Health Discoveries in General Health News
New compounds may reduce component of Alzheimer's
September 10, 2010
New compounds developed by a California-based research team may reduce levels of A-beta 42 peptide, a component of Alzheimer's disease believed to destroy neurons.
At the University of California at San Diego (UCSD) School of Medicine, a collaborative of researchers from universities, hospitals and biotechnology companies synthesized hundreds of new compounds that may be able to reduce A-beta 42 peptide, based on laboratory testing that also left other enzymes in the brain unaffected.
The research was published recently online in the journal Neuron.
"Current drug efforts have tried to broadly knock out peptide activity, but with adverse side effects. Our approach is to target and inhibit only the production of key peptides that may play a pivotal role in the pathogenesis of Alzheimer’s disease, while leaving other catalytic processes alone," said Steve Wagner, a project scientist in the UCSD Department of Neurosciences. "If some of the compounds we've synthesized are shown to do that in humans, we might eventually be able to inhibit or reduce further plaque production and ultimately prevent Alzheimer's before symptoms actually appear."
Within the North Shore-LIJ Health System, experimental drug trials, genetic studies and research on the pathological causes of the disease are done by the Litwin-Zucker Center for Research in Alzheimer's Disease and Memory Disorders.
At the University of California at San Diego (UCSD) School of Medicine, a collaborative of researchers from universities, hospitals and biotechnology companies synthesized hundreds of new compounds that may be able to reduce A-beta 42 peptide, based on laboratory testing that also left other enzymes in the brain unaffected.
The research was published recently online in the journal Neuron.
"Current drug efforts have tried to broadly knock out peptide activity, but with adverse side effects. Our approach is to target and inhibit only the production of key peptides that may play a pivotal role in the pathogenesis of Alzheimer’s disease, while leaving other catalytic processes alone," said Steve Wagner, a project scientist in the UCSD Department of Neurosciences. "If some of the compounds we've synthesized are shown to do that in humans, we might eventually be able to inhibit or reduce further plaque production and ultimately prevent Alzheimer's before symptoms actually appear."
Within the North Shore-LIJ Health System, experimental drug trials, genetic studies and research on the pathological causes of the disease are done by the Litwin-Zucker Center for Research in Alzheimer's Disease and Memory Disorders.