Ganglioside Therapy of Peripheral Neuropathies: A Review of Clinical Literature

Massarotti, M

doi:10.1007/978-1-4757-5309-7_39

Cited by 7 publications

(2 citation statements)

References 8 publications

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“…interest in the treatment of polyneuropathy [9]. However, their involvement in the pathobiochemical events leading to polyneuropathy in man has not been understood until now.…”

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confidence: 99%

Gangliosides in normal human serum

Senn

Orth

Fitzke

et al. 1989

European Journal of Biochemistry

158

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The total content and pattern of gangliosides were determined in the unfractionated sera of 11 healthy human adults and in isolated lipoproteins. The total content of lipid-bound sialic acid was 10.5 3.2 nmol/ml serum. The ganglioside profile consisted of more than ten different components. The major ganglioside was GM3, followed by GD3, GD1,, GM2, GTlb, MG-3 (sialosyllactoneotetraosylceramide), GDlb and GQlb. Traces of four additional gangliosides could not be quantified reliably. Ganglioside patterns did not vary in sera taken from healthy adults of different age and sex. Approximately 98% of human serum gangliosides were transported by serum lipoproteins, predominantly by LDL (66%), followed by HDL (25%) and VLDL (7%). The quantitative distribution of individual gangliosides in VLDL and LDL was almost the same as that in the unfractionated serum; some differences existed with the ganglioside profile in HDL.Gangliosides are sialic-acid-containing glycosphingolipids, ubiquitous in neural and extraneural organs of deuterostomia [l]. They Svennerholm [35, 361, in parenthesis. The nomenclature for MG-3 and MG-4 is according to [17]. GM3, (I13NeuAcLacCer), (N-acetylneuraminosyl)galactosylglucosylceramide; GM2, (I13Neu-AcCgOse3Cer), N-acetylgalactosaminyl-(N-acetylneuraminosy1)galactosylglucosylceramide; G M I , (I13NeuAcGgOse4Cer), galacto-

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“…interest in the treatment of polyneuropathy [9]. However, their involvement in the pathobiochemical events leading to polyneuropathy in man has not been understood until now.…”

mentioning

confidence: 99%

Gangliosides in normal human serum

Senn

Orth

Fitzke

et al. 1989

European Journal of Biochemistry

158

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“…Before treatment, endogenous ganglioside GM, levels were determined in plasma on 3 different days and in urine and feces on 2 different days. The time-concentration curves over 24 hours were investigated on the first and last day of administration at 0, 10, 20, 30, 45, and 60 minutes and at 1 Y2, 2, 3, 5, 7, 9, 12, and 24 hours for intravenous administrations, and at 0, 30, and 60 minutes and at 2,3,4,5,6,7,8,9,10,12, and 24 hours for intramuscular administrations. On these days volunteers were served a controlled low-fat diet.…”

Section: Methodsmentioning

confidence: 99%

Multiple-dose pharmacokinetics of ganglioside GM1 after intravenous and intramuscular administration to healthy volunteers

Rost

Brockmöller

Weber

et al. 1991

Clin Pharmacol Ther

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Ganglioside GM1 multiple-dose pharmacokinetics were investigated in five healthy male volunteers. Doses of 100 mg were administered either intravenously or intramuscularly for 21 days, and the washout was followed-up for a further 21 days. The highly specific binding of the beta-subunit of cholera toxin was used to quantify ganglioside GM1 levels in plasma, urine, and feces. This dose regime increased the ganglioside GM1 steady-state plasma levels two to three orders of magnitude above the endogenous levels of 0.132 mg/L (coefficient of variation, 8.9%). Large and variable amounts of ganglioside GM1 were found in feces before and during treatment without relation to the dosage. No ganglioside GM1 could be detected in urine at any time. Plasma kinetics were linear with a biexponential disposition. Exogenously administered ganglioside GM1 was confined mainly to the blood volume as indicated by a steady-state volume of distribution of 6.98 +/- 3.57 L and appears to be excreted mainly in the form of metabolites. The total clearance was very slow at 1.61 +/- 0.37 ml/min. Absorption after intramuscular administration was slow (time to reach maximum concentration greater than 12 hours) and yielded steady-state concentrations somewhat lower compared with the intravenous infusion.

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