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Neurobiology of Disease

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https://www.readbyqxmd.com/read/28511918/molecular-imaging-of-serotonin-degeneration-in-mild-cognitive-impairment
#1
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, as well as the cell bodies of origin (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
#2
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
https://www.readbyqxmd.com/read/28502805/distinct-phenotypes-of-three-repeat-and-four-repeat-human-tau-in-a-transgenic-model-of-tauopathy
#3
Megan A Sealey, Ergina Vourkou, Catherine M Cowan, Torsten Bossing, Shmma Quraishe, Sofia Grammenoudi, Efthimios M C Skoulakis, Amritpal Mudher
Tau exists as six closely related protein isoforms in the adult human brain. These are generated from alternative splicing of a single mRNA transcript and they differ in the absence or presence of two N-terminal and three or four microtubule binding domains. Typically all six isoforms have been considered functionally similar. However, their differential involvement in particular tauopathies raises the possibility that there may be isoform-specific differences in physiological function and pathological role...
May 11, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28502804/wdr79-tcab1-plays-a-conserved-role-in-the-control-of-locomotion-and-ameliorates-phenotypic-defects-in-sma-models
#4
Maria Laura Di Giorgio, Alessandro Esposito, Paolo Maccallini, Emanuela Micheli, Francesca Bavasso, Ivan Gallotta, Fiammetta Vernì, Fabian Feiguin, Stefano Cacchione, Brian D McCabe, Elia Di Schiavi, Grazia Daniela Raffa
SMN (Survival Motor Neuron) deficiency is the predominant cause of spinal muscular atrophy (SMA), a severe neurodegenerative disorder that can lead to progressive paralysis and death. Although SMN is required in every cell for proper RNA metabolism, the reason why its loss is especially critical in the motor system is still unclear. SMA genetic models have been employed to identify several modifiers that can ameliorate the deficits induced by SMN depletion. Here we focus on WDR79/TCAB1, a protein important for the biogenesis of several RNA species that has been shown to physically interact with SMN in human cells...
May 11, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28502803/gene-co-expression-networks-identify-trem2-and-tyrobp-as-major-hubs-in-human-apoe-expressing-mice-following-traumatic-brain-injury
#5
Emilie L Castranio, Anais Mounier, Cody M Wolfe, Kyong Nyon Nam, Nicholas F Fitz, Florent Letronne, Jonathan Schug, Radosveta Koldamova, Iliya Lefterov
Traumatic brain injury (TBI) is strongly linked to an increased risk of developing dementia, including chronic traumatic encephalopathy and possibly Alzheimer's disease (AD). APOEε4 allele of human Apolipoprotein E (APOE) gene is the major genetic risk factor for late onset AD and has been associated with chronic traumatic encephalopathy and unfavorable outcome following TBI. To determine if there is an APOE isoform-specific response to TBI we performed controlled cortical impact on 3-month-old mice expressing human APOE3 or APOE4 isoforms...
May 11, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28476637/the-critical-role-of-nramp1-in-degrading-%C3%AE-synuclein-oligomers-in-microglia-under-iron-overload-condition
#6
Kuo-Chen Wu, Horng-Huei Liou, Yu-Han Kao, Chih-Yu Lee, Chun-Jung Lin
Oligomeric α-synuclein is a key mediator in the pathogenesis of Parkinson's disease (PD) and is mainly cleared by autophagy-lysosomal pathway, whose dysfunction results in the accumulation and cell-to-cell transmission of α-synuclein. In this study, concomitant with the accumulation of iron and oligomeric α-synuclein, higher expression of a lysosomal iron transporter, natural resistance-associated macrophage protein-1 (Nramp1), was observed in microglia in post-mortem striatum of sporadic PD patients. Using Nramp1-deficient macrophage (RAW264...
May 2, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28476636/differential-effects-of-immunotherapy-with-antibodies-targeting-%C3%AE-synuclein-oligomers-and-fibrils-in-a-transgenic-model-of-synucleinopathy
#7
Omar El-Agnaf, Cassia Overk, Edward Rockenstein, Michael Mante, Jazmin Florio, Anthony Adame, Nishant Vaikath, Nour Majbour, Seung-Jae Lee, Changyoun Kim, Eliezer Masliah, Robert A Rissman
Disorders with progressive accumulation of α-synuclein (α-syn) are a common cause of dementia and parkinsonism in the aging population. Accumulation and propagation of α-syn play a role in the pathogenesis of these disorders. Previous studies have shown that immunization with antibodies that recognize C-terminus of α-syn reduces the intra-neuronal accumulation of α-syn and related deficits in transgenic models of synucleinopathy. These studies employed antibodies that recognize epitopes within monomeric and aggregated α-syn that were generated through active immunization or administered via passive immunization...
May 2, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28473263/differences-in-white-matter-structure-between-seizure-prone-fast-and-seizure-resistant-slow-rat-strains
#8
Pragati Sharma, David K Wright, Leigh A Johnston, Kim L Powell, Mary E Wlodek, Sandy R Shultz, Terence J O'Brien, Krista L Gilby
Alterations in white matter integrity have been well documented in chronic epilepsy and during epileptogenesis. However, the relationship between white matter integrity and a predisposition towards epileptogenesis has been understudied. The FAST rat strain exhibit heightened susceptibility towards kindling epileptogenesis whereas SLOW rats are highly resistant. FAST rats also display behavioral phenotypes reminiscent of those observed in neurodevelopmental disorders that commonly comorbid with epilepsy. In this study, we aim to identify differences in white matter integrity that may contribute to a predisposition towards epileptogenesis and its associated comorbidities in 6month old FAST (n=10) and SLOW (n=10) male rats...
May 1, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28461248/simultaneous-triple-therapy-for-the-treatment-of-status-epilepticus
#9
Jerome Niquet, Roger Baldwin, Keith Norman, Lucie Suchomelova, Lucille Lumley, Claude G Wasterlain
Early maladaptive internalization of synaptic GABAA receptors (GABAAR) and externalization of NMDA receptors (NMDAR) may explain the time-dependent loss of potency of standard anti-epileptic drugs (AED) in refractory status epilepticus (SE). We hypothesized that correcting the effects of changes in GABAAR and NMDAR would terminate SE, even when treatment is delayed 40 minutes. SE was induced in adult Sprague-Dawley rats with a high dose of lithium and pilocarpine. The GABAAR agonist midazolam, the NMDAR antagonist ketamine and the AED valproate were injected 40 min after SE onset in combination or as monotherapy...
April 29, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28461250/deletion-of-exons-9-and-10-of-the-presenilin-1-gene-in-a-patient-with-early-onset-alzheimer-disease-generates-longer-amyloid-seeds
#10
Kilan Le Guennec, Sarah Veugelen, Olivier Quenez, Maria Szaruga, Stéphane Rousseau, Gaël Nicolas, David Wallon, Frédérique Fluchere, Thierry Frébourg, Bart De Strooper, Dominique Campion, Lucía Chávez-Gutiérrez, Anne Rovelet-Lecrux
Presenilin 1 (PSEN1) mutations are the main cause of autosomal dominant Early-onset Alzheimer Disease (EOAD). Among them, deletions of exon 9 have been reported to be associated with a phenotype of spastic paraparesis. Using exome data from a large sample of 522 EOAD cases and 584 controls to search for genomic copy-number variations (CNVs), we report here a novel partial, in-frame deletion of PSEN1, removing both exons 9 and 10. The patient presented with memory impairment associated with spastic paraparesis, both starting from the age of 56years...
April 28, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28461249/neuron-and-neuroblast-numbers-and-cytogenesis-in-the-dentate-gyrus-of-aged-appswe-ps1de9-transgenic-mice-effect-of-long-term-treatment-with-paroxetine
#11
Louise Ørum Olesen, Mithula Sivasaravanaparan, Maurizio Severino, Alicia A Babcock, Elena V Bouzinova, Mark J West, Ove Wiborg, Bente Finsen
Altered neurogenesis may influence hippocampal functions such as learning and memory in Alzheimer's disease. Selective serotonin reuptake inhibitors enhance neurogenesis and have been reported to reduce cerebral amyloidosis in both humans and transgenic mice. We have used stereology to assess the longitudinal changes in the number of doublecortin-expressing neuroblasts and number of granular neurons in the dentate gyrus of APPswe/PS1dE9 transgenic mice. Furthermore, we investigated the effect of long-term paroxetine treatment on the number of neuroblasts and granular neurons, hippocampal amyloidosis, and spontaneous alternation behaviour, a measure of spatial working memory, in transgenic mice...
April 28, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28461247/systemic-antimir-337-3p-delivery-inhibits-cerebral-ischemia-mediated-injury
#12
Xiaomin Wang, Yalikun Suofu, Berkcan Akpinar, Sergei V Baranov, Jinho Kim, Diane L Carlisle, Yu Zhang, Robert M Friedlander
Modulation of miRNA expression has been shown to be beneficial in the context of multiple diseases. The purpose of this study was to determine if an inhibitor of miR-337-3p is neuroprotective for hypoxic injury after tail vein injection. We evaluated miR-337-3p expression levels and in brain tissue in vivo before and after permanent middle cerebral artery occlusion (pMCAO) in mice. Subsequently, a custom locked nucleic acid (LNA) antimir-337-3p oligonucleotide was developed and tested in vitro after induction of oxygen glucose-deprivation (OGD) and in vivo by injection into the mouse tail vein for 3 consecutive days before pMCAO...
April 28, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28457951/hiv-tat-and-dopaminergic-transmission
#13
REVIEW
Peter Gaskill, Doug Miller, Joyonna-Gamble George, Hideaki Yano, Habibeh Khoshbouei
Human Immunodeficiency Virus (HIV) is a progressive infection that targets the immune system, affecting more than 37 million people around the world. While combinatorial antiretroviral therapy (cART) has lowered mortality rates and improved quality of life in infected individuals, the prevalence of HIV associated neurocognitive disorders is increasing and HIV associated cognitive decline remains prevalent. Recent research has suggested that HIV accessory proteins may be involved in this decline, and several studies have indicated that the HIV protein transactivator of transcription (Tat) can disrupt normal neuronal and glial function...
April 27, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28438505/turning-down-the-volume-astrocyte-volume-change-in-the-generation-and-termination-of-epileptic-seizures
#14
REVIEW
Thomas R Murphy, Devin K Binder, Todd A Fiacco
Approximately 1% of the global population suffers from epilepsy, a class of disorders characterized by recurrent and unpredictable seizures. Of these cases roughly one-third are refractory to current antiepileptic drugs, which typically target neuronal excitability directly. The events leading to seizure generation and epileptogenesis remain largely unknown, hindering development of new treatments. Some recent experimental models of epilepsy have provided compelling evidence that glial cells, especially astrocytes, could be central to seizure development...
April 22, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28438504/agomelatine-protects-against-neuronal-damage-without-preventing-epileptogenesis-in-the-kainate-model-of-temporal-lobe-epilepsy
#15
Jana Tchekalarova, Dimitrinka Atanasova, Zlatina Nenchovska, Milena Atanasova, Lidia Kortenska, Rumyana Gesheva, Nikolai Lazarov
Recent studies about the novel antidepressant agomelatine, which is a mixed MT1 and MT2 melatonin receptor agonist and 5HT2C serotonin receptor antagonist possessing an anticonvulsant and neuroprotective action, suggest that it may have potential to contribute against epileptogenesis and epilepsy-induced memory impairment. In order to ascertain whether protection of some brain structures could suppress epileptogenesis, in the present study, we evaluated the effect of chronic post-status treatment with agomelatine on epileptogenesis, behavioral and neuronal damage induced by kainate acid (KA) status epilepticus (SE)...
April 21, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28435104/drosophila-pink1-and-parkin-loss-of-function-mutants-display-a-range-of-non-motor-parkinson-s-disease-phenotypes
#16
Hannah Julienne, Edgar Buhl, David S Leslie, James J L Hodge
Parkinson's disease (PD) is more commonly associated with its motor symptoms and the related degeneration of dopamine (DA) neurons. However, it is becoming increasingly clear that PD patients also display a wide range of non-motor symptoms, including memory deficits and disruptions of their sleep-wake cycles. These have a large impact on their quality of life, and often precede the onset of motor symptoms, but their etiology is poorly understood. The fruit fly Drosophila has already been successfully used to model PD, and has been used extensively to study relevant non-motor behaviours in other contexts, but little attention has yet been paid to modelling non-motor symptoms of PD in this genetically tractable organism...
April 21, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28416393/tdp-43-expression-influences-amyloid%C3%AE-plaque-deposition-and-tau-aggregation
#17
Stephani A Davis, Kok Ann Gan, James A Dowell, Nigel J Cairns, Michael A Gitcho
Although the main focus in Alzheimer's disease (AD) has been an investigation of mechanisms causing Aβ plaque deposition and tau tangle formation, recent studies have shown that phosphorylated TDP-43 pathology is present in up to 50% of sporadic cases. Furthermore, elevated phosphorylated TDP-43 has been associated with more severe AD pathology. Therefore, we hypothesized that TDP-43 may regulate amyloid-beta precursor protein (APP) trafficking and tau phosphorylation/aggregation. In order to examine the role of TDP-43 in AD, we developed a transgenic mouse that overexpresses hippocampal and cortical neuronal TDP-43 in a mouse expressing familial mutations (K595N and M596L) in APP and presenilin 1 (PSEN1ΔE9)...
April 20, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28433741/loss-of-the-neurodevelopmental-gene-zswim6-alters-striatal-morphology-and-motor-regulation
#18
David J Tischfield, Dave K Saraswat, Andrew Furash, Stephen C Fowler, Marc V Fuccillo, Stewart A Anderson
The zinc-finger SWIM domain-containing protein 6 (ZSWIM6) is a protein of unknown function that has been associated with schizophrenia and limited educational attainment by three independent genome-wide association studies. Additionally, a putatively causal point mutation in ZSWIM6 has been identified in several cases of acromelic frontonasal dysostosis with severe intellectual disability. Despite the growing number of studies implicating ZSWIM6 as an important regulator of brain development, its role in this process has never been examined...
April 19, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28411118/regulation-of-motor-proteins-axonal-transport-deficits-and-adult-onset-neurodegenerative-diseases
#19
REVIEW
Scott T Brady, Gerardo A Morfini
Neurons affected in a wide variety of unrelated adult-onset neurodegenerative diseases (AONDs) typically exhibit a "dying back" pattern of degeneration, which is characterized by early deficits in synaptic function and neuritic pathology long before neuronal cell death. Consistent with this observation, multiple unrelated AONDs including Alzheimer's disease, Parkinson's disease, Huntington's disease, and several motor neuron diseases feature early alterations in kinase-based signaling pathways associated with deficits in axonal transport (AT), a complex cellular process involving multiple intracellular trafficking events powered by microtubule-based motor proteins...
April 11, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28411117/in-vitro-%C3%AE-synuclein-neurotoxicity-and-spreading-among-neurons-and-astrocytes-using-lewy-body-extracts-from-parkinson-disease-brains
#20
Fabio Cavaliere, Loic Cerf, Benjamin Dehay, Paula Ramos-Gonzalez, Francesca De Giorgi, Mathieu Bourdenx, Alban Bessede, Jose A Obeso, Carlos Matute, François Ichas, Erwan Bezard
Synucleinopathies are a group of diseases characterized by the presence of intracellular protein aggregates containing α-synuclein (α-syn). While α-syn aggregates have been shown to induce multimodal cellular dysfunctions, uptake and transport mechanisms remain unclear. Using high-content imaging on cortical neurons and astrocytes, we here define the kinetics of neuronal and astrocytic abnormalities induced by human-derived α-syn aggregates grounding the use of such system to identify and test putative therapeutic compounds...
April 11, 2017: Neurobiology of Disease
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