To watch the video associated with this blog post, click here.
In this article, I’m going to tell you how to use an extract from the brains of pigs to rehabilitate your brain, reduce anxiety and depression, reduce withdrawals from drugs, delay tolerance development from drugs, protect yourself from neurodegenerative disease, and more.
How I Found Cerebrolysin
1. I developed an essential tremor in childhood that worsened tremendously when I developed more brain damage in my twenties.
2. I developed an almost crippling anxiety disorder in my 20’s also.
As my research developed, I came to understand that increases in neurogenesis and brain plasticity were those that most helped me overcome my anxiety disorder. Surprisingly, as they did so, I began to heal from my essential tremor. Consequently, I’ve devoted a lot of time in the last two years to the study of neurogenesis – the reason I have a long series on serotonin.
Cerebrolysin is one of the only commercially available formulation of actual neurotrophic molecules. When I discovered it, I experimented with it so extensively that I think I may be the single human who has most used Cerebrolysin.
In this article, I’ll tell you what Cerebrolysin is and what it’s effects are, before I take you through a tour of the most interesting rodent studies on Cerebrolysin followed by a survey of the human clinical studies, which are extensive. Finally, at the end of the article, I’ll tell you how to get Cerebrolysin and how I use it.
What is Cerebrolysin?
In 1949, Gerhart Harrer discovered that enzymatic hydrolysis of brain tissues produced a substance that stimulates nerve cells. It was subsequently registered as a drug in Austria by 1954, known as FPF1070, and has since become a commonly used medicine in East Asia and Eastern Europe, though it has yet to gain popularity in North America and Western Europe.
Cerebrolysin is a protein-based mixture of free amino acids (20%) and active, low molecular weight amino acid sequences (80%) that include the brain growth factors brain-derived neurotrophic factor (BDNF), glial cell-derived neurotrophic factor (GDNF), nerve growth factor (NGF), and ciliary neurotrophic factor (CNF).
Cerebrolysin’s Consistent Effects
1. Endogenous growth factors:
a. Cerebrolysin administration upregulates nerve growth factor, brain derived neurotrophic factor, and IGF-1.
2. Oxidative stress and inflammation:
a. Cerebrolysin administration consistently reduces markers of inflammatory cytokines (e.g. TNF-a), reduces markers of oxidative stress, increases glutathione activity, and consequently protects neurons from apoptosis.
a. Like donepezil, Cerebrolysin has been shown to inhibit glycogen synthase kinase-3-beta (GSK-3B).
b. Inhibition of GSK-3B and cyclin-dependent kinase 5 (CDK5) activity are the reasons Cerebrolysin decreases beta amyloid deposition and microtubule-associated protein tau phosphorylation.
4. Plastic changes:
a. Cerebrolysin induces plastic changes to dendritic morphology. Chronic Cerebrolysin exposure in aging rodents increases dendritic spine density and dendritic length in pyramidal neurons of the PFC and granule cells of the dentate gyrus.
b. Cerebrolysin reverses endothelial permeability dysfunction by reducing proinflammatory and pro-coagulation proteins and by increasing tight junction proteins.
Interesting Rodent Studies
1. Cognitive deficits:
a. In a rodent model of diabetes-induced cognitive decline using streptozotocin, Cerebrolysin treatment reduced HbA1c% elevations, attenuated body weight loss due to diabetes, enhanced learning and memory, reduced serum TNF-a and increased IGF-1beta, glutamate, and serotonin levels. Authors concluded that Cerebrolysin is neuroprotective against diabetes-induced cognitive decline.
b. In a rodent model of aging related cognitive deficits, Cerebrolysin dose-dependently improved antioxidant markers, reduced markers of oxidative stress like malondialdehyde, and reduced apoptosis while improving memory.
2. Parkinson’s disease:
a. In the 6-OHDA rodent model of Parkinson’s disease, post-treatment of rodents with Cerebrolysin restored midbrain and striatum dopamine levels, normalized MDA and NO levels, and replenished glutathione activity in the midbrain.
b. In the MPTP rodent model of Parkinson’s, sustained release, nanoparticle Cerebrolysin treatment had similar effects.
a. Concurrent Cerebrolysin treatment in rodents exposed to ethanol counteracts ethanol-induced oxidative stress and apoptosis.
4. Morphine withdrawal:
a. In a rodent model of morphine withdrawal, pre-treatment with Cerebrolysin limited withdrawal symptoms and heat shock protein elevation while not affecting morphine tolerance.
b. In another rodent model of morphine tolerance and withdrawal, concurrent Cerebrolysin treatment delayed tolerance development and attenuated symptoms of withdrawal from morphine.
5. Sleep deprivation:
a. Sleep-deprived animals experience memory deficits that can be attenuated by concurrent Cerebrolysin administration, likely via reducing oxidative stress at the hippocampus.