“It’s an important step in understanding and ultimately slowing, stopping or even reversing the effects of Alzheimer’s disease.”.....Alzheimer's Reading Room
A new approach developed for studying brain synapses has yielded valuable information about the production of Amyloid-Beta oligomers (clumps of the Abeta peptide) known to play a key role in the onset of Alzheimer’s disease.
Testing of New Drug to Block Alzheimer’s Causing Abeta42 Aggregation Underway
“It is crucial that we understand how Abeta clumping is regulated, especially at the synapse, if we are to learn how to prevent, stop or slow Alzheimer’s pathology. Abeta42 is believed to be the first subtype of the Abeta peptide to oligomerize (clump together), and therefore most harmful to the brain,” Gandy said. “Now that the neurotransmitter receptor, ‘Group II mGluR’, has been identified as a source of Abeta42, we can find ways to reduce Abeta42 generation at the synapse. Lowering levels of Abeta42 would be predicted to hinder formation of poisonous clumps (oligomers).”
Gandy’s new approach is based on the use of isolated intact nerve terminals (synapses) from mice bred specially using human AD genes. Soong Ho Kim, a postdoctoral fellow in Gandy’s lab, has pioneered this approach. The new system aided in isolating a particular receptor at the synapse, known as “Group II Metabotropic Glutamate Receptor” (or mGluR). Group II mGluR selectively controls the formation Abeta42 at the synapse.
Studies have shown Abeta and its variant Abeta42 play a critical role in Alzheimer’s pathology. Previous research backed by CAF has shown that Abeta42 oligomers are formed at the neuronal synapse, a specialized way station where messages pass from one nerve cell to the next cell in the circuit. Disruption of synapses by Abeta42 oligomers is believed to underlie the loss of brain function in AD.
In unrelated work, a neuroscience bio-tech company, in the process of researching anti-depressants, has developed a safe and orally active drug that blocks ‘Group II mGluR’. In light of Gandy’s new discoveries, he and his colleagues are using the new synaptic terminal system to test the drug before moving on to test mice to determine if the drug can block Abeta from aggregating, which could be a leap forward in the search for preventative therapies.
“The development of this innovative approach by Dr. Gandy and his team could open up new doors of research on this devastating disease,” said Tim Armour, President and CEO of Cure Alzheimer’s Fund. “It’s an important step in understanding and ultimately slowing, stopping or even reversing the effects of Alzheimer’s disease.”
About Cure Alzheimer's Fund
Cure Alzheimer's Fund™ is a 501c3 public charity whose mission is to fund research with the highest probability of slowing, stopping or reversing Alzheimer's disease. Cure Alzheimer’s Fund is characterized by a venture approach to philanthropy, which targets funding to specific research objectives. All expenses and overhead is paid for by its founders and all contributions go directly to research. The Foundation has no financial or intellectual property interest in the research funded, and will make known the results of all funded research as soon as possible. Cure Alzheimer’s Fund is a national organization with offices in Boston and Pittsburgh.
For more information, visit www.curealzfund.org.
Media Contact: Contact: David Roscow, 703-276-2772 x21
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Bob DeMarco is the Founder of the Alzheimer's Reading Room and an Alzheimer's caregiver. Bob has written more than 2,101 articles with more than 272,100 links on the Internet. Bob resides in Delray Beach, FL.
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Original content Bob DeMarco, the Alzheimer's Reading Room
