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'Missing link' known to trigger Alzheimer's discovered

By Catholic Online (NEWS CONSORTIUM)
September 6th, 2013
Catholic Online (www.catholic.org)

Alzheimer's remains a perplexing medical mystery to scientists. There is little known about the condition, which typically destroys memory and cognitive skills among the elderly, other than the amyloid plaque that attaches itself to brain cell. Now, researchers say they have discovered a protein they claim is the missing link to the development to Alzheimer's.

LOS ANGELES, CA (Catholic Online) - Researchers found that blocking this protein with an existing drug can restore memory in laboratory mice with brain damage that mimics Alzheimer's. This discovery offers hope of developing drugs to slow the degenerative illness.

"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," the study's senior author Stephen Strittmatter at Yale School of Medicine says.

"This gives us strong hope that we can find a drug that will work to lessen the burden of Alzheimer's."

Alzheimer's patients also have a shortage of important brain chemicals involved with the transmission of messages within the brain. Scientists have already provided a partial molecular map of how Alzheimer's disease destroys brain cells.

Professor Strittmatter's lab in previous work showed that the amyloid-beta peptides, which are a hallmark of Alzheimer's, couple with prion proteins. In a mysterious process, the coupling activates a molecular messenger called Fyn.

As published in the journal Neuron, the study reveals the missing link in the chain, a protein within the cell membrane called metabotropic glutamate receptor 5, or mGluR5.

Whenever 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.

Strittmatter stressed that new drugs may have to be designed to precisely target the amyloid-prion disruption of mGluR5 in human cases of Alzheimer's and said his lab is exploring new ways to achieve this.

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