Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thyrotropin-releasing hormone (TRH) has been reported to improve the clinical picture of patients with the predominantly cerebellar form of spinocerebellar degeneration. The authors performed a double-blind, double cross-over, four-month trial, where TRH, at the daily dose of 2 and 4 mg, and placebo were given intramuscularly over a period of one month each. Sixteen patients with Friedreich's disease and 14 patients with different forms of spinocerebellar degeneration completed the trial. Features of cerebellar involvement, such as dysarthria, dysmetria and stance ataxia, showed a slight but significant improvement during TRH treatment. TRH was well tolerated. Transient nausea was the most frequent side-effect.
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PMID:[Chronic experimentation with TRH administered intramuscularly in spinocerebellar degeneration. Double-blind cross-over study in 30 subjects]. 250 70

Thyrotropin-releasing hormone (TRH) has been reported to be effective in some neuropsychiatric diseases. We examined the effect of TRH on the syndrome of pathologic laughing or crying in four patients with multiple cerebral infarction and one with olivo-ponto-cerebellar atrophy (OPCA). We found a marked therapeutic effect of the peptide on pathologic laughing with a slight improvement in ataxia in a patient with OPCA. A marked diminution in frequency of their pathologic crying with TRH was achieved in two patients with multiple cerebral infarction. The two other patients did not respond to TRH. Levodopa was administered to these patients to compare with TRH in therapeutic efficacy on the symptom and was effective in only one of four patients. The concentration of homovanillic acid in cerebrospinal fluid had diminished in two of the four patients. The results suggest that the tripeptide is effective in the control of this syndrome. We discuss the underlying mechanism(s) of the syndrome and the mode(s) of action of TRH.
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PMID:Treatment of pathologic emotionality with thyrotropin-releasing hormone. 251 62

Thyrotropin-releasing hormone (TRH) and its analog, TA-0910, ameliorate the ataxia of the mutant mouse, rolling mouse Nagoya, by metabolic normalization in the ventral tegmental field (VTF). We here investigated the distribution of cerebral TRH receptors in the rolling mouse to clarify the sites of action of these drugs. TRH receptors were widely distributed in multiple brain areas, including in the VTF and the cuneiform nucleus (CnF) which terminates in the VTF. These results suggest that TRH and TA-0910 directly activate the VTF by acting on TRH receptors in the VTF and indirectly activate it through the receptors in the CnF.
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PMID:Distribution of thyrotropin-releasing hormone (TRH) receptors in the brain of the ataxic mutant mouse, rolling mouse Nagoya. 901 14

1 Nootropic drugs increase glucose uptake into anaesthetised brain and into Alzheimer's diseased brain. Thyrotropin-releasing hormone, TRH, which has a chemical structure similar to nootropics increases cerebellar uptake of glucose in murine rolling ataxia. This paper shows that nootropic drugs like piracetam (2-oxo 1 pyrrolidine acetamide) and levetiracetam and neuropeptides like TRH antagonise the inhibition of glucose transport by barbiturates, diazepam, melatonin and endogenous neuropeptide galanin in human erythrocytes in vitro. 2 The potencies of nootropic drugs in opposing scopolamine-induced memory loss correlate with their potencies in antagonising pentobarbital inhibition of erythrocyte glucose transport in vitro (P<0.01). Less potent nootropics, D-levetiracetam and D-pyroglutamate, have higher antagonist Ki's against pentobarbital inhibition of glucose transport than more potent L-stereoisomers (P<0.001). 3 Piracetam and TRH have no direct effects on net glucose transport, but competitively antagonise hypnotic drug inhibition of glucose transport. Other nootropics, like aniracetam and levetiracetam, while antagonising pentobarbital action, also inhibit glucose transport. Analeptics like bemigride and methamphetamine are more potent inhibitors of glucose transport than antagonists of hypnotic action on glucose transport. 4 There are similarities between amino-acid sequences in human glucose transport protein isoform 1 (GLUT1) and the benzodiazepine-binding domains of GABAA (gamma amino butyric acid) receptor subunits. Mapped on a 3D template of GLUT1, these homologies suggest that the site of diazepam and piracetam interaction is a pocket outside the central hydrophilic pore region. 5 Nootropic pyrrolidone antagonism of hypnotic drug inhibition of glucose transport in vitro may be an analogue of TRH antagonism of galanin-induced narcosis.
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PMID:Piracetam and TRH analogues antagonise inhibition by barbiturates, diazepam, melatonin and galanin of human erythrocyte D-glucose transport. 1514 55