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Published on: July 25, 2012
by Robin Wulffson MD for Exam Health:
Alzheimer’s disease, Parkinson’s disease, Multiple sclerosis (MS), and Parkinson’s disease are disparate brain disorders. Different therapies are under development for treatment of each of them. A team of researchers from Northwestern University Feinberg School of Medicine reported that they have developed a new multipurpose drug that could possibly treat all the conditions.
They published their findings on July 25 in the Journal of Neuroscience.
The researchers noted that overproduction of proinflammatory cytokines in the central nervous system has been implicated as a major contributor to the progression in Alzheimer’s disease. (A cytokine is a small protein released by cells that has a specific effect on the interactions between cells and communications between cells. Proinlammatory cytokines promote inflammation, which can cause cellular damage.)
In addition, numerous studies with animal models have shown that selective suppression of excessive glial proinflammatory cytokines can improve neurologic outcomes. (Glia is the delicate network of branched cells and fibers that supports the tissue of the central nervous system.) The researchers theorized that intervention with drugs targeting dysregulated glial proinflammatory cytokine production might be effective disease-modifying therapeutics if used in the appropriate biological time window.
This type of inflammatory response is known as neuroinflammation. This brain response has become increasingly considered to be a common denominator for many neurological disorders (i.e., Alzheimer’s disease, MS, and Parkinson’s disease), as well as playing a major role in brain injuries.
To test their hypothesis that early stage intervention with such drugs might be therapeutically beneficial, they examined the impact of intervention with MW01-2-151SRM (MW-151) in a mouse model. MW-151 is an experimental therapeutic that reduces proinflammatory cytokine production at low doses. The substance was tested in an mice that had been genetically engineered to develop Alzheimer’s disease, including increases in proinflammatory cytokine levels. The drug was administered during two distinct but overlapping therapeutic time windows of early stage pathology development.
The researchers found that MW-151 treatment attenuated (reduced) the increase in microglial and astrocyte activation and proinflammatory cytokine production in the cortex. This treatment resulted in improved neurologic outcomes, such as protection against synaptic protein loss and synaptic plasticity impairment. (Synapses are the connections between nerve cells.)
They noted that their results also demonstrated that the therapeutic time window is an important consideration in studies of drugs that modulate glia biological responses involved in pathology progression. They added that their results suggest that such models should be considered in the development of new therapeutic regimens that seek to delay the onset or slow the progression of Alzheimer’s disease.
In summary, unlike the majority of existing treatments for neurological disorders, MW-151 takes a new approach by targeting neurological disorders during the early to middle phases of the inflammatory response. Current treatments for these conditions target the development of beta amyloid plaques in the brain, which is a common sign of the progression of the disease.
In contrast, the new drug developed by the researchers targets the increase of the cell-signaling molecule cytokine, a precursor to the development of neurodegenerative disorders.
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