NYC Healthcare News



On-going phase II trial of octagam in AD to be discussed at ICAD 2010

August 26, 2015

Previous studies had found that blocking the AMPA receptor could alleviate the misfiring caused by amyloid plaques in the brain. But the AMPA receptor, which responds to glutamate, is important to learning and memory, so blocking it could also do harm, the researchers said.

"Glutamate is such a ubiquitous neurotransmitter throughout the brain, you can't simply go in and block its actions because if you do, you can just start rounding up the side effects," Cox said.

"Once you block the AMPA receptor you're basically dampening widespread neuronal excitability throughout the whole brain," Cox said. "Now we have something a bit more specific to latch onto: the beta-2 adrenergic receptor."

This receptor offers an attractive alternative target because, the researchers found, amyloid-beta binds to a different part of the receptor than that normally engaged by neurotransmitters and hormones. This means it may be possible to stop amyloid-beta from binding to it without hindering the other functions of the beta-2 adrenergic receptor.

Previous studies have shown that Alzheimer's patients who also take beta-blockers tend to see a slower decline in their mental function. These drugs are meant to treat hypertension and other conditions by targeting beta-adrenergic receptors, including beta-2. This finding provides further support to the idea that the beta-2 adrenergic receptor is a key to the ill effects of Alzheimer's disease.

Xiang and Cox stress that the beta-2 adrenergic receptor is almost certainly not the only important player in the damage that occurs in an Alzheimer's-afflicted brain. But they see it as a promising new potential target for future drug research.

Source: University of Illinois at Urbana-Champaign