Tardive dyskinetic syndrome in rats infected with Borna disease virus.

Abstract:

:Tardive Dyskinesia (TD) is a hyperkinetic movement disorder caused by chronic treatment of psychiatric patients with dopamine (DA) receptor blocking drugs (Stacy & Jankovic 1991). Although TD is one of the most important and frequently encountered iatrogenic disorders in clinical medicine, its pathophysiology is poorly understood. We have observed a hyperkinetic movement disorder in rats experimentally infected with a neurotropic RNA virus, Borna disease virus, that may provide important insights into the pathophysiology of TD. Like TD patients, infected rats show prominent orofacial dyskinesias. In keeping with the dopamine (Goetz & Klawans 1982) and anatomic (Fibiger & Lloyd 1984) hypotheses of TD, the Borna disease rat model shows enhanced behavioural sensitivity to DA agonists and selective striatal cell damage. There is also evidence of DA deafferentation and heterogeneous reduction of D2 binding in the caudate-putamen, particularly from sites implicated in oral behaviour. These observations on a virus-induced movement disorder offer novel approaches to TD pathogenesis.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Solbrig MV,Koob GF,Fallon JH,Lipkin WI

doi

10.1006/nbdi.1994.0014

subject

Has Abstract

pub_date

1994-12-01 00:00:00

pages

111-9

issue

3

eissn

0969-9961

issn

1095-953X

pii

S0969-9961(84)70014-3

journal_volume

1

pub_type

杂志文章
  • Dap12 and Trem2, molecules involved in innate immunity and neurodegeneration, are co-expressed in the CNS.

    abstract::Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL) is a recessively inherited disease characterized by early onset dementia associated with bone cysts. Our group has recently established the molecular background of PLOSL by identifying mutations in DAP12 and TREM2 genes. To understand...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2004.09.007

    authors: Kiialainen A,Hovanes K,Paloneva J,Kopra O,Peltonen L

    更新日期:2005-03-01 00:00:00

  • Decreased stathmin expression ameliorates neuromuscular defects but fails to prolong survival in a mouse model of spinal muscular atrophy.

    abstract::Spinal muscular atrophy (SMA), a genetic neurodegenerative disorder, is caused by mutations or deletions in the survival of motor neuron 1 (SMN1) gene that result in SMN deficiency. SMN deficiency impairs microtubule networks in Smn-deficient cells and in SMA-like motor neuron cultures. Microtubule defects can be rest...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2012.11.015

    authors: Wen HL,Ting CH,Liu HC,Li H,Lin-Chao S

    更新日期:2013-04-01 00:00:00

  • Phenothiazines interfere with dopaminergic neurodegeneration in Caenorhabditis elegans models of Parkinson's disease.

    abstract::Oxidative stress is involved in the pathogenesis of various neurodegenerative disorders, conventional antioxidant strategies have yet been of limited success. We have employed transgenic Caenorhabditis elegans expressing DsRed2 in dopaminergic neurons and CFP pan-neuronally, to characterize in larval and adult animals...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2010.03.019

    authors: Mocko JB,Kern A,Moosmann B,Behl C,Hajieva P

    更新日期:2010-10-01 00:00:00

  • (G2019S) LRRK2 causes early-phase dysfunction of SNpc dopaminergic neurons and impairment of corticostriatal long-term depression in the PD transgenic mouse.

    abstract::Twelve- to sixteen-month-old (G2019S) LRRK2 transgenic mice prepared by us displayed progressive neuronal death of substantia nigra pars compacta (SNpc) dopaminergic cells. In the present study, we hypothesized that prior to a late-phase death of SNpc dopaminergic neurons, (G2019S) LRRK2 also causes an early-phase neu...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2014.04.021

    authors: Chou JS,Chen CY,Chen YL,Weng YH,Yeh TH,Lu CS,Chang YM,Wang HL

    更新日期:2014-08-01 00:00:00

  • BDNF regulates BIM expression levels in 3-nitropropionic acid-treated cortical neurons.

    abstract::3-Nitropropionic acid (3-NP) is an irreversible inhibitor of succinate dehydrogenase that has been used to explore the primary mechanisms of cell death associated with mitochondrial dysfunction and neurodegeneration in Huntington's disease. In this study we investigated the ability of brain-derived neurotrophic factor...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2009.06.006

    authors: Almeida S,Laço M,Cunha-Oliveira T,Oliveira CR,Rego AC

    更新日期:2009-09-01 00:00:00

  • Pridopidine stabilizes mushroom spines in mouse models of Alzheimer's disease by acting on the sigma-1 receptor.

    abstract::There is evidence that cognitive decline in Alzheimer's disease (AD) results from deficiencies in synaptic communication (e.g., loss of mushroom-shaped 'memory spines') and neurodegenerative processes. This might be treated with sigma-1 receptor (S1R) agonists, which are broadly neuroprotective and modulate synaptic p...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2018.12.022

    authors: Ryskamp D,Wu L,Wu J,Kim D,Rammes G,Geva M,Hayden M,Bezprozvanny I

    更新日期:2019-04-01 00:00:00

  • Cardiovascular dysautonomia in Parkinson disease: from pathophysiology to pathogenesis.

    abstract::Signs or symptoms of impaired autonomic regulation of circulation often attend Parkinson disease (PD). This review covers biomarkers and mechanisms of autonomic cardiovascular abnormalities in PD and related alpha-synucleinopathies. The clearest clinical laboratory correlate of dysautonomia in PD is loss of myocardial...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章,评审

    doi:10.1016/j.nbd.2011.10.025

    authors: Jain S,Goldstein DS

    更新日期:2012-06-01 00:00:00

  • Bax deletion does not protect neurons from BSE-induced death.

    abstract::Neurodegeneration is a common neuropathological feature of prion diseases. Although evidence of apoptosis was found in natural and experimental prion diseases, the precise mechanisms by which neurons die are poorly understood. The pro-apoptotic BAX protein, a key factor of the mitochondrial pathway, plays a central ro...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2006.05.013

    authors: Coulpier M,Messiaen S,Hamel R,Fernández de Marco M,Lilin T,Eloit M

    更新日期:2006-09-01 00:00:00

  • Copper/zinc chelation by clioquinol reduces spinal cord white matter damage and behavioral deficits in a murine MOG-induced multiple sclerosis model.

    abstract::The present study aimed to evaluate the therapeutic potential of clioquinol (CQ), a metal chelator, on multiple sclerosis pathogenesis. Experimental autoimmune encephalomyelitis was induced by immunization with myelin oligodendrocyte glycoprotein (MOG(35-55)) in female mice. Three weeks after the initial immunization,...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2013.01.012

    authors: Choi BY,Jang BG,Kim JH,Seo JN,Wu G,Sohn M,Chung TN,Suh SW

    更新日期:2013-06-01 00:00:00

  • Polyglutamine-expanded ataxin-3 causes cerebellar dysfunction of SCA3 transgenic mice by inducing transcriptional dysregulation.

    abstract::In the present study, we prepared a SCA3 animal model by generating transgenic mice expressing polyglutamine-expanded ataxin-3-Q79. Ataxin-3-Q79 was expressed in brain areas implicated in SCA3 neurodegeneration, including cerebellum, pontine nucleus and substantia nigra. Ataxin-3-Q79 transgenic mice displayed motor dy...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2008.03.011

    authors: Chou AH,Yeh TH,Ouyang P,Chen YL,Chen SY,Wang HL

    更新日期:2008-07-01 00:00:00

  • Seasonal affective disorder and serotonin-related polymorphisms.

    abstract::Disturbances in central serotonergic systems have been hypothesized to be involved in seasonal affective disorder (SAD). Association between SAD and the shorter allele of the serotonin transporter promoter repeat length polymorphism (5-HTTLPR) has been reported in an American sample. We have genotyped 82 SAD patients ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1006/nbdi.2000.0373

    authors: Johansson C,Smedh C,Partonen T,Pekkarinen P,Paunio T,Ekholm J,Peltonen L,Lichtermann D,Palmgren J,Adolfsson R,Schalling M

    更新日期:2001-04-01 00:00:00

  • Delayed administration of high dose human immunoglobulin G enhances recovery after traumatic cervical spinal cord injury by modulation of neuroinflammation and protection of the blood spinal cord barrier.

    abstract:BACKGROUND/INTRODUCTION:The neuroinflammatory response plays a major role in the secondary injury cascade after traumatic spinal cord injury (SCI). To date, systemic anti-inflammatory medications such as methylprednisolone sodium succinate (MPSS) have shown promise in SCI. However, systemic immunosuppression can have d...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2020.105187

    authors: Chio JCT,Wang J,Surendran V,Li L,Zavvarian MM,Pieczonka K,Fehlings MG

    更新日期:2021-01-01 00:00:00

  • Bright cyclic light accelerates photoreceptor cell degeneration in tubby mice.

    abstract::Photoreceptor cell death is an irreversible, pathologic event in many blinding retinal diseases including retinitis pigmentosa, age-related macular disease, and retinal detachment. Light exposure can exacerbate a variety of human retinal diseases by increasing the rate of photoreceptor cell death. In the present study...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2005.08.017

    authors: Kong L,Li F,Soleman CE,Li S,Elias RV,Zhou X,Lewis DA,McGinnis JF,Cao W

    更新日期:2006-03-01 00:00:00

  • AT2-receptor stimulation enhances axonal plasticity after spinal cord injury by upregulating BDNF expression.

    abstract::It is widely accepted that the angiotensin AT2-receptor (AT2R) has neuroprotective features. In the present study we tested pharmacological AT2R-stimulation as a therapeutic approach in a model of spinal cord compression injury (SCI) in mice using the novel non-peptide AT2R-agonist, Compound 21 (C21). Complementary ex...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2012.11.008

    authors: Namsolleck P,Boato F,Schwengel K,Paulis L,Matho KS,Geurts N,Thöne-Reineke C,Lucht K,Seidel K,Hallberg A,Dahlöf B,Unger T,Hendrix S,Steckelings UM

    更新日期:2013-03-01 00:00:00

  • Local insulin and the rapid regrowth of diabetic epidermal axons.

    abstract::Insulin deficiency may contribute toward the neurological deficits of diabetic polyneuropathy (DPN). In particular, the unique trophic properties of insulin, acting on sensory neuron and axon receptors offer an approach toward reversing loss of skin axons that develops during diabetes. Here we examined how local cutan...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2011.04.012

    authors: Guo G,Kan M,Martinez JA,Zochodne DW

    更新日期:2011-08-01 00:00:00

  • A single amino acid difference between the intracellular domains of amyloid precursor protein and amyloid-like precursor protein 2 enables induction of synaptic depression and block of long-term potentiation.

    abstract::Alzheimer disease (AD) is initially characterized as a disease of the synapse that affects synaptic transmission and synaptic plasticity. While amyloid-beta and tau have been traditionally implicated in causing AD, recent studies suggest that other factors, such as the intracellular domain of the amyloid-precursor pro...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2016.02.016

    authors: Trillaud-Doppia E,Paradis-Isler N,Boehm J

    更新日期:2016-07-01 00:00:00

  • Brain molecular aging, promotion of neurological disease and modulation by sirtuin 5 longevity gene polymorphism.

    abstract::Mechanisms determining characteristic age-of-onset for neurological diseases are largely unknown. Normal brain aging associates with robust and progressive transcriptome changes ("molecular aging"), but the intersection with disease pathways is mostly uncharacterized. Here, using cross-cohort microarray analysis of fo...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2010.09.016

    authors: Glorioso C,Oh S,Douillard GG,Sibille E

    更新日期:2011-02-01 00:00:00

  • GlialCAM/MLC1 modulates LRRC8/VRAC currents in an indirect manner: Implications for megalencephalic leukoencephalopathy.

    abstract::Megalencephalic leukoencephalopathy with subcortical cysts (MLC) is a rare type of leukodystrophy caused by mutations in either MLC1 or GLIALCAM genes. Previous work indicated that chloride currents mediated by the volume-regulated anion channel (VRAC) and ClC-2 channels were affected in astrocytes deficient in either...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2018.07.031

    authors: Elorza-Vidal X,Sirisi S,Gaitán-Peñas H,Pérez-Rius C,Alonso-Gardón M,Armand-Ugón M,Lanciotti A,Brignone MS,Prat E,Nunes V,Ambrosini E,Gasull X,Estévez R

    更新日期:2018-11-01 00:00:00

  • Inverse association between CSF Aβ 42 levels and years of education in mild form of Alzheimer's disease: the cognitive reserve theory.

    abstract::In Alzheimer's disease (AD), the cognitive reserve theory predicts that at any level of assessed clinical severity, the underlying brain pathology is more advanced in patients with more cognitive reserve. Recent evidences suggest that cerebrospinal fluid (CSF) biomarkers may reflect the brain pathology in AD. We inves...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2010.07.007

    authors: Dumurgier J,Paquet C,Benisty S,Kiffel C,Lidy C,Mouton-Liger F,Chabriat H,Laplanche JL,Hugon J

    更新日期:2010-11-01 00:00:00

  • Neuroprotective effects of the Sigma-1 receptor (S1R) agonist PRE-084, in a mouse model of motor neuron disease not linked to SOD1 mutation.

    abstract::The identification of novel molecular targets crucially involved in motor neuron degeneration/survival is a necessary step for the development of hopefully more effective therapeutic strategies for amyotrophic lateral sclerosis (ALS) patients. In this view, S1R, an endoplasmic reticulum (ER)-resident receptor with cha...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2013.10.010

    authors: Peviani M,Salvaneschi E,Bontempi L,Petese A,Manzo A,Rossi D,Salmona M,Collina S,Bigini P,Curti D

    更新日期:2014-02-01 00:00:00

  • Development of an aggregate-selective, human-derived α-synuclein antibody BIIB054 that ameliorates disease phenotypes in Parkinson's disease models.

    abstract::Aggregation of α-synuclein (α-syn) is neuropathologically and genetically linked to Parkinson's disease (PD). Since stereotypic cell-to-cell spreading of α-syn pathology is believed to contribute to disease progression, immunotherapy with antibodies directed against α-syn is considered a promising therapeutic approach...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2018.10.016

    authors: Weihofen A,Liu Y,Arndt JW,Huy C,Quan C,Smith BA,Baeriswyl JL,Cavegn N,Senn L,Su L,Marsh G,Auluck PK,Montrasio F,Nitsch RM,Hirst WD,Cedarbaum JM,Pepinsky RB,Grimm J,Weinreb PH

    更新日期:2019-04-01 00:00:00

  • Beta synchrony in the cortico-basal ganglia network during regulation of force control on and off dopamine.

    abstract::Beta power suppression in the basal ganglia is stronger during movements that require high force levels and high movement effort but it has been difficult to dissociate the two. We recorded scalp EEG and basal ganglia local field potentials in Parkinson's disease patients (11 STN, 7 GPi) ON and OFF dopaminergic medica...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2019.03.004

    authors: Fischer P,Pogosyan A,Green AL,Aziz TZ,Hyam J,Foltynie T,Limousin P,Zrinzo L,Samuel M,Ashkan K,Da Lio M,De Cecco M,Fornaser A,Brown P,Tan H

    更新日期:2019-07-01 00:00:00

  • Post-seizures amygdaloallocortical microvascular lesion leading to atrophy and memory impairment.

    abstract::Although the incidence of seizures after a cerebrovascular event including intracerebral hemorrhage has been widely recognized, the present studies have demonstrated that generalized convulsive seizures can cause multifocal amygdaloallocortical hemorrhage and tissue necrosis, the origin of which remains to be establis...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2005.01.029

    authors: Mraovitch S,Calando Y,Régnier A,Lamproglou I,Vicaut E

    更新日期:2005-08-01 00:00:00

  • Reducing canonical Wingless/Wnt signaling pathway confers protection against mutant Huntingtin toxicity in Drosophila.

    abstract::Huntington's disease (HD) is a genetic neurodegenerative disease characterized by movement disorders, cognitive decline and neuropsychiatric symptoms. HD is caused by expanded CAG tract within the coding region of Huntingtin protein. Despite major insights into the molecular mechanisms leading to HD, no effective cure...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2012.04.007

    authors: Dupont P,Besson MT,Devaux J,Liévens JC

    更新日期:2012-08-01 00:00:00

  • Finding intestinal fortitude: Integrating the microbiome into a holistic view of depression mechanisms, treatment, and resilience.

    abstract::Depression affects at least 322 million people globally, or approximately 4.4% of the world's population. While the earnestness of researchers and clinicians to understand and treat depression is not waning, the number of individuals suffering from depression continues to increase over and above the rate of global pop...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章,评审

    doi:10.1016/j.nbd.2019.104578

    authors: Flux MC,Lowry CA

    更新日期:2020-02-01 00:00:00

  • Every-other-day feeding exacerbates inflammation and neuronal deficits in 5XFAD mouse model of Alzheimer's disease.

    abstract::Food restriction has been widely associated with beneficial effects on brain aging and age-related neurodegenerative diseases such as Alzheimer's disease. However, previous studies on the effects of food restriction on aging- or pathology-related cognitive decline are controversial, emphasizing the importance of the t...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2020.104745

    authors: Lazic D,Tesic V,Jovanovic M,Brkic M,Milanovic D,Zlokovic BV,Kanazir S,Perovic M

    更新日期:2020-03-01 00:00:00

  • Role of the Fyn-PKCδ signaling in SE-induced neuroinflammation and epileptogenesis in experimental models of temporal lobe epilepsy.

    abstract::Status epilepticus (SE) induces neuroinflammation and epileptogenesis, but the mechanisms are not yet fully delineated. The Fyn, a non-receptor Src family tyrosine kinase (SFK), and its immediate downstream target, PKCδ are emerging as potential mediators of neuroinflammation. In order to first determine the role of F...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2017.11.008

    authors: Sharma S,Carlson S,Puttachary S,Sarkar S,Showman L,Putra M,Kanthasamy AG,Thippeswamy T

    更新日期:2018-02-01 00:00:00

  • Unraveling substantia nigra sequential gene expression in a progressive MPTP-lesioned macaque model of Parkinson's disease.

    abstract::Taking advantage of a progressive nonhuman primate model mimicking Parkinson's disease (PD) evolution, we monitored transcriptional fluctuations in the substantia nigra using Affymetrix microarrays in control (normal), saline-treated (normal), 6 days-treated (asymptomatic with 20% cell loss), 12 days-treated (asymptom...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2005.02.005

    authors: Bassilana F,Mace N,Li Q,Stutzmann JM,Gross CE,Pradier L,Benavides J,Ménager J,Bezard E

    更新日期:2005-10-01 00:00:00

  • Novel presenilin 1 and 2 double knock-out cell line for in vitro validation of PSEN1 and PSEN2 mutations.

    abstract::Mutations in APP (amyloid precursor protein), PSEN1 (presenilin 1) or PSEN2 (presenilin 2) are the main cause of early-onset familial forms of Alzheimer's disease (autosomal dominant AD or ADAD). These genes affect γ-secretase-dependent generation of Amyloid β (Aβ) peptides, the main constituent of amyloid plaques and...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2020.104785

    authors: Pimenova AA,Goate AM

    更新日期:2020-05-01 00:00:00

  • Fibrillation and molecular characteristics are coherent with clinical and pathological features of 4-repeat tauopathy caused by MAPT variant G273R.

    abstract::Microtubule Associated Protein Tau (MAPT) forms proteopathic aggregates in several diseases. The G273R tau mutation, located in the first repeat region, was found by exome sequencing in a patient who presented with dementia and parkinsonism. We herein return to pathological examination which demonstrated tau immunorea...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2020.105079

    authors: Sandberg A,Ling H,Gearing M,Dombroski B,Cantwell L,R'Bibo L,Levey A,Schellenberg GD,Hardy J,Wood N,Fernius J,Nyström S,Svensson S,Thor S,Hammarström P,Revesz T,Mok KY

    更新日期:2020-12-01 00:00:00