Vasogen's drug impacts inflammation-signalling pathways

By Wai Lang Chu

- Last updated on GMT

Related tags Nervous system

Vasogen announced preclinical data this week, demonstrating the
ability of its lead drug candidate to modulate key signalling
pathways associated with inflammation, demonstrating therapeutic
potential in a range of neurological disorders.

In a series of studies presented at the Neuroscience 2005, VP025 showed anti-inflammatory effects that could have significant applications in Alzheimer's disease, Parkinson's disease, and ALS (Lou Gehrig's disease).

These neurological conditions are associated with an inflammatory response in the nervous system, characterised by increased levels of inflammatory mediators, including cytokines, leading to the death of nerve cells and the eventual loss of functional activity.

Due to the prevalence, morbidity, and mortality associated with neuro-inflammatory diseases, they represent a significant medical, social, and financial burden.

"The growing body of evidence demonstrating the ability of VP025 to reduce inflammation within the central nervous system, suggests therapeutic potential in a range of neurological disorders and continues to support our plans to initiate phase II development,"​ said Dr. Anthony Bolton, Vasogen​'s chief scientific officer.

The latest study presented results from a model showing the ability of VP025 to reverse age-related inflammation in the brain.

Researchers from Trinity College Institute of Neuroscience, Dublin, Ireland, headed by Dr. Marina Lynch's team presented results from a model, which when treated with VP025, reversed age-related decreases in CD200 levels in the brain, reducing levels of microglial cell activation, and restoring memory and learning function.

CD200 is a protein that controls inflammation and maintains microglial cells in an unactivated state, decreases with ageing and has become a highly significant drug target

The process of ageing is associated with increased inflammation in the brain resulting from activation of microglial cells, (inflammatory immune cells of the brain), as evidenced by increases in inflammatory cytokines, including IL-1beta, and a reduction in memory and learning function (measured as long-term potentiation).

The study closely follows on from Dr. Yvonne Nolan's team representing the Department of Anatomy/Neuroscience, University College, Cork, Ireland, which presented earlier in the week.

The study presented new data demonstrating the ability of VP025 to inhibit increases in levels of p38 MAP kinase, a key component of the inflammation-signalling pathway, regulating IL-1beta, TNF-alpha, and other immune system responses associated with many inflammatory conditions.

In a preclinical model of Parkinson's disease, VP025 was shown to inhibit both the increase in p38 levels and the associated death of dopaminergic neurons.

The death of dopaminergic neurons in this model system leads to the onset of movement abnormalities that mimic those seen in Parkinson's disease.

A recent conference on Alzheimer's in the US heard that worldwide direct costs of caring for those with the disease and other forms of dementia amount to $156 billion, (€134 billion), based on a worldwide prevalence estimate of 27.7 million people with dementia.

With the current trend in demographics, this figure will rise to 34 million by 2025, presenting clear opportunities for pharmaceuticals targeted at prevention.

Related topics Preclinical Research Ingredients

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