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Thursday, 25.05.2017

Barry Blackwell: Ervin Varga: Family, Culture, Persona and Career

Joseph Knoll’s response to Ervin Varga’s reply to his comment

Answer to your questions.

Ad 1. I never stopped working with deprenyl (DEP). It is still overlooked that DEP is the only catecholaminergic activity enhancer  (CAE)  substance in clinical use. The 10 mg daily dose of DEP has two effects. The known one: it blocks MAO-B in the brain; and the overlooked one: it exerts the non-specific enhancer effect (see my essay: inhn.org.e-books, 2016). The share of the enhancer effect in the beneficial therapeutic effects of DEP remains to be clarified.

 

Ad 2. The discovery of the catecholaminergic and serotoninergic enhancer regulation in the mammalian brain and the realization of β-phenylethylamine (PEA) and tryptamine as natural enhancer substances;  the identification of selegiline/(-)-deprenyl (DEP) as the first PEA-derived synthetic enhancer substance and the development of (2R)-1-(1-benzofuran-2-yl)-N-propylpentane-2-amine (BPAP), a tryptamine-derived synthetic enhancer substance, opened a promising new  brain-research domain. Up to this time we identified and studied by means of DEP and BPAP the enhancer sensitive catecholaminergic and serotonergic neurons only. DEP exerts it specific enhancer effect in 0.001 mg/kg and blocks MAO-B in the brain in 0.25 mg/kg. It is obvious that DEP, used world-wide since decades just as an MAO-B inhibitor, is primarily a PEA-derived synthetic enhancer substance, and this essential point is, unfortunately, still left out of consideration.

 

Joseph Knoll

July 28, 2016