Vasogen Inc. (VSGN)

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Vasogen's Research Published in European Journal of Neuroscience
Monday January 28, 7:00 am ET
- VP025 Provides a Neuroprotective Effect in Preclinical Model of Parkinson's Disease -

MISSISSAUGA, ON, Jan. 28 /PRNewswire-FirstCall/ - Vasogen Inc. (NASDAQ:VSGN - News; TSX:VAS - News), a biotechnology company engaged in the research and commercial development of therapies designed to target the destructive inflammatory process associated with the development and progression of cardiovascular and neurodegenerative disorders, today announced the publication of preclinical findings demonstrating that Vasogen's VP025, the leading candidate from its VP series of drugs, provides a significant neuroprotective effect in a model of Parkinson's disease. The research, which was conducted at the University College Cork, Ireland, was published in the European Journal of Neuroscience (Vol 27, pp.294-300, 2008).

Evidence is accumulating that inflammation plays an important role in the pathogenesis of Parkinson's disease. Microglial cells (immune cells resident in the brain) are activated in Parkinson's disease, producing pro-inflammatory factors that result in the death of nerve cells in an area of the brain called the nigrostriatal pathway. The published research was based on a well-established model of Parkinson's disease that involves the generation of a lesion on one side of the brain by the introduction of 6-hydroxydopamine (6-OHDA), inducing abnormal behaviour resulting in rotational movement. Both Parkinson's disease and 6-OHDA administration are associated with inflammatory processes that lead to the death of certain nerve cells, the dopaminergic neurons, which produce the neurotransmitter dopamine. It is the loss of these neurons and thereby the dopamine they produce that results in the movement abnormalities seen in this model.

The published study assessed the effect of pre-treatment with VP025 on 6-OHDA-induced rotational behaviour in response to amphetamine. Treatment with VP025 prior to 6-OHDA administration led to behavioural improvement demonstrated by a substantial (50-75%) and significant (p<0.001) reduction in rotation rate. VP025 also protected against the loss of dopaminergic neurons and provided significant protection against the reduction in levels of striatal dopamine induced by OHDA. The absence of rotations was maintained for up to three weeks while partial protection against the loss of dopaminergic neurons and reduction in striatal dopamine levels was still evident four weeks after lesion induction, indicating that VP025 has a potential long-term neuroprotective effect in this model.

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