Effect of isoniazid on cerebrospinal fluid and plasma GABA levels in Huntington's disease

Manyam, N.V.Bala; Hare, Theodore A.; Katz, Leonard

doi:10.1016/0024-3205(80)90089-2

Cited by 33 publications

(7 citation statements)

References 26 publications

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“…We have, in fact, selected t,he mass fragmentographic approach to measure authentic GABA as the radioreceptor assay which may be influenced by substances other than GABA. The GABA concentrations that we found in human plasma are in keeping with previous reports (9), although lower values have also been obtained (19,20).…”

Section: Discussionsupporting

confidence: 93%

“…It is worthwhile to remember that the concentration of GABA in the nervous tissue is at least 10,000 times higher than in CSF. Nevertheless, drugs which are able to increase brain GABA content (and probably GABA concentration in the synaptic clefts) also increase the concentration of the amino acid in CSF in animals (28) and in humans (29,30). Therefore, values of CSF GABA could be considered, at least to a certain extent, as an index of the cerebral GABA function.…”

Section: Discussionmentioning

confidence: 99%

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Hepatic encephalopathy: Lack of changes of γ-aminobutyric acid content in plasma and cerebrospinal fluid

Moroni¹,

Riggio²,

Carlà³

et al. 1987

Hepatology

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The aim of the study was to verify the role of gamma-aminobutyric acid in the pathogenesis of hepatic encephalopathy occurring in cirrhotic patients by attempting to correlate plasma and cerebrospinal fluid content of authentic gamma-aminobutyric acid with the neurological manifestations of hepatic encephalopathy. For this purpose, plasma and cerebrospinal fluid gamma-aminobutyric acid levels were measured by means of mass fragmentography in 17 cirrhotic patients with hepatic encephalopathy and in 6 cirrhotics without neurological symptoms. Moreover, in all patients, a second sample was obtained during the clinical course of hepatic encephalopathy. The mean plasma and cerebrospinal fluid gamma-aminobutyric acid levels were not different in patients with or without hepatic encephalopathy and did not change during the evolution of the neurological symptoms. The lack of changes in the gamma-aminobutyric acid content in plasma and cerebrospinal fluid during hepatic encephalopathy is in contrast with the hypothesized importance of increased entry into the brain of gamma-aminobutyric acid in the pathogenesis of hepatic encephalopathy.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Hepatic encephalopathy: Lack of changes of γ-aminobutyric acid content in plasma and cerebrospinal fluid

Moroni¹,

Riggio²,

Carlà³

et al. 1987

Hepatology

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“…In contrast Bonnet et al found total GABA and homocarnosine to be significantly higher in HD CSF, in conflict with previous results [28]. The promise of GABA-related markers was further dampened after results of a randomized, double-blind, placebo-controlled crossover, clinical trial in 4 HD patients using Isoniazid (with pyridoxine), a treatment which increased GABA [29]. This failed to produce significant improvement in clinical measurements [30] but did produce side effects.…”

Section: Neurotransmittersmentioning

confidence: 84%

Cerebrospinal Fluid Biomarkers for Huntington’s Disease

Byrne¹,

Wild

2016

JHD

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Abstract. Cerebrospinal fluid (CSF) is enriched in brain-derived components and represents an accessible and appealing means of interrogating the CNS milieu to study neurodegenerative diseases and identify biomarkers to facilitate the development of novel therapeutics. Many such CSF biomarkers have been proposed for Huntington's disease (HD) but none has been validated for clinical trial use. Across many studies proposing dozens of biomarker candidates, there is a notable lack of statistical power, consistency, rigor and validation. Here we review proposed CSF biomarkers including neurotransmitters, transglutaminase activity, kynurenine pathway metabolites, oxidative stress markers, inflammatory markers, neuroendocrine markers, protein markers of neuronal death, proteomic approaches and mutant huntingtin protein itself. We reflect on the need for large-scale, standardized CSF collections with detailed phenotypic data to validate and qualify much-needed CSF biomarkers for clinical trial use in HD.

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“…Three patients with torticollis subsequently received isoniazid in a dosage ranging from 400 to 600 mg per day for a period of four to six weeks. Although larger doses of this drug have been advocated for this disorder [ 5 ] , in all three patients an elevation in serum aspartate transaminase was found, and one suffered severe nausea and vomiting. The treatment was stopped and liver function returned to normal rapidly.…”

Section: Department Ofmentioning

confidence: 92%

Postvaccinal encephalitis

Poser

1983

Annals of Neurology

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Effect of isoniazid on cerebrospinal fluid and plasma GABA levels in Huntington's disease

Cited by 33 publications

References 26 publications

Hepatic encephalopathy: Lack of changes of γ-aminobutyric acid content in plasma and cerebrospinal fluid

Hepatic encephalopathy: Lack of changes of γ-aminobutyric acid content in plasma and cerebrospinal fluid

Cerebrospinal Fluid Biomarkers for Huntington’s Disease

Postvaccinal encephalitis

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