More Questions answered
I received this in an email concerning this thread:
>Deprenyl is a great example of a nootropics by its
> numerous benefits. Thus making it one of the most popular prescription drugs
> in the cognitive enhancement field. This drug is also known as L-deprenyl
> and selegiline and is one of the most widely researched nootropics for
> nearly forty years with over two hundred research papers on it.
> Selegiline works by preserving the brain as a protector and a neuro-rescue
> agent in times of stress and injury while being an antidepressant and
> cognitive enhancement agent.
Perhaps? But terms such as “protector” are vague. Gotta get more
specific on what it does?
Here is the best answer I could come up with as the Neuro-protector.
DEPRENYL: THE NEUROPROTECTOR
DPR has been shown to protect nerve cells from an ever-growing list of neurotoxins. Some of these neurotoxins can actually be produced within the brain under certain conditions, while others come from the environment or diet.
MPTP is a chemical first identified as a contaminant in synthetic heroin. In the 1980s young men using synthetic heroin suddenly developed a Parkinson-like disease. It was then discovered that the MPTP was taken up by glial cells surrounding nigrostriatal neurons, where it was converted by glial MAO-B enzymes into the real toxin, MPP+. The nigral neurons then absorbed MPP+ into their mitochondria, where MPP+ poisoned the mitochondria, killing the DA-using neurons.(15) The MAO-B inhibiting dose of DPR (10 mg/day) has been shown to prevent MPTP from being converted to the neurotoxin MPP+.(4) And as Lange and colleagues note, Compounds with a chemical structure similar to MPTP include both natural and synthetic products (e.g. paraquat) that are used in agriculture! (15)
6-hydroxydopamine (6-OHDA) is a potent neurotoxin that can spontaneously form from DA in DA-using neurons. (11,13) 6-OHDA may then further auto-oxidize to generate toxic superoxide and hydroxyl free radicals and hydrogen peroxide. (11,13) Knolls research has shown that pre-treatment of striatal DA-neurons with DPR can completely protect them from 6-OHDA toxicity. (4,11,13) Even in those not suffering from Parkinsons disease, the nigrostriatal neurons are the fastest aging neuron population in the human brain - an average 13% loss every decade from the 40s on. (1,13) Knoll and others believe that 6-OHDA neurotoxicity is a key cause of this normal nigral death, and that DPR may be just what the doctor ordered to retard this debilitating downhill neural slide.
DSP-4 is a synthetic NA-nerve toxin. In rodents DPR has been shown to prevent the depletion of NA in NA-using neurons and NA-nerve degeneration that DSP-4 causes. (4) AF64A is a cholinergic toxin - it damages brain cells that use acetylcholine. DPR pre-treatment has been shown to protect cholinergic neurons from AF64A toxicity. (4)
DPR has also protected human nerve cells from peroxynitrite and nitric oxide toxicity. Peroxynitrite is formed naturally in the brain when nitric oxide reacts with superoxide radical. Peroxynitrite causes apoptosis, a programmed suicide cell death that can be triggered in neurons by various agents. DPR was found to inhibit peroxynitrite-caused apoptosis, even after the DPR was washed from DPR pre-treated cells. (3)
Methyl-salsolinol is another MAO-B produced endogenous neurotoxin. Salsolinol is a tetra-hydroisoquinoline produced from the interaction of DA and acetaldehyde, the first-stage breakdown product of alcohol.
Once formed, salsolinol can then be further modified by MAO-B to generate methyl-salsolinol. DPRs MAO-B inhibiting activity can prevent the DNA damage caused by this toxin. (3,4)
By inhibiting MAO-B, DPR reduces the toxic load on the brain that is routinely produced through the normal operation of MAO-B. MAO-B digests not just DA and PEA, but also tryptamine, tyramine and various other secondary and tertiary amines. (15)
As noted earlier, PEA is the substance MAO-B is most efficient at digesting, so that the half-life of PEA is estimated at only 0.4 minutes. (21)
This continuous high level breakdown of PEA (and other amines) produces aldehydes, hydrogen peroxide and ammonia as automatic MAO-B reaction products, and they are all toxins. (4) Thus by reducing age-elevated MAO-B activity, DPR reduces the toxin burden on DA/NA neurons (where PEA is primarily produced).
…L-deprenyl provides neuroprotection against growth factor withdrawal in PC12 cells, oxidative stress in mesencepahalic neurons, and the genotoxic compound, Ara C, in cerebellar granule neurons, and against axotomy-induced motoneuronal degeneration and delayed neuronal death in hippocampus after global ischaemia. (24) And these are just some of the many reports in the scientific literature on DPRs versatile neuroprotection.
The answer came from this website, so you can check the references if you wish. http://www.bjklein.com/forum/topic….E=&TOPIC_ID=582
“You see, I don’t want to do good things, I want to do great things.” ~Alexander Joseph Luthor
I know Lewd Ferrigno personally.