Beta burst coupling across the motor circuit in Parkinson's disease.

Abstract:

:Exaggerated activity in the beta band (13-35 Hz) is a hallmark of basal ganglia signals in patients with Parkinson's disease (PD). Beta activity however is not constantly elevated, but comes in bursts. In previous work we showed that the longer beta bursts are maintained, the more the oscillatory synchronisation within the subthalamic nucleus (STN) increases, which is posited to limit the information coding capacity of local circuits. Accordingly, a higher incidence of longer bursts correlates positively with clinical impairment, while the opposite is true for short, more physiological bursts. Here, we test the hypothesis that beta bursts not only indicate local synchronisation within the STN, but also phasic coupling across the motor network and hence entail an even greater restriction of information coding capacity in patients with PD. Local field potentials from the subthalamic nucleus and EEG over the motor cortex area were recorded in nine PD patients after temporary lead externalization after surgery for deep brain stimulation and overnight withdrawal of levodopa. Beta bursts were defined as periods exceeding the 75th percentile of signal amplitude and the coupling between bursts was considered using two distinct measurements, first the % overlapping (%OVL) as a feature of the amplitude coupling and secondly the phase synchrony index (PSI) to measure the phase coupling between regions. %OVL between STN and cortex and between the left and the right STN was higher than expected between the regions than if they had been independent. Similarly, PSI was higher during bursts as opposed to non-bursts periods. In addition, %OVL was greater for long compared to short bursts. Our results support the hypothesis that beta bursts involve long-range coupling between structures in the basal ganglia-cortical network. The impact of this is greater during long as opposed to short duration beta bursts. Accordingly, we posit that episodes of simultaneously elevated coupling across multiple structures in the basal ganglia-cortical circuit further limit information coding capacity and may have further impact upon motor impairment.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Tinkhauser G,Torrecillos F,Duclos Y,Tan H,Pogosyan A,Fischer P,Carron R,Welter ML,Karachi C,Vandenberghe W,Nuttin B,Witjas T,Régis J,Azulay JP,Eusebio A,Brown P

doi

10.1016/j.nbd.2018.06.007

subject

Has Abstract

pub_date

2018-09-01 00:00:00

pages

217-225

eissn

0969-9961

issn

1095-953X

pii

S0969-9961(18)30182-7

journal_volume

117

pub_type

杂志文章
  • TDP-43 proteinopathy in aging: Associations with risk-associated gene variants and with brain parenchymal thyroid hormone levels.

    abstract::TDP-43 proteinopathy is very prevalent among the elderly (affecting at least 25% of individuals over 85 years of age) and is associated with substantial cognitive impairment. Risk factors implicated in age-related TDP-43 proteinopathy include commonly inherited gene variants, comorbid Alzheimer's disease pathology, an...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2019.01.013

    authors: Nelson PT,Gal Z,Wang WX,Niedowicz DM,Artiushin SC,Wycoff S,Wei A,Jicha GA,Fardo DW

    更新日期:2019-05-01 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

  • Astrocytic Ca(2+) waves mediate activation of extrasynaptic NMDA receptors in hippocampal neurons to aggravate brain damage during ischemia.

    abstract::Excitotoxicity plays a central role in the neuronal damage during ischemic stroke. Although growing evidence suggests that activation of extrasynaptic NMDA receptors initiates neuronal death, no direct evidence demonstrated their activation during ischemia. Using rat hippocampal slices, we detected oxygen-glucose depr...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2013.05.005

    authors: Dong QP,He JQ,Chai Z

    更新日期:2013-10-01 00:00:00

  • Elevated plasma triglyceride levels precede amyloid deposition in Alzheimer's disease mouse models with abundant A beta in plasma.

    abstract::Dietary or pharmacological manipulation of plasma lipids markedly influences amyloid deposition in animal models of Alzheimer's Disease (AD). However, it is not known whether baseline plasma lipids in AD models differ from wild-type littermates throughout the natural history of disease. To address this question, we me...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2006.06.007

    authors: Burgess BL,McIsaac SA,Naus KE,Chan JY,Tansley GH,Yang J,Miao F,Ross CJ,van Eck M,Hayden MR,van Nostrand W,St George-Hyslop P,Westaway D,Wellington CL

    更新日期:2006-10-01 00:00:00

  • Heritability and genetic variance of dementia with Lewy bodies.

    abstract::Recent large-scale genetic studies have allowed for the first glimpse of the effects of common genetic variability in dementia with Lewy bodies (DLB), identifying risk variants with appreciable effect sizes. However, it is currently well established that a substantial portion of the genetic heritable component of comp...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2019.04.004

    authors: Guerreiro R,Escott-Price V,Hernandez DG,Kun-Rodrigues C,Ross OA,Orme T,Neto JL,Carmona S,Dehghani N,Eicher JD,Shepherd C,Parkkinen L,Darwent L,Heckman MG,Scholz SW,Troncoso JC,Pletnikova O,Dawson T,Rosenthal L,Ansor

    更新日期:2019-07-01 00:00:00

  • Tissue-specific variation of Ube3a protein expression in rodents and in a mouse model of Angelman syndrome.

    abstract::Angelman syndrome (AS) is a neurogenetic disorder caused by loss of maternal UBE3A expression or mutation-induced dysfunction of its protein product, the E3 ubiquitin-protein ligase, UBE3A. In humans and rodents, UBE3A/Ube3a transcript is maternally imprinted in several brain regions, but the distribution of native UB...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2010.04.012

    authors: Gustin RM,Bichell TJ,Bubser M,Daily J,Filonova I,Mrelashvili D,Deutch AY,Colbran RJ,Weeber EJ,Haas KF

    更新日期:2010-09-01 00:00:00

  • Induction of apoptosis in cells expressing exogenous Hippi, a molecular partner of huntingtin-interacting protein Hip1.

    abstract::To decipher the pathway of apoptosis induction downstream to caspase-8 activation by exogenous expression of Hippi, an interactor of huntingtin-interacting protein Hip1, we studied apoptosis in HeLa and Neuro2A cells expressing GFP-tagged Hippi. Nuclear fragmentation, caspase-1, caspase-8, caspase-9/caspase-6 and casp...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2005.11.003

    authors: Majumder P,Chattopadhyay B,Mazumder A,Das P,Bhattacharyya NP

    更新日期:2006-05-01 00:00:00

  • The vasculature as a neural stem cell niche.

    abstract::Neural stem cells (NSCs) are multipotent, self-renewing progenitors that generate progeny that differentiate into neurons and glia. NSCs in the adult mammalian brain are generally quiescent. Environmental stimuli such as learning or exercise can activate quiescent NSCs, inducing them to proliferate and produce new neu...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章,评审

    doi:10.1016/j.nbd.2017.01.010

    authors: Otsuki L,Brand AH

    更新日期:2017-11-01 00:00:00

  • Interictal spikes, seizures and ictal cell death are not necessary for post-traumatic epileptogenesis in vitro.

    abstract::Clinical studies indicate that phenytoin prevents acute post-traumatic seizures but not subsequent post-traumatic epilepsy. We explored this phenomenon using organotypic hippocampal slice cultures as a model of severe traumatic brain injury. Hippocampal slices were cultured for up to eight weeks, during which acute an...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2011.11.001

    authors: Berdichevsky Y,Dzhala V,Mail M,Staley KJ

    更新日期:2012-02-01 00:00:00

  • Formoterol, a β2-adrenoreceptor agonist, induces mitochondrial biogenesis and promotes cognitive recovery after traumatic brain injury.

    abstract::Traumatic brain injury (TBI) leads to acute necrosis at the site of injury followed by a sequence of secondary events lasting from hours to weeks and often years. Targeting mitochondrial impairment following TBI has shown improvements in brain mitochondrial bioenergetics and neuronal function. Recently formoterol, a h...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2020.104866

    authors: Vekaria HJ,Hubbard WB,Scholpa NE,Spry ML,Gooch JL,Prince SJ,Schnellmann RG,Sullivan PG

    更新日期:2020-07-01 00:00:00

  • Isoform-level brain expression profiling of the spermidine/spermine N1-Acetyltransferase1 (SAT1) gene in major depression and suicide.

    abstract::Low brain expression of the spermidine/spermine N-1 acetyltransferase (SAT1) gene, the rate-limiting enzyme involved in catabolism of polyamines that mediate the polyamine stress response (PSR), has been reported in depressed suicides. However, it is unknown whether this effect is associated with depression or with su...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2015.04.014

    authors: Pantazatos SP,Andrews SJ,Dunning-Broadbent J,Pang J,Huang YY,Arango V,Nagy PL,John Mann J

    更新日期:2015-07-01 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

  • Endocannabinoids affect neurological and cognitive function in thioacetamide-induced hepatic encephalopathy in mice.

    abstract::Endocannabinoids function as neurotransmitters and neuromodulators in the central nervous system via specific receptors and apparently have a neuroprotective role. We assumed that the endocannabinoid system could be involved in the pathogenesis of hepatic encephalopathy (HE), a neuropsychiatric syndrome due to liver d...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2005.07.008

    authors: Avraham Y,Israeli E,Gabbay E,Okun A,Zolotarev O,Silberman I,Ganzburg V,Dagon Y,Magen I,Vorobia L,Pappo O,Mechoulam R,Ilan Y,Berry EM

    更新日期:2006-01-01 00:00:00

  • White matter connectivity reflects clinical and cognitive status in Huntington's disease.

    abstract:OBJECTIVE:To investigate structural connectivity and the relationship between axonal microstructure and clinical, cognitive, and motor functions in premanifest (pre-HD) and symptomatic (symp-HD) Huntington's disease. METHOD:Diffusion tensor imaging (DTI) data were acquired from 35 pre-HD, 36 symp-HD, and 35 controls. ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2014.01.013

    authors: Poudel GR,Stout JC,Domínguez D JF,Salmon L,Churchyard A,Chua P,Georgiou-Karistianis N,Egan GF

    更新日期:2014-05-01 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

  • Neuronal tissue-specific ribonucleoprotein complex formation on SOD1 mRNA: alterations by ALS SOD1 mutations.

    abstract::Amyotrophic lateral sclerosis (ALS) is a fatal disease of unknown etiology. Mutations in copper/zinc superoxide dismutase (SOD1) are the most commonly associated genetic abnormality. Given that SOD1 is ubiquitously expressed, the exclusive vulnerability of motor neurons is one of the most puzzling issues in ALS resear...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2006.03.007

    authors: Ge WW,Leystra-Lantz C,Sanelli TR,McLean J,Wen W,Strong W,Strong MJ

    更新日期:2006-08-01 00:00:00

  • beta-amyloid peptides are cytotoxic to astrocytes in culture: a role for oxidative stress.

    abstract::beta-Amyloid is cytotoxic to neurons in culture by increasing hydrogen peroxide and altering calcium homeostasis. We have evaluated the cytotoxicty of beta-amyloid peptides (betaA(25-35) and betaA(1-40)) and generation of hydrogen peroxide on cortical cultured astrocytes. Twenty-four hours after a single addition of e...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1006/nbdi.2000.0313

    authors: Brera B,Serrano A,de Ceballos ML

    更新日期:2000-08-01 00:00:00

  • The dynamics of cortico-thalamo-cortical interactions at the transition from pre-ictal to ictal LFPs in absence epilepsy.

    abstract:PURPOSE:Generalized spike and wave discharges (SWD) are generated within the cortico-thalamo-cortical system. However the exact interactions between cortex and different thalamic nuclei needed for the generation and maintenance of SWD are still to be elucidated. This study aims to shed more light on these interactions ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2012.03.023

    authors: Lüttjohann A,van Luijtelaar G

    更新日期:2012-07-01 00:00:00

  • Cln5-deficiency in mice leads to microglial activation, defective myelination and changes in lipid metabolism.

    abstract::CLN5 disease, late infantile variant phenotype neuronal ceroid lipofuscinosis, is a severe neurodegenerative disease caused by mutations in the CLN5 gene, which encodes a lysosomal protein of unknown function. Cln5-deficiency in mice leads to loss of thalamocortical neurons, and glial activation, but the underlying me...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2011.12.009

    authors: Schmiedt ML,Blom T,Blom T,Kopra O,Wong A,von Schantz-Fant C,Ikonen E,Kuronen M,Jauhiainen M,Cooper JD,Jalanko A

    更新日期:2012-04-01 00:00:00

  • The role of cannabinoid 1 receptor expressing interneurons in behavior.

    abstract::Schizophrenia is a devastating neurodevelopmental disorder that affects approximately 1% of the population. Reduced expression of the 67-kDa protein isoform of glutamic acid decarboxylase (GAD67) is a hallmark of the disease and is encoded by the GAD1 gene. In schizophrenia, GAD67 downregulation occurs in multiple int...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2013.11.001

    authors: Brown JA,Horváth S,Garbett KA,Schmidt MJ,Everheart M,Gellért L,Ebert P,Mirnics K

    更新日期:2014-03-01 00:00:00

  • Oxidative insults are associated with apolipoprotein E genotype in Alzheimer's disease brain.

    abstract::The epsilon4 allele of the apolipoprotein E gene (APOE) is associated with sporadic and familial late-onset Alzheimer's disease (AD). Oxidative stress is believed to play an important role in neuronal dysfunction and cell death in AD. We now provide evidence that in the hippocampus of AD, the level of thiobarbituric a...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1006/nbdi.1999.0273

    authors: Ramassamy C,Averill D,Beffert U,Theroux L,Lussier-Cacan S,Cohn JS,Christen Y,Schoofs A,Davignon J,Poirier J

    更新日期:2000-02-01 00:00:00

  • Coincident thresholds of mutant protein for paralytic disease and protein aggregation caused by restrictively expressed superoxide dismutase cDNA.

    abstract::Familial amyotrophic lateral sclerosis (FALS) has been modeled in transgenic mice by introducing mutated versions of human genomic DNA encompassing the entire gene for Cu,Zn superoxide dismutase (SOD1). In this setting, the transgene is expressed throughout the body and results in mice that faithfully recapitulate man...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2005.06.005

    authors: Wang J,Xu G,Slunt HH,Gonzales V,Coonfield M,Fromholt D,Copeland NG,Jenkins NA,Borchelt DR

    更新日期:2005-12-01 00:00:00

  • Ethanol-induced death of postnatal hippocampal neurons.

    abstract::Fetal alcohol exposure causes severe neuropsychiatric problems, but mechanisms of the ethanol-associated changes in central nervous system development are unclear. In vivo, ethanol's interaction with N-methyl-D-aspartate (NMDA) and gamma-aminobutyric acid type A (GABA(A)) receptors may cause increased apoptosis in the...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1006/nbdi.2002.0523

    authors: Moulder KL,Fu T,Melbostad H,Cormier RJ,Isenberg KE,Zorumski CF,Mennerick S

    更新日期:2002-08-01 00:00:00

  • Expression analysis of genes responsible for serotonin signaling in the brain.

    abstract::To thoroughly understand the function and regulation of neurotransmitter systems in the brain, as well as the underlying disease mechanisms, it is important to comprehensively analyze the expression patterns of genes participating in such systems. Using functional annotated cDNA clones (FANTOM), we examined the gene e...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2005.01.021

    authors: Ichikawa M,Okamura-Oho Y,Okunishi R,Kanamori M,Suzuki H,Ritani A,Nitta H,Eguchi N,Urade Y,Hayashizaki Y

    更新日期:2005-08-01 00:00:00

  • Implantable brain computer interface: challenges to neurotechnology translation.

    abstract::This article reviews three concepts related to implantable brain computer interface (BCI) devices being designed for human use: neural signal extraction primarily for motor commands, signal insertion to restore sensation, and technological challenges that remain. A significant body of literature has occurred over the ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章,评审

    doi:10.1016/j.nbd.2009.12.007

    authors: Konrad P,Shanks T

    更新日期:2010-06-01 00:00:00

  • Beta-amyloid 42 accumulation in the lumbar spinal cord motor neurons of amyotrophic lateral sclerosis patients.

    abstract::Amyotrophic lateral sclerosis (ALS) is characterized by a progressive loss of large motor neurons in the brain and spinal cord. Amyloid precursor protein (APP), the transmembrane precursor of beta-amyloid (A beta), accumulates in the anterior horn motor neurons of ALS patients with mild lesions. APP undergoes an alter...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2005.01.012

    authors: Calingasan NY,Chen J,Kiaei M,Beal MF

    更新日期:2005-06-01 00:00:00

  • Human Rab7 mutation mimics features of Charcot-Marie-Tooth neuropathy type 2B in Drosophila.

    abstract::Charcot-Marie-Tooth disease type 2B (CMT2B) is an inherited axonal peripheral neuropathy. It is characterised by prominent sensory loss, often complicated by severe ulcero-mutilations of toes or feet, and variable motor involvement. Missense mutations in RAB7A, the gene encoding the small GTPase Rab7, cause CMT2B and ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2014.01.021

    authors: Janssens K,Goethals S,Atkinson D,Ermanoska B,Fransen E,Jordanova A,Auer-Grumbach M,Asselbergh B,Timmerman V

    更新日期:2014-05-01 00:00:00

  • The metabolism of glycosaminoglycans is impaired in prion diseases.

    abstract::It is well established that the conversion of PrP(C) to PrP(Sc) is the key event in prion disease biology. In addition, several lines of evidence suggest that glycosaminoglycans (GAGs) and in particular heparan sulfate (HS) may play a role in the PrP(C) to PrP(Sc) conversion process. It has been proposed that PrP(Sc) ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2005.05.009

    authors: Mayer-Sonnenfeld T,Zeigler M,Halimi M,Dayan Y,Herzog C,Lasmezas CI,Gabizon R

    更新日期:2005-12-01 00:00:00

  • Neuronal pentraxin 1: A synaptic-derived plasma biomarker in Alzheimer's disease.

    abstract::Synaptic neurodegeneration is thought to be an early event initiated by soluble β-amyloid (Aβ) aggregates that closely correlates with cognitive decline in Alzheimer disease (AD). Apolipoprotein ε4 (APOE4) is the most common genetic risk factor for both familial AD (FAD) and sporadic AD; it accelerates Aβ aggregation ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2018.02.014

    authors: Ma QL,Teng E,Zuo X,Jones M,Teter B,Zhao EY,Zhu C,Bilousova T,Gylys KH,Apostolova LG,LaDu MJ,Hossain MA,Frautschy SA,Cole GM

    更新日期:2018-06-01 00:00:00

  • Genetically determined susceptibility to neurodegeneration is associated with expression of inflammatory genes.

    abstract::Axonal damage, a core feature of neurological diseases, induces a retrograde reaction in neurons and surrounding glia. We determined transcriptional profiles of this reaction using Affymetrix oligonucleotide arrays. Gene expression was examined in spinal cord tissue prior to injury and following ventral root avulsion ...

    journal_title:Neurobiology of disease

    pub_type: 杂志文章

    doi:10.1016/j.nbd.2006.05.016

    authors: Swanberg M,Duvefelt K,Diez M,Hillert J,Olsson T,Piehl F,Lidman O

    更新日期:2006-10-01 00:00:00