A Multiple Front War Against Alzheimer's Disease
Alzheimer's Disease (AD) accounts for about 60% of dementia cases in the elderly. Although current treatments for AD try mainly to maximise Acetylcholine levels in the brain, there are many other approaches to treatment for AD that are in the pipeline.
Genentech is buying licenses for antibody-based compounds that attack amyloid plaques in the brain.
GlaxoSmithKline (GSK) is partnering with Epix to develop a G Coupled Protein Receptor (GCPR) agonist that both increases Acetylcholine (ACh) levels and decreases formation of new amyloid plaques.
Samaritan Pharmaceuticals has developed a drug labeled SP 233 that not only blocks formation of new amyloid plaques, but also causes the removal of pre-existing plaques. Such elimination of plaques may hold promise for retrieval of mental function that was assumed lost.
Researchers at Washington University School of Medicine in St. Louis have developed a matrix metalloproteinase enzyme (MMP 9) that contributes to the clearance of Abeta plaques from between neurons.
Finally, Neuropharma has developed an enzyme inhibitor that may slow the formation of neurofibrillary tangles, the other principle neuropathology seen in AD. Their compound is labeled NP-12. If this inhibitor is effective in preventing neurofibrillary tangles, it may provide a complementary approach to anti-amyloid treatments of AD.
Although AD is not the only cause of dementia and neurodegeneration in the elderly, it is likely that at least some of the treatments being developed for AD will also benefit people who suffer from other degenerative conditions. The multiplicity of approaches to treatment of this disease is heartening, and provides hope that more people in the future will be able to enjoy a greater part of their lifespan.
Genentech is buying licenses for antibody-based compounds that attack amyloid plaques in the brain.
GlaxoSmithKline (GSK) is partnering with Epix to develop a G Coupled Protein Receptor (GCPR) agonist that both increases Acetylcholine (ACh) levels and decreases formation of new amyloid plaques.
Samaritan Pharmaceuticals has developed a drug labeled SP 233 that not only blocks formation of new amyloid plaques, but also causes the removal of pre-existing plaques. Such elimination of plaques may hold promise for retrieval of mental function that was assumed lost.
Researchers at Washington University School of Medicine in St. Louis have developed a matrix metalloproteinase enzyme (MMP 9) that contributes to the clearance of Abeta plaques from between neurons.
Finally, Neuropharma has developed an enzyme inhibitor that may slow the formation of neurofibrillary tangles, the other principle neuropathology seen in AD. Their compound is labeled NP-12. If this inhibitor is effective in preventing neurofibrillary tangles, it may provide a complementary approach to anti-amyloid treatments of AD.
Although AD is not the only cause of dementia and neurodegeneration in the elderly, it is likely that at least some of the treatments being developed for AD will also benefit people who suffer from other degenerative conditions. The multiplicity of approaches to treatment of this disease is heartening, and provides hope that more people in the future will be able to enjoy a greater part of their lifespan.
Labels: Alzheimer's
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