Froud, K.; Saffrey, M. J.; Stewart, M. G.; Banks, D. and Wardhaugh, T.
The protective effect of colostrinin CLN(TM) against beta-amyloid and an oxidative stress inducer, menadione, in primary hippocampal cultures.
In: FENS Forum 2008, 12-16 Jul 2008, Geneva.
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The proline rich polypeptide ColostrininTM (CLN) isolated from early ovine or bovine milk has been found to have beneficial effects in slowing the course of Alzheimer’s disease (AD) in humans  although the mechanism by which this benefit occurs is still unclear. It has previously been shown that CLN can protect against beta-amyloid induced toxicity in SHSY-5Y cells by decreasing beta-amyloid aggregation and can prevent the beta-amyloid induced impairment of learning in newly hatched chicks. Moreover, a potential protective effect of CLN has been seen against oxidative stress induced damage including lipid peroxidation products in the PC12 cell line.
One of the key areas known to be affected in neurodegenerative diseases such as AD, is the
hippocampus. The aim of the present experiments was to investigate the putative protective effects of
CLN on primary hippocampal cultures treated with beta-amyloid or the oxidative stress inducer menadione. Initial experiments with 5ng/ml CLN show that CLN leads to a significant reversal of the beta-amyloid induced reduction in MAP-2 positive neurons. In addition menadione at 10uM causes a significant reduction in the number of MAP-2 positive neurons but treatment of cultures with CLN at 100ng/ml along with menadione causes a non-significant trend towards an increase in MAP-2 positive cells compared to menadione alone. Furthermore investigation of whether CLN is capable of affecting caspase 3 activation and therefore apoptosis in primary rat hippocampal cells showed that CLN may reduce a menadione mediated increase in caspase 3 activation.
Therefore CLN in primary hippocampal cultures may a) have a protective effect against beta-amyloid or menadione induced toxicity and b) reduce the menadione mediated increase in caspase 3 activation.
Acknowledgments: Regen Therapeutics
1. Boldogh, I, Kruzel, M. L (2008) J. Alzheimers Disease (in press)
2. Banks D, Stewart M. G. (2006) Soc Neurosci Abstr proceedings 674.5.
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