Colostrinin Shows Promise as a Retardant to the Development of Dementia and Alzheimer’s Disease

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Colostrinin is a naturally occurring mixture of at least 32 peptides (proline-rich polypeptides) derived from colostrum.  Colostrum is a form of milk produced in late pregnancy of mammals, including humans, by their mammary glands.  Colostrum delivers its nutrients in a very concentrated low-volume form to the delicate and immature digestive systems of a newborn.

Colostrinin may appear under various names in the literature, including:

  • CLN
  • Transfer factor
  • Proline-rich polypeptides (PRPs)

Numerous studies on Colostrinin have indicated that it has profound effects on cognitive performance and improvements in cognitive function.  Research demonstrates that an increase in new nerve cell growth and connectivity is observed after supplementing with Colostrinin.

Studies on cultured cells showed that Colostrinin modulates intracellular levels of reactive oxygen species (ROS), via regulation of glutathione metabolism, activity of antioxidant enzymes and mitochondria function. Due to an improvement in senescence-associated mitochondrial dysfunction and a decrease in ROS generation, Colostrinin decelerates the aging processes of both cultured cells and experimental animals. When given orally to mice, Colostrinin increased the lifespan and improved various motor and sensory activities.   1

Colostrinin’s Impact on Dementia and Alzheimer’s disease

There has been significant and considerable research on Colostrinin’s therapeutic value in dementia and Alzheimer’s disease.  Results from one study showed that oral administration of Colostrinin improves the outcome of Alzheimer’s disease patients with mild to moderate dementia.  2 

Specifically, the various neurological mechanisms of Colostrinin have been identified as the following:  3

  • changes the expression of molecular networks involved in beta amyloid protein production and in the changes to tau proteins that trigger formation of neurofibrillary tangles
  • alters the expression of genes to increase the production of enzymes that break down and eliminate beta amyloid as part of the natural clearance process
  • enhances defenses against chemical stresses and decreased expression of cytokines that promote inflammation

The studies on Colostrinin applied to dementia and Alzheimer’s disease have been encouraging and positive. 

A summary of these studies include:

In a study from 1996, 46 Alzheimer’s disease patients were randomly assigned to receive, every second day, either 100 mcg of colostrum, 100 mcg of selenium, or placebo tablets.  The patients took the supplements for three weeks, followed by 2 weeks of no treatment, and repeated this cycle 10 times over the one-year trial.

Subjects were then assessed using the standard Mini-Mental State Examination score. In the Colostrinin group, 54% of Alzheimer’s patients showed improved scores.  In the other 46% of Alzheimer’s patients receiving Colostrinin, the dementia progression stabilized and did not worsen.

In the placebo group, Alzheimer’s patients with mild and moderate disease saw their mental test scores decrease by 36% and 55%, respectively. 4

Another study from 2010 demonstrated that Colostrinin significantly relieved amyloid-beta induced cytotoxicity and alleviated the effect of amyloid-beta induced cytotoxicity.  5 

Colostrinin induces neurite outgrowth of pheochromocytoma cells and inhibits beta amyloid-induced apoptosis.  6  Colostrinin treatment may control the expression of genes that are involved in the development, maintenance, and regeneration of neurons in the central nervous system, and thus may also explain the improvements observed in Alzheimer’s patients with mild-to-moderate dementia during treatment with Colostrinin.

Low doses of Colostrinin (2.5 nM) can attain cytotoxic protection levels similar to those of highest doses (0.25 microM).  Thus, the time course for the appearance of beta-amyloid fibrils coincides with that for cytotoxicity, and that the reduction of fibrils of beta-amyloid peptides by Colostrinin is concomitant with the reduction of the cytotoxic effects of beta-amyloid on SHSY-5Y neuroblastoma cells.  These studies suggest that the neuroprotective effects exerted by Colostrinin are related to the reduction of beta-amyloid fibrils.   7

Colostrinin, which has efficacy in counteracting neural degradation and in stimulating neural growth, might prove to be a more effective means to deal with the causes of Alzheimer’s and other neurodegenerative diseases.  Evidence for the clinical efficacy of Colostrinin shows the remarkable ability of Colostrinin to reduce oxidative stress, prevent beta-amyloid aggregation and prolong the lifespan in a laboratory model of premature ageing.   8

Transcriptomal analysis showed that Colstrinin alters gene expression of molecular networks implicated in Abeta precursor protein synthesis, Tau phosphorylation and increased levels of enzymes that proteolitically eliminate Abeta.   9

A study from 2013 the beneficial effects of Colostrinin in the case of Alzheimer’s disease were shown in double-blind placebo-controlled trials, in long-term open-label studies and in multicenter clinical trials. A very important property of Colostrinin and one of its components, a nonapeptide (NP), is the prevention of amyloid-beta aggregation and the disruption of aggregates already formed. Moreover, Colostrinin has been found to modulate neurite outgrowth, suppress uncontrolled activation of cells, and reduce 4-HNE-mediated cellular damage.  10

These various studies demonstrate that Colostrinin is a very promising preparation which can be used to retard the development of dementia and Alzheimer’s disease.