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Plasma levels of the β‐carbolines harman and norharman in Parkinson's disease
Author(s) -
Kuhn W.,
Müller T.,
Große H.,
Dierks T.,
Rommelspacher H.
Publication year - 1995
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.1995.tb00479.x
Subject(s) - harmine , parkinson's disease , selegiline , endogeny , pathogenesis , rotenone , medicine , pathophysiology , beta (programming language) , endocrinology , chemistry , disease , pharmacology , biochemistry , mitochondrion , computer science , programming language
Several lines of evidence suggest that endogenous and exogenous toxins may play a major role in the pathogenesis of Parkinson's disease (PD). In vivo aromatic β‐carbolines, like harman or norharman, may easily be formed by cyclization of indoleamines with e.g. aldehydes. Because of the structural similarity to MPTP, β‐carbolines have been proposed as endogenous toxins. For further elucidation of the role of β‐carbolines in neurodegenerative disorders, harman and norharman plasma levels were measured in 36 patients with PD and compared to an age‐ and sex‐matched control group. Plasma levels of norharman in PD were significantly higher compared to the control group. Harman in the plasma of Parkinsonian patients was also elevated compared to controls, but this difference was not significant. Correlation of β‐carbolines with plasma levels of L‐dopa, oral doses of bromocriptine and selegiline in treated Parkinsonian patients showed no significant results. On the one hand these results may suggest a possible role of β‐carbolines in the pathophysiological processes initiating PD, by, e.g., inducing mitochondrial respiratory inhibition like MPP + . One may speculate, however, that elevated levels of norharman and harman are due to an endogenous upregulation caused by unknown metabolic processes.