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Researchers discover weak link in Alzheimer's drug candidates
Date:4/1/2010

Some current therapies being investigated for Alzheimer's disease may cause further neural degeneration and cell death, according to a breakthrough discovery by UC San Diego researchers. By combining three dimensional computer simulations with high resolution atomic force microscopy membrane protein and cell imaging, electrical recording and various cellular assays, UCSD nano-biophysicist Ratnesh Lal and his colleagues investigated the structure and function of truncated peptides, known as nonamyloidgenic peptides, formed by some Alzheimer's drug candidates. The researchers found that the nonamyloidgenic peptides formed active ion channels that caused the cells to take in very high levels of calcium ions, which damaged synaptic efficiency and eventually killed neurons, neurons that are linked to memory loss in human brain.

As a result of their current findings and related previous work, Lal and his colleagues believe that aggregate-forming amyloidogenic peptides promote neurological diseases by forming holes or channels in cell membranes, disturbing ionic homeostasis by allowing unwanted ion flow in-and-out of cells, and most importantly allowing toxic amounts of calcium ions into neural cells. Truncated, shorter non-amyloidogenic peptide fragments that also form ion channels and alter neuronal viability, are assumed by biomedical researchers to be non-toxic and are currently targeted to treat Alzheimer's disease patients. Details of their research were recently published in a paper entitled "Truncated β-amyloid peptide channels provide an alternative mechanism for Alzheimer's Disease and Down syndrome" in the Proceedings of the National Academy of Sciences.

"There are several drugs to treat Alzheimer's in Trials I and II, but we don't believe that they will be adopted for clinical usage," said Lal, a joint professor in the UCSD Jacobs School of Engineering's Department of Mechanical and Aerospace Engineering and Bioengineering. We belie
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Contact: Andrea Siedsma
asiedsma@soe.ucsd.edu
858-822-0899
University of California - San Diego
Source:Eurekalert  

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