Literature DB >> 11061214

(-)Deprenyl (Selegiline): past, present and future.

J Knoll1.   

Abstract

(-)Deprenyl (Selegiline), the N-propargyl analogue of (-)methamphetamine, is the only drug in clinical case which, by enhancing the impulse propagation mediated release of noradrenaline and dopamine in the brain (catecholaminergic activity enhancer, CAE, effect), keeps in small doses without side-effects the catecholaminergic brain system on a higher activity level. (-)Deprenyl stimulates the catecholaminergic neurons selectively in the brain because, in contrast to PEA and the amphetamines which induce the continuous release of noradrenaline and dopamine from their intraneuronal stores, (-)deprenyl is devoid of this property. It is due to the CAE effect that a) the maintenance of rats on (-)deprenyl during the postdevelopmental phase of their life slows the age-related decline of sexual and learning performances and prolongs life significantly; b) patients with early, untreated Parkinson's disease maintained on (-)deprenyl need levodopa significantly later than their placebo-treated peers, and when on levodopa plus (-)deprenyl, they live significantly longer than patients on levodopa alone; and c) in patients with moderately severe impairment from Alzheimer's disease, treatment with (-)deprenyl slows the progression of the disease. It is reasonable to expect that a prophylactic low dose administration of a safe catecholaminergic activity enhancer substance during the postdevelopmental phase of life will slow the age-related decline of behavioral performances, delay natural death and decrease susceptibility to Parkinson's disease and Alzheimer's disease.

Entities:  

Mesh:

Substances:

Year:  2000        PMID: 11061214

Source DB:  PubMed          Journal:  Neurobiology (Bp)        ISSN: 1216-8068


  7 in total

1.  Acidic vesicles of the endo-exocytic pathways as targets for some anti-monoamine oxidase drugs.

Authors:  Paolo Dell'Antone; Meryem IbnLkayat; Denise Drago; Paolo Zatta
Journal:  Metab Brain Dis       Date:  2007-07-12       Impact factor: 3.584

2.  Trans-differentiation of the adipose tissue-derived stem cells into neuron-like cells expressing neurotrophins by selegiline.

Authors:  Alireza Abdanipour; Taki Tiraihi; Alireza Delshad
Journal:  Iran Biomed J       Date:  2011

Review 3.  Perspectives on MAO-B in aging and neurological disease: where do we go from here?

Authors:  M Jyothi Kumar; Julie K Andersen
Journal:  Mol Neurobiol       Date:  2004-08       Impact factor: 5.590

Review 4.  Monoamine oxidase inactivation: from pathophysiology to therapeutics.

Authors:  Marco Bortolato; Kevin Chen; Jean C Shih
Journal:  Adv Drug Deliv Rev       Date:  2008-07-04       Impact factor: 15.470

5.  The effects of rivastigmine plus selegiline on brain acetylcholinesterase, (Na, K)-, Mg-ATPase activities, antioxidant status, and learning performance of aged rats.

Authors:  Haris Carageorgiou; Antonios C Sideris; Ioanna Messari; Chrissoula I Liakou; Stylianos Tsakiris
Journal:  Neuropsychiatr Dis Treat       Date:  2008-08       Impact factor: 2.570

6.  Effects of the DT-diaphorase inhibitor dicumarol on striatal monoamine levels in L-DOPA and L-deprenyl pre-treated rats.

Authors:  Diego Bustamante; L Bustamante; Juan Segura-Aguilar; Michel Goiny; Mario Herrera-Marschitz
Journal:  Neurotox Res       Date:  2004       Impact factor: 3.978

7.  Hydride Abstraction as the Rate-Limiting Step of the Irreversible Inhibition of Monoamine Oxidase B by Rasagiline and Selegiline: A Computational Empirical Valence Bond Study.

Authors:  Tana Tandarić; Alja Prah; Jernej Stare; Janez Mavri; Robert Vianello
Journal:  Int J Mol Sci       Date:  2020-08-26       Impact factor: 5.923

  7 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.