Please Scroll Down to See Forums Below
napsgear
genezapharmateuticals
domestic-supply
puritysourcelabs
UGL OZ
UGFREAK
napsgeargenezapharmateuticals domestic-supplypuritysourcelabsUGL OZUGFREAK

Deprenyl & ALCAR

split endz

New member
Any problems taking these together? Deprenyl has many neurotransmitter enhancing effects. ALCAR is involved in the production of acetylcholine, a key neurotransmitter. Is there any risk of damage to neurotransmitter or synaptic pathways when combining these two. Any risk of overstimulation?
 
Last edited:
split endz said:
Any problems taking these together? Deprenyl has many neurotransmitter enhancing effects. ALCAR is involved in the production of acetylcholine, a key neurotransmitter. Is there any risk of damage to neurotransmitter or synaptic pathways when combining these two. Any risk of overstimulation?
I don't think so,since selegeline prevents re-uptake of dopamine,serotonin and norepinephrine but does not display significant affinity for acetylcholine.
However over-stimulation is possible,so it is recomended to start on one of these then add the 2nd agent and gradually titrate to achieve the desired effect while keeping adverse effects to a minimum.


J Neural Transm Park Dis Dement Sect. 1991;3(1):63-72. Related Articles, Links

Acetyl-levo-carnitine protects against MPTP-induced parkinsonism in primates.

Bodis-Wollner I, Chung E, Ghilardi MF, Glover A, Onofrj M, Pasik P, Samson Y.

Department of Neurology, Mount Sinai School of Medicine, C.U.N.Y., New York.

Acetyl-levo-carnitine (ALC) protects against 1-methyl, 4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced toxicity in the nonhuman primate. ALC pretreated monkeys do not show signs of parkinsonism or electroretinographic changes typical of dopaminergic deficiency when given MPTP. In addition, pilot neurochemical and morphological data confirm a partial protection effect. While MAO-B inhibitors, like L-Deprenyl, are thought to protect dopaminergic neurons from MPTP-induced cell death by preventing the conversion of MPTP to its toxic metabolite MPP+, ALC is not known to have MAO-B affinity. Converging evidence suggests that ALC may affect directly mitochondrial respiration, which is known to be the target of MPP+ and affected in human neurodegenerative diseases, including Parkinson's disease. The results of this study point to new therapeutic avenues for the treatment of these nosologic entities.
 
Thanks bro, that is the kind of info I was looking for. Many of the cautions about deprenyl point to mood enhancer/ stimulatory type drugs which when combined, can cause overstimulation.
 
Top Bottom