The AMAZING Properties of 9‐Methyl‐β‐carboline (9-me-BC)


9-me-BC

Overview of 9-Me-BC

β-carbolines are potential endogenously produced and exogenously introduced neurotoxins that may contribute to the development of Parkinson’s disease (PD).

9-methyl-β-carboline has a wide range of activities that might be helpful in treating PD.

It stimulates dopaminergic neurons by boosting tyrosine hydroxylase and transcription factors in pre-existing dopa decarboxylase immunoreactive neurons, which increases the amount of dopamine produced.

Furthermore, 9-methyl-β-carboline has been found to have survival and regenerative/restorative potential for dopaminergic neurons by modulating the expression of multiple neurotrophic proteins as well as decreasing apoptotic cell signals.

Finally, 9-methyl-β-carboline targets a variety of inflammatory pathway components by blocking the proliferation of microglia, lowering chemotactic cytokines, and fostering an anti-inflammatory environment in the brain.

 

What is 9-Me-BC?

9-Me-BC, also known as 9-methoxy-β carboline, is a methylated variant of β carboline with the formula C12H10N2 [R].

The endocannabinoid system includes the enzymes that modulate the activity of neurotransmitters.

The brain contains eicosanoids, which are derivatives of tryptophan and its derivatives.

They occur in the human brain, spinal fluid, and plasma.

It was discovered for the first time in a 2008 study of the 9-methyl-β-carboline that it has a neuroprotective effect [R].

The Caspase-3 activity catalyzes programmed cell death, was decreased, while the ATP level was increased.

The researchers also noted an increase in the cell types that produce dopamine, which resulted in a larger amount of dopamine and uptake.

Furthermore, there was an increase in neuroprotectin, a protein that promotes neuron survival.

 

How does 9-Me-BC work in the brain?

9-me-BC_brain

In vitro studies with dopaminergic neuron cell cultures demonstrated greater tyrosine hydroxylase expression and associated transcription factors, enhanced neurite outgrowth, regeneration of neurons after chronic rotenone treatment, and decreased pro-inflammatory cytokines.

The substance increased the number of mature dopaminergic neurons and promoted expression factors linked with dopaminergic maturity in cell culture studies of primary mesencephalic dopaminergic neuron cells.

In addition, arabinoxylan nitrile, a 9-Me-BC derivative, inhibited the MPTP oxidation to MPP+ in vitro.

In vivo rodent research revealed increased dopamine levels in the hippocampus, improved spatial learning performance in a radial maze test, and increased dendrite outgrowth in the dentate gyrus of the hippocampus, as well as restoration of the number of tyrosine hydroxylase expressing neurons in the left striatum after an injection of MPP+.

The drug has been investigated in the treatment of Parkinson’s disease, and it is thought that 9-Me-BC inhibits monoamine oxidase A and B, which have been proposed for further study.

 

What are the benefits?

9-Methyl-β-carboline is a psychotropic substance that has a wide range of effects on human body functioning.

It’s a nootropic drug with a longer half-life than the lengthy list of other similar cognitive boosters.

People who take 9-Me-BC report the following benefits:

  • It improves executive functioning & alertness: It increases dopamine production and stimulation of dopamine receptors, resulting in an improvement in motivation and memory retention. It’s distinct from caffeine and other well-known stimulants in that it depletes norepinephrine but not through excessive firing.
  • Euphoria is increased: Dopamine is the major neurotransmitter of the pleasure and satisfaction reward system.
  • Apart from its dopamine production, it increases cognitive performance by improving hippocampal-dependent functions (short-term memory).
  • 9-Me-BC improves mitochondrial respiratory: Which is the process by which energy is made in cells and tissues, allowing them to operate properly. A number of organs are developed thanks to this efficiency, including the heart and brain. They include a wide range of functions linked with good brain health.

How much 9-Me-BC should you take?

The capsule and powder do not have a recommended dosage because research is still in its early stages.

However, some people believe that a 9-Me-BC dose ranges from 15 to 30 mg per day. At these doses, the majority of consumers report positive results.

That depends on the user. For some people, 15 milligrams of 9-MBC per day may be sufficient; while for others, 30 milligrams may be required.

 

9-Me-BC Mechanism of Action

mechanism_of_Action

It’s been shown to improve cognitive performance in people with age-related memory loss, including those who had no prior knowledge of the disease.

It works by stimulating neurons as well as promoting their growth. It’s neuroprotective, which means it protects our brain and central nervous system from toxin-induced damage.

It has a variety of effects, which may be due to its several mechanisms of action:

  • Interacting with the dopamine synthesis pathway via the tyrosine hydroxylase enzyme
  • The monoamine oxidase A and B (MAOA and MAOB) are both inhibited by harmaline, which is why it works as a MAOI.
  • It inhibits the breakdown of dopamine, resulting in higher levels of dopamine.

9-Me-BC is a dopaminergic compound as well. This basically implies that it increases dopamine-linked activity in the brain.

Some people enjoy this because it aids in the regeneration of dead dopaminergic neurons.

To put it another way, some users find 9-Me-BC helpful in recovering from stimulant abuse.

9-Me-BC also has Nootropic effects, which we briefly outlined above.

Because of this, it may enhance our cognitive abilities.

This is also why 9-Me-BC belongs to the nootropic family. Not only that, but 9-Me-BC also encourages the formation of new neurons, resulting in improved memory and learning.

As mentioned previously, 9-Me-BC also promotes the functioning of the respiratory chain. This can lead to potential cognitive advantages as well as a higher athletic performance.

All in all, 9-Me-BC is a highly versatile and effective nootropic.

It’s probably one of the most well rounded nootropics on the market today.

Because of this, it’s especially important to avoid using 9-Me-BC late in the afternoon, since unlike other nootropics, it delivers long-term benefits that don’t wear off in a few hours.

The half-life is certainly a factor here.

 

9-Me-BC and inflammation

9-methyl-carboline-9-me-BC-stimulates

Inflammatory processes are involved in the degeneration of dopaminergic neurons, and anti-inflammatory medications have been linked to a reduced risk of Parkinson’s disease (and Alzheimer’s disease).

9-Me-BC is also anti-inflammatory, in addition to its neurotrophic and neuroprotective effects on dopaminergic neurons.

9-Me-BC was tested in vitro on dopaminergic neurons to determine whether it could reduce the pro-inflammatory effect of lipopolysaccharides (LPS), the harmful endotoxins generated by gastrointestinal bacteria.

LPS upregulated the inflammatory cytokines and receptors CCL-1, CCL-2, CCL-4, CCL-5, complement factor 3 (C3), CVCL1, beta 2 microglobulin (b2m), chemokine ligand 10 (CVCL-10) and nitric oxide synthase (iNOS) cytokine expression.

9-Me-BC is thought to have anti-inflammatory effects in part by blocking the production of inflammatory cytokines such as interleukin-10.

Sources (references):

  • Adachi J., Mizoi Y., Naito T., Ogawa Y., Uetani Y. and Ninomiya I. (1991) Identification of tetrahydro-beta-carboline-3-carboxylic acid in foodstuffs, human urine and human milk. J. Nutr.121, 646– 652.
  • Ambrosini E. and Aloisi F. (2004) Chemokines and glial cells: a complex network in the central nervous system. Neurochem. Res.29, 1017– 1038.
  • Anderson D. W., Bradbury K. A. and Schneider J. S. (2006) Neuroprotection in Parkinson models varies with toxin administration protocol. Eur. J. Neurosci.24, 3174– 3182.
  • Ang S. L. (2006) Transcriptional control of midbrain dopaminergic neuron development. Development133, 3499– 3506.
  • Collins M. A., Neafsey E. J., Matsubara K., Cobuzzi R. J. Jr and Rollema H. (1992) Indole-N-methylated beta-carbolinium ions as potential brain-bioactivated neurotoxins. Brain Res.570, 154– 160.
  • Ghee M., Baker H., Miller J. C. and Ziff E. B. (1998) AP-1, CREB and CBP transcription factors differentially regulate the tyrosine hydroxylase gene. Brain Res. Mol. Brain Res.55, 101– 114.

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