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Parkinsonism Relat Disord. 2015 May;21(5):500-3. doi: 10.1016/j.parkreldis.2015.02.020. Epub 2015 Feb 28.

Cerebrospinal fluid concentrations of N-acetylcysteine after oral administration in Parkinson's disease.

Author information

1
Neurology Service, San Francisco Veterans Affairs Medical Center, 4150 Clement Street, San Francisco, CA 94121, USA; Department of Neurology, University of California, San Francisco Medical Center, 675 Nelson Rising Lane, San Francisco, CA 94143, USA. Electronic address: maya.katz@ucsfmedctr.org.
2
Neurology Service, San Francisco Veterans Affairs Medical Center, 4150 Clement Street, San Francisco, CA 94121, USA; Department of Neurology, University of California, San Francisco Medical Center, 675 Nelson Rising Lane, San Francisco, CA 94143, USA.
3
Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Emory University, 615 Michael Street, Suite 205, Atlanta, GA 30322, USA.

Abstract

INTRODUCTION:

Depletion of neuronal glutathione may contribute to the pathogenesis of Parkinson's disease (PD). N-acetylcysteine (NAC) can restore neuronal glutathione levels, but it has not been established whether NAC can cross the blood-brain barrier in humans.

METHODS:

Twelve patients with PD were given oral NAC twice daily for 2 days. Three doses were compared: 7 mg/kg, 35 mg/kg, and 70 mg/kg. NAC, cysteine, and glutathione were measured in the cerebrospinal fluid (CSF) at baseline and 90 min after the last dose. Cognitive and motor functions were assessed pre- and post-NAC administration using the Montreal Cognitive Assessment (MoCA) and the Unified Parkinson's Disease Rating Scale part III motor subscore (UPDRS-III).

RESULTS:

Oral NAC produced a dose-dependent increase in CSF NAC concentrations (p < 0.001), with the highest dose producing a CSF concentration of 9.26 ± 1.62 μM. There were no significant adverse events. NAC had no acute effect on motor or cognitive function.

CONCLUSION:

Orally administered NAC produces biologically relevant CSF NAC concentrations at doses that are well tolerated. The findings support the feasibility of NAC as a potential disease-modifying therapy for PD.

KEYWORDS:

Cysteine; Glutathione; Neuroprotection; Parkinson's disease; Therapeutics

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