How Colostrinin Helps the Aging Brain - Life Extension Blog


Colostrinin is a polypeptide derived from colostrum, which lactating mothers produce prior to the
production of breast milk. Colostrum ensures the delivery of disease-protecting antibodies to newborn mammals. Polypeptides are chains of approximately 50 or fewer bonded amino acids.

Colostrinin is rich in the amino acid proline, which is one of the amino acids recommended by Linus Pauling to lower the risk of cardiovascular disease.

Some of the earliest published research concerning colostrinin suggests an immune system benefit. It has been reported that colostrinin induces the maturation and differentiation of thymus cells in mice.1

Experimental research suggests that colostrinin could benefit those with allergies. In a mouse model of allergic airway inflammation, IgE/IgG1 production, airway eosinophilia, mucin production and hypersensitivity were reduced in response to exposure to extracts from ragweed pollen grains and house dust mites.2

While colostrinin has many published studies focusing on immune support, it has also shown the ability to modulate production of tau and amyloid beta proteins, which are associated with cognitive decline.

Alzheimer’s Disease and Cognitive Decline

Recently, colostrinin has shown promise against cognitive dysfunction and Alzheimer’s disease. In experiments with rats, intraperitoneal (abdominal cavity) injection of colostrinin improved spatial learning in 13-month-old rats, but not in young, 3-month old-animals.3 Incidental learning was also enhanced in association with colostrinin. “Given the fact that colostrum is the first nutritive agent of neonates, it might be speculated that its peptides may facilitate the early postnatal development of the cerebral neurons and their plasticity,” write authors P. Popik and colleagues at the Polish Academy of Sciences.

Acting on these and other positive animal findings, colostrinin was evaluated in a clinical trial.4 Forty-six patients with Alzheimer’s disease were assigned to receive 100 micrograms of colostrinin every other day, 100 micrograms of selenium every other day, or a placebo for 3 weeks, followed by a 2-week period during which no treatment was received. After ten cycles, 15 patients who received colostrinin experienced improvement and seven of them had stabilized. While selenium was associated with disease stabilization in 13 out of 15 who received it, just half of the placebo patients had stabilized by the end of the trial evaluation.

In a similar trial, 105 participants with Alzheimer’s disease received 100 micrograms of colostrinin or a placebo on alternate days for three weeks followed by two treatment-free weeks for three cycles.5 This was followed by a 15 week phase during which all subjects received colostrinin. Tests that evaluated cognitive function, instrumental activities of daily living, and other areas were administered at the beginning of the study and at weeks 15 and 30. At 15 weeks, colostrinin was associated with stabilization of cognitive and daily living functions. Overall patient response also favored colostrinin. A better cognitive response to colostrinin was observed among those with less advanced disease.

In chicks trained in a task involving memory, injection of colostrinin into the mesopallium intermediomediale (a region of bird brains that is important for memory formation) prior to training improved long term memory retention, while control animals injected with saline failed to show improvement.6 Injection of colostrinin into the peritoneum was also effective. “These data extend the known efficacy of colostrinin from mammals demonstrating its widespread efficacy as a cognitive enhancer,” authors M. G. Stewart and D. Banks observe.

While some of the research has evaluated the use of colostrinin as an injection, it can also be taken orally as a supplement.

How Colostrinin Works

Research has revealed that colostrinin decreases lipid peroxidation and reduces intracellular levels of reactive oxygen species.7 In an in vitro study, colostrinin inhibited the aggregation of amyloid beta that results in the brain plaques characteristic of Alzheimer’s disease.8 It was observed that amyloid beta formed fibrils after 24 to 48 hours, however, colostrinin completely abolished fibril formation. As late as the 17th day, preformed fibers were dissolved upon the addition of colostrinin. When the effects of amyloid beta were evaluated in human neuroblastoma cells, preincubation of colostrinin with amyloid nearly completely prevented cell toxicity that would have otherwise occurred. Lower doses of colostrinin appeared to be as effective as high doses. The researchers concluded that colostrinin’s neuroprotective effects are related to the reduction of amyloid beta fibrils. Similar anti-amyloid effects have been demonstrated for colostrinin in other experiments.

Aging

In mouse diploid fibroblast cells, which are used as a model of cellular aging, the administration of colostrinin slowed senescence and increased population doubling levels.9 This was associated with a decrease in intracellular reactive oxygen species levels. “These data suggest that colostrinin may delay the development of cellular aging at the level of the organism,” A. Bacsi and colleagues conclude. “Thus, colostrinin may be used in the prevention and/or therapy of diseases associated with aging processes.”

In a review of colostrinin’s effects, I. Boldogh and M. L. Kruzel of the University of Texas Medical Branch at Galveston note that “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.”10

They conclude that “Although the molecular basis by which colostrinin exerts its diverse effects are still under investigation, the regulatory effect on the cellular redox state via maintenance of mitochondrial function and modification of ROS-induced cell signaling seem to be of great importance.”10

References

  1. Sokal I et al. Arch Immunol Ther Exp (Warsz). 1998;46(3):193-8.
  2. Boldogh I et al. Int Arch Allergy Immunol. 2008;146(4):298-306.
  3. Popkik P et al. Pharmacol Biochem Behav. 1999 Sep;64(1):183-9.
  4. Leszek J et al. Arch Immunol Ther Exp (Warsz). 1999;47(6):377-85.
  5. Bilikiewicz A et al. J Alzheimers Dis. 2004 Feb;6(1):17-26.
  6. Stewart MG et al. Neurobiol Learn Mem. 2006 Jul;86(1):66-71.
  7. Boldogh I et al. J Mol Neurosci. 2003 Apr;20(2):125-34.
  8. Schuster D et al. Neuropeptides. 2005 Aug;39(4):419-26.
  9. Bacsi A et al. Neuropeptides. 2007 Apr;41(2):93-101.
  10. Boldogh I et al. J Alzheimers Dis. 2008 Apr;13(3):303-21.

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