Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0270736 (Essential tremor)
 404 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Deep brain stimulation (DBS) within the basal ganglia complex is an effective neurosurgical approach for treating symptoms of Parkinson's disease (PD), Essential Tremor, Dystonia, Depression, Obssessive Compulsive Disorder, and Tourette's Syndrome, among others. Elucidating DBS mechanism has become a critical clinical and research goal in stereotactic and functional neurosurgery and in neural engineering. Along with electro-physiological and microdialysis techniques, two additional powerful technologies, notably functional Magnetic Resonance Imaging (fMRI) and in vivo neurochemical monitoring have recently been used to investigate DBS-mediated activation of basal ganglia network circuitry. For this purpose, we have previously developed WINCS (Wireless Instantaneous Neurotransmitter Concentration Sensor System), which is an MRI-compatible wireless monitoring device to obtain chemically resolved neurotransmitter measurements at implanted microsensors in a large mammalian model (pig) as well as in human patients. This device supports an array of electrochemical measurements that includes fast-scan cyclic voltammetry (FSCV) for real-time simultaneous in vivo monitoring of dopamine and adenosine release at carbon-fiber microelectrodes as well as fixed potential amperometry for monitoring of glutamate at enzyme-linked biosensors. In addition, we have utilized fMRI to investigate subthalamic nucleus (STN) DBS activation in the pig with 3Tesla MR scanner. We demonstrate the activation of specific basal ganglia circuitry during STN DBS using both fMRI and FSCV in the pig model. Our results suggest that fMRI and electrochemistry are important emerging techniques for use in elucidating mechanism of action of DBS.
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PMID:Emerging techniques for elucidating mechanism of action of deep brain stimulation. 2225

Essential tremor (ET) is one of the most common and most disabling movement disorders among adults. The drug treatment of essential tremor remains unsatisfactory. Additional therapies are required for patients with inadequate response or intolerable side effects. Thus, we aimed to investigate the therapeutic effects of riluzole on harmaline-induced tremor and ataxia in rat, and determining whether riluzole exerts its effect through modulation of glutamate levels in cerebellum. The study included 5 groups of Wistar rats weighing 80-100g, injected with harmaline (50mg/kg i.p.) for inducing experimental tremors and ataxia. The rats in group 1 served as control (saline induced) and group 2 received harmaline alone, whereas the animals in groups 3, 4 and 5, were also given riluzole intraperitoneally at doses of 2, 4 and 8 mg/kg 10 min after harmaline administration, respectively. The intensity and duration of tremor were recorded. Rotarod test, distance traveled and number of crossings were used to evaluate motor performance. Results of this study demonstrated that riluzole dose dependently attenuated duration and intensity of harmaline-induced tremors. Also, riluzole significantly improves time to fall, distance traveled and number of crossings in combined riluzole and harmaline treated rats. Histological analysis indicated that harmaline could cause vermis Purkinje cell (PC) loss and riluzole prevented this toxic effect. Harmaline also could increase glutamate levels in vermis and treatment with riluzole restored glutamate levels. In conclusion, riluzole has relatively protective effects on harmaline-induced tremor, probably related to its inhibitory effect on glutamatergic neurotransmission.
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PMID:Effects of riluzole on harmaline induced tremor and ataxia in rats: biochemical, histological and behavioral studies. 2297 88

Essential tremor (ET), which is one of the most common movement disorders, may lead to severe interference in quality of life. The first genome-wide association study (GWAS) has identified an association of the LINGO1 variant (rs9652490) with ET in Americans and Europeans. Recently, a second GWAS that was performed in a European population has discovered a new variant (rs3794087) of the main glial glutamate transporter (SLC1A2) that increases the risk of ET with an odds ratio of about 1.4. SLC1A2 encodes for the major glial high-affinity glutamate reuptake transporter in the brain and is a potential ET susceptibility gene. Because replication in a different ethnic population is important for validating a finding, we conducted a case-control study to investigate the SLC1A2 variant in an Asian cohort with ET in Taiwan. A total of 542 subjects (273 ET patients and 269 controls) were included. The results showed that rs3794087 was associated with ET among the Taiwanese. The odds ratio was 1.37. Our results were similar to those of the second GWAS of ET in Europeans, and this confirms that SLC1A2 may be a good functional candidate gene for ET. A replication study in another independent population is of importance to validate this association.
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PMID:SLC1A2 variant is associated with essential tremor in Taiwanese population. 2395 Dec 68

Essential tremor (ET) is a progressive neurological disorder with motor and non-motor symptoms. It has conclusively been shown that modulation of glutamate receptors could ameliorate ET. Recent studies have suggested that Berberine (BBR) has an inhibitory effect on glutamate receptors. Therefore, BBR may have therapeutic effects on ET. In this study, male Wistar rats (n=10 in each group) weighing 40-60 g were divided into control, harmaline (30 mg/kg, i.p.) and berberine (10, 20 or 50mg/kg, i.p, 15 min before harmaline injection) groups. Open field, rotarod, wire grip and foot print tests were used to evaluate motor performance. The results indicated that the administration of BBR (10 and 20mg/kg) attenuated harmaline-induced tremor in rats, but the beneficial effects of BBR could not be identified at dose 50mg/kg. In addition, BBR ameliorated gait disturbance in doses of 10 and 20mg/kg. The high dose of BBR not only failed to recover step width but also showed an adverse effect on left and right step length. The results indicate that BBR only in dose of 20mg/kg recovers mobility duration. The current study found a dose-dependent manner for the therapeutic effects of BBR in ET. Our study provides the initial evidence for the effects of BBR on motor function. Since BBR exerts its effects mainly through regulation of neurotransmitter release or blocke of NMDA receptors, thus, it is predicted that BBR ameliorate harmaline effect through blockade of NMDA receptors or glutamate release. This is an important issue for future research to evaluate the possible mechanisms involved.
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PMID:The therapeutic potential of Berberine chloride hydrate against harmaline-induced motor impairments in a rat model of tremor. 2564 20