Pubmed - The protective effects of the nutraceutical, colostrinin, against Alzheimer's disease, is mediated via prevention of apoptosis in human neurones induced by aggregated beta-amyloid

Neurodegeneration Unit, Basic Medical Sciences, St. George's, University of London, Cranmer Terrace, Tooting, London, UK.

Abstract

OBJECTIVE:

It has previously been demonstrated that oral administration of ovine Colostrinin (CLN), a proline-rich polypeptide isolated from ovine colostrum, can effectively treat Alzheimer's disease patients. This study aims to determine whether CLN has effects on the aggregation and toxicity of synthetic beta-amyloid (Abeta), implicated as a causative agent of AD.

DESIGN AND MEASUREMENTS:

Using cell assays, we examined if pre-treatment of neuronal cells with CLN confers protection.

RESULTS:

The data from cytotoxicity assays (using MTT and LDH) demonstrated that pre-treatment of human neuronal SHSY-5Y cells with 5 microg/ml CLN, for 24 hours, confers neuroprotection against Abeta-induced neurotoxicity. Twenty-four hour pre-treatment with 5 microg/ml CLN was also shown to reduce Abeta 1-40-induced apoptosis in human neuronal cells as determined via qualitative and quantitative apoptosis assays.

CONCLUSION:

The neuroprotection conferred with CLN pre-treatment was reduced with the Fas ligand (FasL) binding antibody Nok1, suggesting that the effects of CLN may involve a Fas:soluble FasL interaction. These findings indicate that CLN could possibly play a role in the prevention of AD pathogenesis, though the inhibition of Fas-mediated apoptosis.

http://www.ncbi.nlm.nih.gov/pubmed/19536420