• Disease
  • Induced
  • Induced Dyskinesia
  • Qin Li

    Prominent publications by Qin Li

    KOL Index score: 14441

    Involuntary movements, or dyskinesia, represent a debilitating complication of levodopa therapy for Parkinson's disease. Although changes affecting D(1) and D(2) dopamine receptors have been studied in association with this condition, no causal relationship has yet been established. Taking advantage of a monkey brain bank constituted to study levodopa-induced dyskinesia, we report changes affecting D(1) and D(2) dopamine receptors within the striatum of normal, parkinsonian, ...

    Also Ranks for: D1 Dopamine |  induced dyskinesia |  dyskinetic animals |  cyclin dependent |  involuntary movements
    KOL Index score: 13956

    Appearance of dyskinesia is a common problem of long-term l-DOPA treatment in Parkinson's disease patients and represents a major limitation for the pharmacological management of the motor symptoms in advanced disease stages. We have recently demonstrated that dopamine released from serotonin neurons is responsible for l-DOPA-induced dyskinesia in 6-hydroxydopamine (6-OHDA)-lesioned rats, raising the possibility that blockade of serotonin neuron activity by combination of 5-HT(1A) and ...

    Also Ranks for: Receptor Agonists |  induced dyskinesia |  serotonin 5 |  dopa treatment |  motor symptoms
    KOL Index score: 12906

    Spinal cord injury disrupts the communication between the brain and the spinal circuits that orchestrate movement. To bypass the lesion, brain-computer interfaces have directly linked cortical activity to electrical stimulation of muscles, and have thus restored grasping abilities after hand paralysis. Theoretically, this strategy could also restore control over leg muscle activity for walking. However, replicating the complex sequence of individual muscle activation patterns underlying ...

    Also Ranks for: Spinal Cord Injury |  cord stimulation |  motor cortex |  macaca mulatta |  natural activation
    KOL Index score: 12862

    The serotonin (5-hydroxytryptamine [5HT]) system has recently emerged as an important player in the appearance of l-3,4-dihydroxyphenylalanine (levodopa [l-dopa])-induced dyskinesia in animal models of Parkinson's disease. In fact, dopamine released as a false transmitter from serotonin neurons appears to contribute to the pulsatile stimulation of dopamine receptors, leading to the appearance of the abnormal involuntary movements. Thus, drugs able to dampen the activity of serotonin ...

    Also Ranks for: Animal Models |  induced dyskinesia |  serotonin neurons |  antidyskinetic amantadine |  ldopa eltoprazine
    KOL Index score: 12498

    Dyskinesias represent a debilitating complication of levodopa therapy for Parkinson's disease (PD). While we recently demonstrated that levodopa-induced dyskinesia results from increased dopamine D(1) receptor-mediated transmission, we also questioned the possible role of subcellular localization of D(1) and D(2) receptors in mediating these effects as we previously showed that D(1) receptors undergo differential trafficking in striatal neurons of non-dyskinetic PD patients. Taking ...

    Also Ranks for: D1 Dopamine |  striatal neurons |  receptor trafficking |  parkinsonian monkeys |  ldopa dyskinesia
    KOL Index score: 10711

    BACKGROUND: In rodents, the development of dyskinesia produced by L-DOPA in the dopamine-depleted striatum occurs in response to increased dopamine D1 receptor-mediated activation of the cAMP - protein kinase A and of the Ras-extracellular signal-regulated kinase (ERK) signalling pathways. However, very little is known, in non-human primates, about the regulation of these signalling cascades and their association with the induction, manifestation and/or maintenance of ...

    Also Ranks for: Protein Kinase |  extracellular signal |  dyskinesia erk |  camp regulated |  increased phosphorylation
    KOL Index score: 10679

    BACKGROUND: A role for enhanced opioid peptide transmission has been suggested in the genesis of levodopa-induced dyskinesia. However, basal ganglia nuclei other than the striatum have not been regarded as potential sources, and the opioid precursors have never been quantified simultaneously with the levels of opioid receptors at the peak of dyskinesia severity.

    METHODS: The levels of messenger RNA (mRNA) encoding the opioid precursors preproenkephalin-A and preproenkephalin-B in the ...

    Also Ranks for: Subthalamic Nucleus |  induced dyskinesia |  opioid transmission |  basal ganglia |  globus pallidus
    KOL Index score: 10559

    BACKGROUND: ΔFosB is a surrogate marker of L-DOPA-induced dyskinesia (LID), the unavoidable disabling consequence of Parkinson's disease L-DOPA long-term treatment. However, the relationship between the electrical activity of FosB/ΔFosB-expressing neurons and LID manifestation is unknown.

    METHODS: We used the Daun02 prodrug-inactivation method associated with lentiviral expression of β-galactosidase under the control of the FosB promoter to investigate a causal link between the activity ...

    Also Ranks for: Induced Dyskinesia |  selective inactivation |  expressing neurons |  disease dopa |  spraguedawley receptors
    KOL Index score: 10370

    Parkinson's disease is caused primarily by degeneration of brain dopaminergic neurons in the substantia nigra and the consequent deficit of dopamine in the striatum. Dopamine replacement therapy with the dopamine precursor l-dopa is the mainstay of current treatment. After several years, however, the patients develop l-dopa-induced dyskinesia, or abnormal involuntary movements, thought to be due to excessive signaling via dopamine receptors. G protein-coupled receptor kinases (GRKs) ...

    Also Ranks for: Induced Dyskinesia |  dopamine receptors |  parkinsons disease |  parkinsonian rats |  animal doseresponse relationship
    KOL Index score: 10257

    The classic view of anatomofunctional organization of the basal ganglia is that striatopallidal neurons of the "indirect" pathway express D2 dopamine receptors and corelease enkephalin with GABA, whereas striatopallidal neurons of the "direct" pathway bear D1 dopamine receptors and corelease dynorphin and substance P with GABA. Although many studies have investigated the pathophysiology of the basal ganglia after dopamine denervation and subsequent chronic levodopa (L-dopa) treatment, ...

    Also Ranks for: Basal Ganglia |  medium spiny neurons |  dopamine receptors |  nonhuman primates |  opioid peptides
    KOL Index score: 9642

    INTRODUCTION: Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons as well as the presence of proteinaceous inclusions named Lewy bodies. α-synuclein (α-syn) is a major constituent of Lewy bodies, and the first disease-causing protein characterized in PD. Several α-syn-based animal models of PD have been developed to investigate the pathophysiology of PD, but none of them recapitulate the full picture of the disease. ...

    Also Ranks for: Α Syn |  nigrostriatal neurodegeneration |  mice rats |  lewy bodies |  substantia nigra
    KOL Index score: 9521

    In the present study we investigated whether the neuropeptide nociceptin/orphanin FQ (N/OFQ), previously implicated in the pathogenesis of Parkinson's disease, also affects L-DOPA-induced dyskinesia. In striatal slices of naive rodents, N/OFQ (0.1-1 μm) prevented the increase of ERK phosphorylation and the loss of depotentiation of synaptic plasticity induced by the D1 receptor agonist SKF38393 in spiny neurons. In vivo, exogenous N/OFQ (0.03-1 nmol, i.c.v.) or a synthetic N/OFQ receptor ...

    Also Ranks for: Induced Dyskinesia |  receptor agonist |  orphanin fq |  synaptic plasticity |  substantia nigra
    KOL Index score: 9493

    BACKGROUND: Involuntary movements, or dyskinesia, represent a debilitating complication of dopamine replacement therapy for Parkinson disease (PD). The transcription factor DeltaFosB accumulates in the denervated striatum and dimerizes primarily with JunD upon repeated L-3,4-dihydroxyphenylalanine (L-DOPA) administration. Previous studies in rodents have shown that striatal DeltaFosB levels accurately predict dyskinesia severity and indicate that this transcription factor may play a ...

    Also Ranks for: Parkinson Disease |  striatal overexpression |  induced dyskinesia |  primate model |  involuntary movements
    KOL Index score: 9489

    Amantadine, an N-methyl-D-aspartate glutamate receptor antagonist, is currently the only pharmacological treatment for levodopa-induced dyskinesia (LID) in Parkinson's disease (PD), but causes adverse effects on the central nervous system at therapeutic doses. Fenobam, a negative modulator of metabotropic glutamate receptor subtype 5, has recently been reported to attenuate LID in MPTP-treated macaques. The aim of the current study was to investigate the treatment interactions of fenobam ...

    Also Ranks for: Amantadine Treatment |  combination dyskinesia |  parkinsons disease |  central nervous |  drug induced
    KOL Index score: 9220

    Dyskinesia represents a debilitating complication of L-3,4-dihydroxyphenylalanine (L-dopa) therapy for Parkinson's disease. Such motor manifestations are attributed to pathological activity in the motor parts of basal ganglia. However, because consistent funneling of information takes place between the sensorimotor, limbic, and associative basal ganglia domains, we hypothesized that nonmotor domains play a role in these manifestations. Here we report the changes in 2-deoxyglucose (2-DG) ...

    Also Ranks for: Basal Ganglia |  induced dyskinesia |  motor manifestations |  debilitating complication |  limbic cognitive


    Qin Li: Influence Statistics

    Sample of concepts for which Qin Li is among the top experts in the world.
    Concept World rank
    animal dyskinesia #1
    represent debilitating #2
    symptoms unbiased #2
    30 amantadine #2
    worsening therapeutic effects #2
    symptoms pathological features #2
    istradefylline adjunct treatment #2
    common breeding processes #2
    dyskinetic dopa #2
    multifactorial correspondence #2
    brain bioavailability drugs #2
    farmbred cynomolgus monkeys #2
    phase levodopa #2
    istradefylline optimal doses #2
    mptptreated macaques #2
    profiles reminiscent #2
    5ht neurons dyskinesia #2
    monoamines human #2
    dyskinesia therapeutic #2
    activity fosb #2
    locations cage #2
    background brain bioavailability #2
    therapeutic effects ldopa #2
    ldopaprimed mptptreated macaques #2
    monoamines breeding #2
    single socially #2
    combination dyskinesia amantadine #2
    unbiased ethological #2
    robust antidyskinetic #2
    parkinsonian macaque monkeys #2
    optimal doses time #2
    dyskinesia impairing #2
    male oxidopamine #2
    combination fenobam #2
    ganglia lid #2
    reminiscent depressive #2
    evaluation istradefylline #2
    secondary permeability pyridines #2
    dyskinesia experimental #2

    Key People For Induced Dyskinesia

    Top KOLs in the world
    Maria Angela Cenci
    rat model induced dyskinesia parkinsons disease
    Erwan Bezard
    parkinsons disease basal ganglia induced dyskinesia
    Jonathan Michael Brotchie
    parkinsons disease basal ganglia globus pallidus
    Anders Björklund Björklund
    parkinsons disease dopamine neurons substantia nigra
    Martin Lundblad
    rat model dopamine release induced dyskinesia
    Manolo Carta
    induced dyskinesia animal models serotonin neurons

    Qin Li:Expert Impact

    Concepts for whichQin Lihas direct influence:Induced dyskinesia,  Parkinsons disease,  Animal dyskinesia,  Basal ganglia,  Parkinson disease,  Spraguedawley receptors,  Primate model,  Macaca fascicularis.

    Qin Li:KOL impact

    Concepts related to the work of other authors for whichfor which Qin Li has influence:Parkinson disease,  Basal ganglia,  Spinal cord,  Induced dyskinesia,  Animal models,  Dopamine receptors,  Rat model.



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