor (BDNF) expression in the brain regions of high-fat-diet-induced obese and db/db mice...
July 5, 2018: Neurobiology of Disease
Chantell S Evans, Erika L F Holzbaur
Amyotrophic lateral sclerosis (ALS) is a debilitating and incurable disease involving the loss of motor neurons and subsequent muscle atrophy. Genetic studies have implicated deficits in autophagy and/or mitophagy in the onset of the disease. Here we review recent progress in our understanding of the pathways for autophagy and mitophagy in neurons, and how these pathways may be affected by mutations in genes including DCTN1, OPTN, TBK1, VCP, and C9ORF72. We also discuss the implications of modulating autophagy in ALS, highlighting both the potential of the approach and the concerns raised by targeting this pathway as a therapeutic strategy in neurodegenerative disease...
July 5, 2018: Neurobiology of Disease
Goda Tarcijonas, Deepak K Sarpal
Antipsychotic drugs are the primary treatment for psychosis, yet individual response to their administration remains variable. At present, no biological predictors of response exist to guide clinicians as they select treatments for patients, and our understanding of the neurobiology underlying the heterogeneity of outcomes remains limited. Magnetic Resonance Imaging (MRI) has been applied by numerous studies to examine the response to antipsychotic treatment, though a large gap remains between their results and our clinical practice...
June 25, 2018: Neurobiology of Disease
Chinthasagar Bastian, John Quinn, Ajai Tripathi, Danielle Aquila, Andrew McCray Ranjan Dutta, Selva Baltan, Sylvain Brunet
White matter (WM) is injured in most strokes, which contributes to functional deficits during recovery. Casein kinase 2 (CK2) is a protein kinase that is expressed in brain, including WM. To assess the impact of CK2 inhibition on axon recovery following oxygen glucose deprivation (OGD), mouse optic nerves (MONs), which are pure WM tracts, were subjected to OGD with or without the selective CK2 inhibitor CX-4945. CX-4945 application preserved axon function during OGD and promoted axon function recovery when applied before or after OGD...
June 23, 2018: Neurobiology of Disease
Preeti Dohare, Bokun Cheng, Ehsan Ahmed, Vivek Yadala, Pranav Singla, Sunisha Thomas, Robert Kayton, Zoltan Ungvari, Praveen Ballabh
Intraventricular hemorrhage (IVH) in preterm infants results in reduced proliferation and maturation of oligodendrocyte progenitor cells (OPCs), and survivors exhibit reduced myelination and neurological deficits. Wnt signaling regulates OPC maturation and myelination in a context dependent manner. Herein, we hypothesized that the occurrence of IVH would downregulate Wnt signaling, and that activating Wnt signaling by GSK-3β inhibition or Wnt3A recombinant human protein (rh-Wnt3A) treatment might promote maturation of OPCs, myelination of the white matter, and neurological recovery in premature rabbits with IVH...
June 22, 2018: Neurobiology of Disease
Shi Quan Wong, Matthew G Pontifex, Marie M Phelan, Chandra Pidathala, Brian C Kraemer, Jeff W Barclay, Neil G Berry, Paul M O'Neill, Robert D Burgoyne, Alan Morgan
The antiepileptic drug ethosuximide has recently been shown to be neuroprotective in various Caenorhabditis elegans and rodent neurodegeneration models. It is therefore a promising repurposing candidate for the treatment of multiple neurodegenerative diseases. However, high concentrations of the drug are required for its protective effects in animal models, which may impact on its translational potential and impede the identification of its molecular mechanism of action. Therefore, we set out to develop more potent neuroprotective lead compounds based on ethosuximide as a starting scaffold...
June 22, 2018: Neurobiology of Disease
Mattia Bonzanni, Jacopo C DiFrancesco, Raffaella Milanesi, Giulia Campostrini, Barbara Castellotti, Annalisa Bucchi, Mirko Baruscotti, Carlo Ferrarese, Silvana Franceschetti, Laura Canafoglia, Francesca Ragona, Elena Freri, Angelo Labate, Antonio Gambardella, Cinzia Costa, Ilaria Rivolta, Cinzia Gellera, Tiziana Granata, Andrea Barbuti, Dario DiFrancesco
No abstract text is available yet for this article.
June 21, 2018: Neurobiology of Disease
Estefania Rojo-Bustamante, Miguel Angel Abellanas, Pedro Clavero, Marie-Laure Thiolat, Qin Li, Maria Rosario Luquin, Erwan Bezard, Maria S Aymerich
Management of levodopa-induced dyskinesias (LID) is one of the main challenges in the treatment of Parkinson's disease patients. Mechanisms involved in the appearance of these involuntary movements are not well known but modifications in the activity of different neurotransmitter pathways seem to play an important role. The objective of this study was to determine differences in the expression levels of the endocannabinoid system (ECS) elements that would support a role in LID. The basal ganglia nuclei, putamen, external segment of the globus pallidus (GPe), internal segment of the globus pallidus (GPi), subthalamic nucleus (STN) and substantia nigra (SN) were dissected out from cryostat sections obtained from two groups of parkinsonian monkeys treated with levodopa to induce dyskinesias...
June 21, 2018: Neurobiology of Disease
Liane E Hunter, Craig A Branch, Michael L Lipton
It is now recognized that repetitive head impacts (RHI) in sport have the potential for long-term neurological impairments. In order to identify targets for intervention and/or pharmacological treatment it is necessary to characterize the neurobiological mechanisms associated with RHI. This review aims to summarize animal and human studies that specifically address Blood Brain Barrier (BBB) dysfunction, abnormal neuro-metabolic and neuro-inflammatory processes as well as Tau aggregation associated with RHI in collision sports...
June 21, 2018: Neurobiology of Disease
Federica Morelli, Margherita Romeo, Maria Monica Barzago, Marco Bolis, Davide Mattioni, Giacomina Rossi, Fabrizio Tagliavini, Antonio Bastone, Mario Salmona, Luisa Diomede
Mutations in the microtubule-associated protein tau (MAPT) gene have been linked to a heterogeneous group of progressive neurodegenerative disorders commonly called tauopathies. From patients with frontotemporal lobar degeneration with distinct atypical clinical phenotypes, we recently identified two new mutations on the same codon, in position 363 of the MAPT gene, which resulted in the production of Val-to-Ala (tauV363A ) or Val-to-Ile (tauV363I ) mutated tau. These substitutions specifically affected microtubule polymerization and propensity of tau to aggregate in vitro suggesting that single amino acid modification may dictate the fate of the neuropathology...
June 21, 2018: Neurobiology of Disease
Patricia G Saletti, Idrish Ali, Pablo M Casillas-Espinosa, Bridgette D Semple, Christos Lisgaras, Solomon L Moshé, Aristea S Galanopoulou
Post-traumatic epilepsy (PTE) occurs in 20% of individuals with acquired epilepsy, and can impact significantly the quality of life due to the seizures and other functional or cognitive and behavioral outcomes of the traumatic brain injury (TBI) and PTE. There is no available antiepileptogenic or disease modifying treatment for PTE. Animal models of TBI and PTE have been developed, offering useful insights on the value of inflammatory, neurodegenerative pathways, hemorrhages and iron accumulation, calcium channels and other target pathways that could be used for treatment development...
June 21, 2018: Neurobiology of Disease
Samuel J Dienel, David A Lewis
Certain clinical features of schizophrenia, such as working memory disturbances, appear to emerge from altered gamma oscillatory activity in the prefrontal cortex (PFC). Given the essential role of GABA neurotransmission in both working memory and gamma oscillations, understanding the cellular substrate for their disturbances in schizophrenia requires evidence from in vivo neuroimaging studies, which provide a means to link markers of GABA neurotransmission to gamma oscillations and working memory, and from postmortem studies, which provide insight into GABA neurotransmission at molecular and cellular levels of resolution...
June 21, 2018: Neurobiology of Disease
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