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Neurobiology of Disease

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https://www.readbyqxmd.com/read/28630030/alzheimer-s-brains-show-inter-related-changes-in-rna-and-lipid-metabolism
#1
Shahar Barbash, Benjamin P Garfinkel, Rotem Maoz, Alon Simchovitz, Bettina Nadorp, Alessandro Guffanti, Estelle R Bennett, Courtney Nadeau, Andreas Türk, Lukas Paul, Torsten Reda, Yan Li, Aron S Buchman, David S Greenberg, Alexander Seitz, David A Bennett, Patrick Giavalisco, Hermona Soreq
Alzheimer's disease (AD) involves changes in both lipid and RNA metabolism, but it remained unknown if these differences associate with AD's cognition and/or post-mortem neuropathology indices. Here, we report RNA-sequencing evidence of inter-related associations between lipid processing, cognition level, and AD neuropathology. In two unrelated cohorts, we identified pathway-enriched facilitation of lipid processing and alternative splicing genes, including the neuronal-enriched NOVA1 and hnRNPA1. Specifically, this association emerged in temporal lobe tissue samples from donors where postmortem evidence demonstrated AD neuropathology, but who presented normal cognition proximate to death...
June 16, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28624415/aging-rather-than-aneuploidy-affects-monoamine-neurotransmitters-in-brain-regions-of-down-syndrome-mouse-models
#2
Alain D Dekker, Yannick Vermeiren, Christelle Albac, Eva Lana-Elola, Sheona Watson-Scales, Dorota Gibbins, Tony Aerts, Debby Van Dam, Elizabeth M C Fisher, Victor L J Tybulewicz, Marie-Claude Potier, Peter P De Deyn
Altered concentrations of monoamine neurotransmitters and metabolites have been repeatedly found in people with Down syndrome (DS, trisomy 21). Because of the limited availability of human post-mortem tissue, DS mouse models are of great interest to study these changes and the underlying neurobiological mechanisms. Although previous studies have shown the potential of Ts65Dn mice - the most widely used mouse model of DS - to model noradrenergic changes, a comprehensive monoaminergic characterization in multiple brain regions has not been performed so far...
June 14, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28624414/corneal-kindled-c57bl-6-mice-exhibit-saturated-dentate-gyrus-long-term-potentiation-and-associated-memory-deficits-in-the-absence-of-overt-neuron-loss
#3
Gregory J Remigio, Jaycie L Loewen, Sage Heuston, Colin Helgeson, H Steve White, Karen S Wilcox, Peter J West
Memory deficits have a significant impact on the quality of life of patients with epilepsy and currently no effective treatments exist to mitigate this comorbidity. While these cognitive comorbidities can be associated with varying degrees of hippocampal cell death and hippocampal sclerosis, more subtle changes in hippocampal physiology independent of cell loss may underlie memory dysfunction in many epilepsy patients. Accordingly, animal models of epilepsy or epileptic processes exhibiting memory deficits in the absence of cell loss could facilitate novel therapy discovery...
June 14, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28619545/blast-related-disinhibition-and-risk-seeking-in-mice-and-combat-veterans-potential-role-for-dysfunctional-phasic-dopamine-release
#4
A G Schindler, J S Meabon, K F Pagulayan, R C Hendrickson, K D Meeker, M Cline, G Li, C Sikkema, C W Wilkinson, D P Perl, M R Raskind, E R Peskind, J J Clark, D G Cook
Mild traumatic brain injury (mTBI) caused by exposure to high explosives has been called the "signature injury" of the wars in Iraq and Afghanistan. There is a wide array of chronic neurological and behavioral symptoms associated with blast-induced mTBI. However, the underlying mechanisms are not well understood. Here we used a battlefield-relevant mouse model of blast-induced mTBI and in vivo fast-scan cyclic voltammetry (FSCV) to investigate whether the mesolimbic dopamine system contributes to the mechanisms underlying blast-induced behavioral dysfunction...
June 12, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28610892/novel-human-neuronal-tau-model-exhibiting-neurofibrillary-tangles-and-transcellular-propagation
#5
Patrick Reilly, Charisse N Winston, Kelsey Baron, Margarita Trejo, Edward M Rockenstein, Johnny C Akers, Najla Kfoury, Marc Diamond, Eliezer Masliah, Robert A Rissman, Shauna H Yuan
Tauopathies are a class of neurodegenerative diseases, including Alzheimer's disease, frontotemporal dementia and progressive supranuclear palsy, that are associated with the pathological aggregation of tau protein in neurofibrillary tangles (NFT). Studies have characterized tau as a "prion-like" protein given its ability to form distinct, stable amyloid conformations capable of transcellular and multigenerational propagation in clonal fashion. It has been proposed that progression of tauopathy could be due to the prion-like propagation of tau, suggesting the possibility that end-stage pathologies like NFT formation may require an instigating event such as tau seeding...
June 10, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28610891/n-butyl-deoxynojirimycin-delays-motor-deficits-cerebellar-microgliosis-and-purkinje-cell-loss-in-a-mouse-model-of-mucolipidosis-type-iv
#6
Lauren C Boudewyn, Jakub Sikora, Ladislav Kuchar, Jana Ledvinova, Yulia Grishchuk, Shirley L Wang, Kostantin Dobrenis, Steven U Walkley
Mucolipidosis type IV (MLIV) is a lysosomal storage disease exhibiting progressive intellectual disability, motor impairment, and premature death. There is currently no cure or corrective treatment. The disease results from mutations in the gene encoding mucolipin-1, a transient receptor potential channel believed to play a key role in lysosomal calcium egress. Loss of mucolipin-1 and subsequent defects lead to a host of cellular aberrations, including accumulation of glycosphingolipids (GSLs) in neurons and other cell types, microgliosis and, as reported here, cerebellar Purkinje cell loss...
June 10, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28602856/genetic-resistance-to-kindling-associated-with-alterations-in-circuit-function
#7
M Tansel Kendirli, Edward H Bertram
How a seizure spreads from a focal onset zone to other regions of the brain is not well understood, and animal studies suggest that there is a genetic influence. To understand how genetic factors may influence seizure spread, we examined whether the kindling resistance of WAG/Rij rats, which are slow to develop kindled motor seizures, is independent of the site of seizure induction and thus a global phenomenon, or whether it is circuit specific. We compared the kindling rates (number of stimulations to induce kindled motor seizures) of WAG/Rij rats to the rates of kindling in Sprague Dawley rats...
June 9, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28602636/extensive-phenotyping-of-two-arx-polyalanine-expansion-mutation-mouse-models-that-span-clinical-spectrum-of-intellectual-disability-and-epilepsy
#8
Matilda R Jackson, Kristie Lee, Tessa Mattiske, Emily J Jaehne, Ezgi Ozturk, Bernhard T Baune, Terence J O'Brien, Nigel Jones, Cheryl Shoubridge
The Aristaless-related homeobox gene (ARX) is a known intellectual disability (ID) gene that frequently presents with X-linked infantile spasm syndrome as a comorbidity. ID with epilepsy in children is a chronic and devastating disorder that has poor treatment options and disease outcomes. To gain a better understanding of the role that mutations in ARX play in ID and epilepsy, we investigate ARX patient mutations modelled in mice. Over half of all ARX mutations result from expansions of the first two polyalanine (PA1 and PA2 respectively) tracts...
June 7, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28587921/cxcl1-cxcr2-signaling-in-pathological-pain-role-in-peripheral-and-central-sensitization
#9
REVIEW
Rangel L Silva, Alexandre H Lopes, Rafaela M Guimarães, Thiago M Cunha
Pathological pain conditions can be triggered after peripheral nerve injury and/or inflammation. It is associated with plasticity of nociceptive pathway in which pain is prolonged even after healing of the injured tissue. Generally combinations of analgesic drugs are not sufficient to achieve selective palliation from chronic pain, besides causing a greater number of side effects. In order to identify novel alternatives for more effective treatments, it is necessary to clarify the underlying mechanisms of pathological pain...
June 3, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28578004/alterations-of-striatal-indirect-pathway-neurons-precede-motor-deficits-in-two-mouse-models-of-huntington-s-disease
#10
Irene Sebastianutto, Maria Angela Cenci, Tim Fieblinger
Striatal neurons forming the indirect pathway (iSPNs) are particularly vulnerable in Huntington's disease (HD). In this study we set out to investigate morphological and physiological alterations of iSPNs in two mouse models of HD with relatively slow disease progression (long CAG repeat R6/2 and zQ175-KI). Both were crossed with a transgenic mouse line expressing eGFP in iSPNs. Using the open-field and rotarod tests, we first defined two time points in relation to the occurrence of motor deficits in each model...
June 1, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28578003/generating-level-dependent-models-of-cervical-and-thoracic-spinal-cord-injury-exploring-the-interplay-of-neuroanatomy-physiology-and-function
#11
Jared T Wilcox, Kajana Satkunendrarajah, Yasmin Nasirzadeh, Alex M Laliberte, Alyssa Lip, David W Cadotte, Warren D Foltz, Michael G Fehlings
The majority of spinal cord injuries (SCI) occur at the cervical level, which results in significant impairment. Neurologic level and severity of injury are primary endpoints in clinical trials; however, how level-specific damages relate to behavioural performance in cervical injury is incompletely understood. We hypothesized that ascending level of injury leads to worsening forelimb performance, and correlates with loss of neural tissue and muscle-specific neuron pools. A direct comparison of multiple models was made with injury realized at the C5, C6, C7 and T7 vertebral levels using clip compression with sham-operated controls...
May 31, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28576707/development-of-transcripts-regulating-dendritic-spines-in-layer-3-pyramidal-cells-of-the-monkey-prefrontal-cortex-implications-for-the-pathogenesis-of-schizophrenia
#12
Samuel J Dienel, Holly H Bazmi, David A Lewis
Certain cognitive deficits in schizophrenia appear to emerge from altered postnatal development of the dorsolateral prefrontal cortex (DLPFC). Dendritic spines on DLPFC layer 3 pyramidal cells are essential for certain cognitive functions, change in density over development, and are reduced in number in schizophrenia. Altered expression of molecular regulators of actin filament assembly and stability, which are essential for spine formation and maintenance, is thought to contribute to the pathogenesis of spine deficits in the disease...
May 31, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28576705/the-pathogenic-lrrk2-r1441c-mutation-induces-specific-deficits-modeling-the-prodromal-phase-of-parkinson-s-disease-in-the-mouse
#13
F Giesert, L Glasl, A Zimprich, L Ernst, G Piccoli, C Stautner, J Zerle, S M Hölter, D M Vogt Weisenhorn, W Wurst
The aim of the present study was to further explore the in vivo function of the Leucine-rich repeat kinase 2 (LRRK2)-gene, which is mutated in certain familial forms of Parkinson's disease (PD). We generated a mouse model harboring the disease-associated point mutation R1441C in the GTPase domain of the endogenous murine LRRK2 gene (LRRK2 R1441C line) and performed a comprehensive analysis of these animals throughout lifespan in comparison with an existing knockdown line of LRRK2 (LRRK2 knockdown line). Animals of both lines do not exhibit severe motor dysfunction or pathological signs of neurodegeneration neither at young nor old age...
May 31, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28576709/rescue-of-altered-hdac-activity-recovers-behavioural-abnormalities-in-a-mouse-model-of-angelman-syndrome
#14
Imran Jamal, Vipendra Kumar, Naman Vatsa, Shashi Shekhar, Brijesh Kumar Singh, Ankit Sharma, Nihar Ranjan Jana
Angelman syndrome (AS) is a neurodevelopmental disorder characterized by severe intellectual and developmental disabilities. The disease is caused by the loss of function of maternally inherited UBE3A, a gene that exhibits paternal-specific imprinting in neuronal tissues. Ube3a-maternal deficient mice (AS mice) display many classical features of AS, although, the underlying mechanism of these behavioural deficits is poorly understood. Here we report that the absence of Ube3a in AS mice brain caused aberrant increase in HDAC1/2 along with decreased acetylation of histone H3/H4...
May 30, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28576708/a-systems-level-analysis-of-epileptogenesis-associated-proteome-alterations
#15
Michael Keck, Ganna Androsova, Fabio Gualtieri, Andreas Walker, Eva-Lotta von Rüden, Vera Russmann, Cornelia A Deeg, Stefanie M Hauck, Roland Krause, Heidrun Potschka
Despite intense research efforts, the knowledge about the mechanisms of epileptogenesis and epilepsy is still considered incomplete and limited. However, an in-depth understanding of molecular pathophysiological processes is crucial for the rational selection of innovative biomarkers and target candidates. Here, we subjected proteomic data from different phases of a chronic rat epileptogenesis model to a comprehensive systems level analysis. Weighted Gene Co-expression Network analysis identified several modules of interconnected protein groups reflecting distinct molecular aspects of epileptogenesis in the hippocampus and the parahippocampal cortex...
May 30, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28576706/rhigm22-enhances-remyelination-in-the-brain-of-the-cuprizone-mouse-model-of-demyelination
#16
Ariana P Mullin, Charlene Cui, Yu Wang, Jing Wang, Erika Troy, Anthony O Caggiano, Tom J Parry, Raymond W Colburn, Elias Pavlopoulos
Failure of oligodendrocyte precursor cells (OPCs) to differentiate and remyelinate axons is thought to be a major cause of the limited ability of the central nervous system to repair plaques of immune-mediated demyelination in multiple sclerosis (MS). Current therapies for MS aim to lessen the immune response in order to reduce the frequency and severity of attacks, but these existing therapies do not target remyelination or stimulate repair of the damaged tissue. Thus, the promotion of OPC differentiation and remyelination is potentially an important therapeutic goal...
May 30, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28576704/%C3%AE-synuclein-fibril-induced-inclusion-spread-in-rats-and-mice-correlates-with-dopaminergic-neurodegeneration
#17
Hisham Abdelmotilib, Tyler Maltbie, Vedad Delic, Zhiyong Liu, Xianzhen Hu, Kyle B Fraser, Mark S Moehle, Lindsay Stoyka, Nadia Anabtawi, Valentina Krendelchtchikova, Laura A Volpicelli-Daley, Andrew West
Proteinaceous inclusions in neurons, composed primarily of α-synuclein, define the pathology in several neurodegenerative disorders. Neurons can internalize α-synuclein fibrils that can seed new inclusions from endogenously expressed α-synuclein. The factors contributing to the spread of pathology and subsequent neurodegeneration are not fully understood, and different compositions and concentrations of fibrils have been used in different hosts. Here, we systematically vary the concentration and length of well-characterized α-synuclein fibrils and determine their relative ability to induce inclusions and neurodegeneration in different hosts (primary neurons, C57BL/6J and C3H/HeJ mice, and Sprague Dawley rats)...
May 30, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28552387/-brain-barriers-in-health-and-disease
#18
EDITORIAL
Richard Daneman, Britta Engelhardt
No abstract text is available yet for this article.
May 24, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28511918/molecular-imaging-of-serotonin-degeneration-in-mild-cognitive-impairment
#19
Gwenn S Smith, Frederick S Barrett, Jin Hui Joo, Najlla Nassery, Alena Savonenko, Devin J Sodums, Christopher M Marano, Cynthia A Munro, Jason Brandt, Michael A Kraut, Yun Zhou, Dean F Wong, Clifford I Workman
Neuropathological and neuroimaging studies have consistently demonstrated degeneration of monoamine systems, especially the serotonin system, in normal aging and Alzheimer's disease. The evidence for degeneration of the serotonin system in mild cognitive impairment is limited. Thus, the goal of the present study was to measure the serotonin transporter in vivo in mild cognitive impairment and healthy controls. The serotonin transporter is a selective marker of serotonin terminals and of the integrity of serotonin projections to cortical, subcortical and limbic regions and is found in high concentrations in the serotonergic cell bodies of origin of these projections (raphe nuclei)...
May 13, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28502806/treadmill-exercise-delays-the-onset-of-non-motor-behaviors-and-striatal-pathology-in-the-cag140-knock-in-mouse-model-of-huntington-s-disease
#20
D P Stefanko, V D Shah, W K Yamasaki, G M Petzinger, M W Jakowec
Depression, cognitive impairments, and other neuropsychiatric disturbances are common during the prodromal phase of Huntington's disease (HD) well before the onset of classical motor symptoms of this degenerative disorder. The purpose of this study was to examine the potential impact of physical activity in the form of exercise on a motorized treadmill on non-motor behavioral features including depression-like behavior and cognition in the CAG140 knock-in (KI) mouse model of HD. The CAG140 KI mouse model has a long lifespan compared to other HD rodent models with HD motor deficits emerging after 12months of age and thus provides the opportunity to investigate early life interventions such as exercise on disease progression...
May 11, 2017: Neurobiology of Disease
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