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Cerebrosene = cerebrolysin?

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#31 chrono

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Posted 02 June 2010 - 03:35 PM

I read the full text of the aforementioned oral study. IMO, pretty weak stuff.

The study was conducted on 6 healthy adults, aged 51-76. The first day they were brought in for a baseline EEG reading and cognitive testing. The second day, they were administered 30ml cerebrolysin in OJ. Cognitive impact was measured using the ADAS (Alzheimer's Disease Assessment Scale) and SKT neuropsychological test. Readings were taken with EEG and transcranial Doppler ultrasonograph.

Scores improved slightly on the ADAS (lower is better):

Posted Image

And there was a change in brain waves; most notably, increased alpha waves, as well as decreased beta and delta waves.

Posted Image

Here's what I see (possibly) wrong with this trial:
  • Very small sample size (n=6)
  • ADAS and SKT tests are both used to assess dementia. While many of the principles are probably the same, why were normal tests of cognition not used for healthy subjects?
  • No controls. This renders results from the cognitive tests essentially meaningless, as test scores usually improve upon re-taking tests.
  • While ADAS showed improvement in a few categories, no significant improvements were shown in the SKT test. No explanation given.
  • Baseline EEG readings were taken once during the previous day, and not on the same day, before CL administration. While some of the results (esp. alpha wave) were quite pronounced, no attempt was made to account for normal variations in brainwave patterns between days, or throughout the 6h period of the test, either by control group or a 6h baseline test.
  • The SKT was administered during the timeframe of EEG measurement; complex cognitive tasks have the capability to change brain waves, skewing the measurements (see here, for example). Presumably the ADAS was administered during this same timeframe, but was omitted from the timeframe table. Controls who had received CL, but were not subjected to rigorous mental testing, would have been useful here.
  • Attempts to reconcile some of the differences in the brain wave results with existing literature were pretty weak, speculating on unsupported differences between age groups, rather than acknowledging limitations of the current study.
  • The study was funded by Ebewe Pharma (manufacturer of Cerebrolysin)
If anything, the study might show that CL is having some kind of effect when taken orally, increasing alpha waves and decreasing the slower waves. The study authors suggest that this is indicative of heightened attention; the SKT test (which measures attention) showed no such improvement, so I suggest it may be due to taking two cognitive tests in quick succession. It may correspond to a feeling described by several people in the cerebrolysin thread, of being more on-point and mentally capable, but I believe they mentioned this was not apparent after the first dosage.

None of the CRB literature that I'm aware of attempts to demonstrate cognitive or behavioral efficacy over the timeframe of a single dosage; many of the mechanisms at play require much more time to exert an effect.

If anyone has more knowledge of brain wave dynamics or peptide absorption, I'd appreciate more thoughts on the matter.

Edited by chrono, 26 August 2010 - 02:11 PM.

#32 chrono

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Posted 03 June 2010 - 06:45 PM

Back to the business of reverse-engineering Cerebrolysin: these papers give us an idea of the actual amount of peptides in the solution.

Antiapoptotic effects of the peptidergic drug cerebrolysin on primary cultures of embryonic chick cortical neurons.
Hartbauer M, Hutter-Paier B, Skofitsch G, Windisch M.
Institute of Zoology, Department of Neurobiology, Karl-Franzens University, Graz, Austria.

Cerebrolysin (EBEWE Arzneimittel, Austria, Europe) is a widely used drug relieving the symptoms of a variety of neurological disorders, particularly of neurodegenerative dementia of the Alzheimer's type. It consists of approximately 25% of low molecular weight peptides (<10k DA) and a mixture of approximately 75% free amino acids, this being based on the total nitrogen content...

PMID: 11475013 [PubMed - indexed for MEDLINE]

This paper confirms this composition:

A 24-week, double-blind, placebo-controlled study of three dosages of Cerebrolysin in patients with mild to moderate Alzheimer's disease.

The drug Cerebrolysin (Cere) is a peptide preparation produced by biotechnological methods, using a standardized proteolytic breakdown of purified porcine brain proteins. It consists of approximately 25% biologically active low molecular weight peptides and amino acids. One millilitre of Cere contains 9 mg of peptides and the consistent qualitative and quantitative composition of the compound is ensured by rigorous quality control procedures, including amino acid analysis and HPLC peptide mapping.

As does Int Clin Psychopharmacol. 2001 Sep;16(5):253-63, and others by this research group.

Here's the AA composition, outlined in their 1991 patent (see this post):

The bioactive substance used in the present invention which is obtained from enzymatic hydrolysis of swine brain protein fraction is available from the applicants under the trade name Cerebrolysin. Each ml of this drug contains 3.00mg of alanine, 0.25mg of arginine, 3.00mg of asparaginic acid, 0.06mg of cystine, 4.30mg of glutaminic acid, 1.50mg of glycine, 1.30mg of histidine, 2.00mg of isoleucine, 6.00mg of leucine, 0.50mg of methionine, 2.00mg of phenylalanine, 2.00mg of proline, 0.30mg of serine, 0.30mg of threonine, 0.50mg of tryptophane and 2.00mg of thyrosine as amino acids as well as peptides having a molecular weight of 10,000 or less...

(I've changed four of the units from g to mg, because as trevyn pointed out, those quantities in grams wouldn't fit in solution even by themselves.)

The total is 29.01mg AAs /mL of Cerebrolysin. If this is 75% of the constituent weight, that indicates 9.67mg/mL peptides—a daily dose of about 48mg in a 5mL injection. This calculation is confirmed by the paper Eur J Neurol. 2006 Jan;13(1):43-54, above.

This paper gives a slightly different figure:

Trophic effects of nootropic peptide preparations cerebrolysin and semax on cultured rat pheochromocytoma.

CL is a protein hydrolysate of porcine brain consisting of free amino acids (85%) and peptides with molecular weights below 10 kD (15%).

The 15% figure is also mentioned in the introductions of these papers: Exp Brain Res. 2004 Dec;159(4):425-32, J Neural Transm. 1997;104(11-12):1319-27, and others.

This figure suggests the peptide content is 5.12mg /mL. It's worth keeping in mind that this preparation has been played with for 40 years, and this probably represents a possible range of peptide content. I believe the source of this number to be No To Shinkei. 1993 Apr;45(4):325-31. This relatively early paper by a Japanese research group referse to Cerebrolysin as FPF-1070. Other Japanese papers [1, 2] using this moniker also mention the 15% figure. If this is the case, I believe that this can't be said to reflect the formulation used by Ebewe, and the amount of AAs described in their patent can't be used to derive peptide weight.

I'm most inclined to use the 25%/9mg figure from the first paper (J Neural Transm. 2001;108(4):459-73); they used CL and a special control mixture with the exact content of AAs sans peptides (both sourced from Ebewe) in their lyophilized forms to investigate the differential in function. This paper, and others by this same research group mentioning this figure, include scientists from Ebewe among the authors.

Pharmacol Biochem Behav. 1994 Dec;49(4):1105-7 says that CL is a 6% saline solution.

Edited by chrono, 20 November 2010 - 05:29 AM.

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#33 chrono

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Posted 13 July 2010 - 05:49 AM

I finally got a chance to read through Ebewe's new patent application that synapse posted. I'm still not clear on whether these peptides are derived from CRB. They are fragments of ciliary neurotrophic factor (CNTF), but cerebrolysin's peptides might well derive from this brain peptide as well. Anyway, here's the relevant composition and neurogenesis data:

Ciliary neurotrophic factor (CNTF) is a survival factor for various neuronal cell types. The human CNTF protein comprises 200 amino acid residues and shares significant sequence homology with CNTF proteins from other mammalian sources...CNTF is believed to induce the differentiation of bipotential glial progenitor cells in the perinatal rat optic nerve and brain. Furthermore, it has been observed to promote the survival of embryonic chick dorsal root ganglion sensory neurons. In addition, CNTF supports the survival and differentiation of motor neurons, hippocampal neurons and presympathetic spinal cord neurons.
Therefore, the present invention relates to a neurotrophic and/or neurogenic peptide having an amino acid sequence selected from the group consisting of VGDGGLFEKKL (SEQ ID No. 1), EDQQVHFTPTEG (SEQ ID No. 2) or IPENEADGMPATV (SEQ ID No. 3).

It has surprisingly been found that the peptides of the present invention, which are derivable from rat or human CNTF, show neurotrophic and/or neurogenic (causing growth of nerve tissue) effects which are comparable to the wild-type CNTF. Furthermore due to their small size these peptides are also able to pass the blood brain barrier.
The inorganic cation at the C-terminal end of the peptide according to the present invention may be an alkali metal or alkali earth metal cation, preferably a lithium, sodium, potassium, magnesium or calcium cation.

The organic cation may be a quaternary ammonium ion.

If the N-terminal end of the peptide according to the present invention comprises a positive charge, said charge may be preferably compensated by an equivalent of an inorganic or organic anion. The organic anion can be, for instance, acetate anion.

Another aspect of the present invention relates to a pharmaceutical composition comprising at least one peptide according to the present invention and/or at least one peptide having an amino acid sequence selected from the group consisting of GDGGLFEK (SEQ ID No. 5), GLFEKKLW (SEQ ID No. 6), VGDG (SEQ ID No. 7), GDGG (SEQ ID No. 8), DGGL (SEQ ID No. 9) and GGLF (SEQ ID No. 10) and optionally at least one pharmaceutically acceptable excipient and/or carrier.
The composition of the present invention may further comprise at least one additional pharmaceutically active component, which is preferably IPRNEADGMPINV (SEQ ID No. 4).
According to another preferred embodiment of the present invention the composition is provided for intravenous, intramuscular, spinal, epidural, transdermal, intranasal, mucosal, parenteral, oral, enteral or rectal administration.
The peptides are preferably comprised in the composition in an amount between 0.1 μg/g to 100 mg/g, preferably 1 μg/g to 80 mg/g.
According to a preferred embodiment of the present invention the peptide is administered to said individual at a dose of 0.1 μg/kg to 20 mg/kg body weight, preferably 0.5 μg/kg to 10 mg/kg body weight.

The amounts given for the composition and administration comprise so many orders of magnitude that they're essentially useless. Guidelines for these amounts would have to be determined through experimental titration, or extrapolation from other drugs like CRB (see previous post).

Examples 1, 3 and 4 tested the neurogenic potential of a few of these peptides. I'll summarize the data here, rather than try to quote the somewhat disjointed experiments:

CNTF position 133-145, MW 1384

  • Increased proliferation of DG progenitor cells
  • Increased proliferation in SGZ and oGCL of the DG (indicates progenitor migration)
CNTF position 145-155, MW 1203
  • Increased proliferation of DG progenitor cells
  • Increased proliferation in SGZ and oGCL of the DG (indicates progenitor migration)
  • Induced twofold increase in differentiation of DG progenitor cells into DCX-expressing (new immature) neurons
  • Increased MAP2 (arborization) and synaptophysin (synapse activity) in the DG
  • In mice, SC administration over 30 days improved performance on Morris water maze test over placebo

CNTF position 147-150

  • Increased BrdU-active neurons in GCL by 31%
  • Increased DCX (young neurons) in GCL by 91%
  • Increased BrdU-NeuN (mature neurons) in GCL by 62%
  • Increased BrdU-NeuN-c fos (integrated neurons) in GCL by 47%
  • Increased MAP2 (neurite arborization) in GCL by 31%
  • Increased synaptophysin (synapse activity) in GCL by 26%
  • Increased measures of retention in Morris water maze (better memory consolidation)

CNTF position 91-102, MW 1427
  • Increased proliferation of DG progenitor cells (less than 5 and 6)
  • Increased proliferation in the SGZ of the DG only

Notice that they switched up the numbering scheme of the peptides; does anyone know if these numbered fragments (CNTF 5, 6 and 9) are part of a more general convention for dividing up the CNTF protein?

As this is all the data on neurogenesis (or indeed any effect), I'm not clear on what the other 7 peptides (seq. 3, 5-10) are intended for. They may be based on previously-identified neuroactive sequences; I haven't had time to go through the references yet.

Here's the two versions of this patent. I can't get any of my browsers to view or download the TIFF files from the USPTO site, so I relied on the mostly-similar European version for tables and figures. If anyone has a PDF of the US application, or any version wherein the color histological pictures are at all discernible, please upload/link. (come on, guys...this is 2010, patents don't need to look like crappy Xeroxes any more)

United States Patent Application 20100029572

Patent WO/2008/113536 (European version)

#34 IronFanatic

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Posted 15 July 2010 - 04:03 AM

Does anyone have any information on cerebrolyzat? It seems like cerebrolyzat is cattle derived and lysin porcine derive.

#35 chrono

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Posted 15 July 2010 - 06:35 AM

Not really. Cerebrolysat seems to be the more common spelling, though there's still not much out there. Nothing from medline, only 2 mentions in google scholar (nothing useful). Russianbear mentioned it once on the board:

Is Cerebrolysat as effective as Cerebrolysin? It seems to be much cheaper...

Anyways cerebrolysat is a pain in the butt to inject (literally) unlike cerebrolysine which I'm convinced is laced with some kind of a painkiller. There's also a higher risk of gettin some mad cow encephalopathy from it since it's made out of a bull's brain basically :)

It also didnt seem as powerful too me, there's a clear price to quality correlation here, cerebrolysine is about 10-15 times more expensive (dependin on ampule size) but it IS worth it all the way.

The general process for deriving peptides from animals in this way is about 50 years old. I think cow brain was the material used in the first patent (that I'm aware of). Back then there was barely any purification; after they did the dialysis and protein digestion, filtering was actually considered optional. The first studies (in schizophrenics, as it happened) really did just inject cow brain soup.

My feeling is that it's pretty sketchy. I couldn't find any brand or product information, even from generally reputable places like pharmacy1010. Part of the reason Cerebrolysin is a good bet is that it has a big pharma company doing the extraction, with hundreds of studies conducted to establish its safety and efficacy. This isn't the kind of product that I would want just anyone to be manufacturing. As trevyn mentioned in the main thread, there are no known transferable prions from pigs, but this isn't the case with cows. Even assuming there's a way to lessen this kind of risk, it would involve precise and well-studied methodology, and probably complicated technique. The extremely low price doesn't necessarily imply that's going on.

I'll keep my eye out for any more info!

#36 chrono

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Posted 16 July 2010 - 01:18 AM

Found a really good paper which is the first definitive research I've seen into the peptide composition of Cerebrolysin. The main thrust of the paper is examining the effect CRB has on FGF-2, which in elevated levels (as in AD) prevents effective progenitor differentiation into neurons.

I'll focus first on the composition information, then move on to the very interesting experiments involving neural differentiation.

Trophic factors counteract elevated FGF-2-induced inhibition of adult neurogenesis. [free full PDF]
Chen H, Tung YC, Li B, Iqbal K, Grundke-Iqbal I.
New York State Institute for Basic Research in Developmental Disabilities

The dentate gyrus of adult mammalian brain contains neural progenitor cells with self-renewal and multi-lineage potential. The lineage and maturation of the neural progenitors are determined by the composition and levels of the trophic factors in their microenvironment. In Alzheimer disease (AD) brain, especially the hippocampus, the level of basic fibroblast growth factor (FGF-2) is markedly elevated. Here we show that elevated FGF-2 enhances the division and nestin levels of cultured adult rat hippocampal progenitors but impairs neuronal lineage determination and maturation of these cells in culture. The trophic factors ciliary neurotrophic factor (CNTF), glial-derived neurotrophic factor (GDNF), and insulin-like growth factors-1 and -2 (IGF-1, IGF-2) as well as an Alzheimer peptidergic drug, Cerebrolysin(®) (CL), in which we found these neurotrophic activities, counteract the effect of FGF-2 in inducing neuronal lineage (early neurogenesis). Whereas CNTF is the most active of the neurotrophic factors studied in promoting neurogenesis, CL, probably because of a combined effect of these factors, induces similar changes but without inhibiting cell proliferation. These findings suggest that CNTF, GDNF, IGF-1, and IGF-2 are promising therapeutic targets for AD and other diseases in which neurogenesis is probably inhibited.

PMID: 16859812 [PubMed - indexed for MEDLINE]

3.3. CL contains CNTF, GDNF, IGF-2 and IGF-1 activities
Based on the above findings that CL is neurotrophic/neurogenic, it appeared likely that some of the biologically active peptides in CL might be the proteolytic products of some of the known neurotrophic factors. Therefore, we chose the ELISA to screen CL for the presence of such peptides. Because regular ELISA plates might not bind all peptides in CL equally well, we covalently linked them to Covalink plates for this assay. We found that CL contained peptides reacting with neutralizing antibodies to human CNTF, GDNF, IGF-1, and IGF-2 (Fig. 4A).
Posted Image

Proteolysis is enzymatic protein digestion. So this antibody reaction indicates that CRB contains active peptide fragments of these growth factors, which have some portion of the same effect.

This paper also examines the ability of CRB to encourage differentiation of adult hippocampal progenitor (AHP) cells. Nestin is a marker for immature cells that have not yet differentiated into neurons, astroglia, or oligodendroglia. Class III β-tubulin (TuJ1) is a marker for differentiated neural stem cells, and microtubule-associated protein 2 (MAP2) indicates neurons a little further along in development. Glial fibrillary acidic protein (GFAP) indicates astroglia.

They compare the effect of CRB alone to the four growth factors

As compared with the control AHPs, which were cultured in FGF-2 alone, CL decreased the percentage of nestin-positive cells by ∼20% and simultaneously increased the Tuj1- and MAP2a,b-positive cell populations by a similar percentage. CL also slightly increased the GFAP-positive cells, but had no effect on the percentage of O4-positive oligodendroglia.
In the presence of 5 ng/ml FGF-2, CNTF (at 1, 5, and 10 ng/ml) reduced the nestin level of these cells by almost 50%.
Posted Image

At the same time, at 10 ng/ml, CNTF increased MAP2a,b and, most strongly, Tuj1 levels at 5 and 10 ng/ml. Unexpectedly, 1 ng/ml, the lowest concentration of CNTF, decreased the levels of Tuj1 and MAP2a,b.
Posted Image

Both CL and CNTF increased the GFAP level
Posted Image
The most dramatic dose response reaction, however, was obtained with CNTF, which already at 10 ng/ml induced Tuj1 expression well above the levels observed in cells treated with 5 ng/ml FGF-2. CNTF, GDNF and IGF-1 increased Tuj1 expression in a dose-dependent manner up to a concentration of 100 ng/ml studied.
...all four factors, like CL, increased the Tuj1-positive cell population, with CNTF having the highest (~50%) and IGF-2 the lowest (20%) effect. Similarly, all factors except IGF-2 increased the percentages of BrdU-positive neurons (Tuj1-positive) from ~20% to 60% in the case of CNTF and to ∼45% in the case of GDNF, IGF-1, and CL.
3.5. CNTF neutralizing antibody inhibits the neurogenic effects of CNTF and CL
We postulated that the neurotrophic/neurogenic activity of CL was at least partly due to the presence of an active fragment of CNTF in this preparation. To test this hypothesis, we investigated the effect of a CNTF neutralizing antibody on CL-, and as a positive control, on CNTF-induced changes on the levels of nestin and Tuj1 in AHPs...Western blot analysis of the treated cells revealed that addition of the antibody to CNTF indeed inhibited the neurotrophic/neurogenic activities of both CL and CNTF, as determined by an increase in the level of nestin, a marker for immature cells, and a decrease in the level of the neuronal marker Tuj1.

4. Discussion
In CL, we found CNTF, GDNF, IGF-1, and IGF-2 peptides presumed to be biologically active. Of these trophic factors, CNTF was by far the most active towards neurogenesis, followed by GDNF and IGF-1, which had approximately the same activity as CL. In contrast, IGF-2 had lesser neurogenic activity at high FGF-2 but had the strongest ability of all factors to drive the AHPs towards more mature neuronal stages at low FGF-2 concentration.
By far the most important amongst the four trophic factors found in CL is CNTF because of its strong neurotrophic and neurogenic characteristics and, importantly, because it was the only factor studied that not only fully counteracted the strong mitogenic activity of elevated FGF-2 but also reduced nestin to the same level as was found at low-level FGF-2.
CNTF is known to be a strong inducer of the glial lineage in cultured fetal precursors, which almost totally differentiate into astroglia within 2 days. In contrast, in the present study, the effect of CNTF on adult hippocampal progenitors was different. Only a few cells presumed to be previously uncommitted differentiated into astroglia, whereas the large majority of the cells strongly expressed the early neuronal marker Tuj1.

This was obviously a limited model, primarily relevant to increased FGF-2 in AD. Presumably, the 5ng/mL amount of FGF-2 used as a control in some instances is closer to normal amounts in the healthy brain. So to some extent, these actions can probably be expected in healthy individuals, and likely constitute a large portion of CRB's actions.

I don't know if we've arrived yet at a comprehensive idea of active components. They didn't test for presence of NGF or BDNF fragments; perhaps their presence is ruled out somehow. The study demonstrates that CNTF fragments are responsible for a large portion of the effects in this model. Whether this would be true for other measures remains to be seen. But as CNTF Peptide 6 was selected for development because of its strong performance in a largely AD-specific model, I think a strong case can be made that full-spectrum Cerebrolysin might still be a better choice for general nootropic usage. At least until a wide range of studies are available.

Speaking of which, a later research summary by these same authors links this work to the new Ebewe patent, and Peptide 6:

Development of neurotrophic peptides for enhancement of neurogenesis and associated behavioral improvement
Inge Grundke-Iqbal, Muhammad O. Chohan, Bin Li, Julie Blanchard, Lukas Wanka, Khalid Iqbal

Background: Levels of neurotrophic factors and the dentate gyrus neurogenesis are dysregulated in AD brain. The anti-dementia drug Cerebrolysin, which contains several neurotrophic activities, enhances the dentate gyrus neurogenesis and improves cognition in adult rats. To assess the neurogenic/neurotrophic (ngc/ntc) activities and corresponding neurobehavioral effect in mice of 4-11 mer synthetic peptides corresponding to the active regions of CNTF and the possible molecular mechanisms of action of these peptides. Methods: An 11-mer peptide, Peptide 6, and several 4-mer peptides of Peptide 6 were designed based on a biologically active region of CNTF. These peptides were administered to female retired breeders (C57 BL6 mice) either subcutaneously as a slow release bolus or daily IP injections at a dose of 5 to 50 nmoles peptide/day for 4-5 weeks. On days 2-6 of the treatment with the test peptide, the animals received IP 100 mg BrdU/kg/day. Results: Administration of Peptide 6 subcutaneously as a slow release bolus at a dose of 5 nmoles/day for 4 weeks enhanced the dentate gyrus neurogenesis and hippocampal-dependent spatial memory in normal adult mice. This peptide increased proliferation/survival of newborn neurons, along with a general neurotrophic effect. Of the four 4-mer peptides (Peptides 6A, 6B, 6C, and 6D), Peptide 6C was found to enhance most the dentate gyrus neurogenesis in mice. Both Peptide 6 and Peptide 6C increased the expression levels of MAP2 and synaptophysin in the dentate gyrus, and improved cognition in Morris water maze. These peptides had plasma half-lives of over 6 hours and were blood brain permeable. Peptide 6 was found to inhibit LIF-induced haptoglobin secretion from HepG2 cells. Thus, Peptide 6 appears to enhance neurogenesis in adult mice as a competitive inhibitor to LIF which is known to decrease overall neurogenesis in the subventricular zone. Conclusions: Peptide 6 and its neurogenic/neurotrophic fragments are promising candidate drugs for enhancing cognition through increase in ntg/ntc activity in AD and other learning and memory disorders as well as for promoting general cognitive health.

Edited by chrono, 16 July 2010 - 01:23 AM.

#37 synapse

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Posted 08 December 2010 - 10:49 PM

I finally did get the patent paperwork in on Cerebrosene (Cerebroprotein Hydrolysate). I don't know if it will really do much good, but my thoughts were on using it as a medical food for concussions, traumatic brain injury, and other neurodegenrative conditions. I VERY briefly discuss using it in both oral and injectable forms. Although more discussion has been on potential uses of neuropeptides for Alzheimer's, I see more potential uses in head traumas and brain injuries.

#38 bowling

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Posted 12 May 2011 - 06:07 AM

You know Cerebrolysin the production process it?http://www.stowarzys...pproach.ppt"]My link[/url]These may be useful to you.Do you think Cerebrolysin amino acids added, if not, how enzyme technology can achieve that effect?
So far, no one knows what they are extracted and then to hydrolysis of the protein

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#39 kevinseven11

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Posted 20 March 2012 - 05:11 AM

Why does transdermal cerebrolysin not work? If dissolved in something like DMSO then applied, why couldn't it work?

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