Blocking the Action of Alzheimer's in Mice

The best cure for Alzheimer's disease would be to revert all of the changes in brain tissue characteristic of the disease. This is in general the best approach to age-related degeneration overall. A lot of research falls outside this paradigm, however, looking for ways to work around these changes, or block the mechanisms by which the changes cause specific forms of damage. This can produce good therapies, but is usually the worse approach as there are potentially very many ways in which the underlying changes can cause harm - striking at the root should always be more cost-effective.

Here is news of a potential path to block the main destructive action of Alzheimer's:

Researchers have discovered a protein that is the missing link in the complicated chain of events that lead to Alzheimer's disease. Researchers also found that blocking the protein with an existing drug can restore memory in mice with brain damage that mimics the disease. "What is very exciting is that of all the links in this molecular chain, this is the protein that may be most easily targeted by drugs. This gives us strong hope that we can find a drug that will work to lessen the burden of Alzheimer's."

Scientists have already provided a partial molecular map of how Alzheimer's disease destroys brain cells. In earlier work, [researchers] showed that the amyloid-beta peptides, which are a hallmark of Alzheimer's, couple with prion proteins on the surface of neurons. By an unknown process, the coupling activates a molecular messenger within the cell called Fyn. [This latest research] reveals the missing link in the chain, a protein within the cell membrane called metabotropic glutamate receptor 5 or mGluR5. When the protein is blocked by a drug similar to one being developed for Fragile X syndrome, the deficits in memory, learning, and synapse density were restored in a mouse model of Alzheimer's.

New drugs may have to be designed to precisely target the amyloid-prion disruption of mGluR5 in human cases of Alzheimer's and [the researchers are] exploring new ways to achieve this.

Link: http://www.eurekalert.org/pub_releases/2013-09/yu-aml083013.php

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