The colostrum-based product increased the lifespan of cells isolated from mice predisposed to premature ageing and therefore, death, researchers will report today at the 21st International Conference of Alzheimer's Disease International taking place in Istanbul.
They tested the impact of Colostrinin on the mitochondria of cells isolated from strains of senescence-prone (SAMP1) and senescence-resistant (SAMR1) mice.
While cells from SAMP1 mice produce more reactive oxygen species (ROS), exhibit severe mitochondrial dysfunction, and have a decreased lifespan compared to the cells from SAMR1 mice, adding Colostrinin significantly decreased ROS levels, normalized mitochondrial function and increased the lifespan to levels similar to those in SAMR1 cells.
"This is an exciting finding that may go toward explaining the cognitive benefits of Colostrinin seen in clinical studies," said the study's lead investigator, Dr Istvan Boldogh based at University of TexasMedical Branch, Galveston.
"In-vivo experiments are nowongoing to test if these effects are evident when SAMP1 and SAMR1 miceare given Colostrinin over their lifetime," he added.
Continuous low levels of oxidative damage to cells, caused by ROS, play a key role in age-associatedneurodegenerative diseases such as Alzheimer's, Parkinson's disease andother disorders of the central nervous system.
A clinical trial on the ReGen product - a mixture of peptides isolated from colostrum - showed an improvement in cognitive function in Alzheimer's patients.
Percy Lomax, executive chairman of ReGen, noted: "If the ongoing in-vivo studies show similar results, this will be a very powerful message, which will support the marketing ofColostrinin as a nutraceutical."
A complete copy of the poster will be added to the ReGen website in the next few days.