This is a promising experimental protocol that may lead to exact knowledge of the underlying issues and perhaps from there to actual treatment. I have never thought the disease was anything like intractable like our old enemy cancer. It really begged recognizing a specific failure similar to insulin failure in diabetes. This protocol allows us to ask questions and easily test interventions.
A pathway exists that is not yet understood. I hope progress is now swift. This disease is not just personally tragic; it imposes a huge healthcare burden that needs to be ameliorated. We want the elderly to retain personal independence to the end. This also suggests that progress may be possible on comparable ailments for the same reasons.
A new discovery by University of Central Florida researchers has revealed a previously unknown mechanism that may drive the early brain function deterioration of Alzheimer's victims, thus opening a new exploratory path in the quest for an Alzheimer's cure
The research was published in the science and medicine journal PLoS ONE, also demonstrates how the unique application of an existing cell research technique could accelerate the discovery of treatments to exploit the new findings.
Most Alzheimer's studies have focused on brain cells already damaged by amyloid-beta or the effects of high concentration of amyloid-beta. The University of Central Florida team, led by James Hickman, head of the UCF NanoScience Technology Center's Hybrid Systems Laboratory, instead explored impacts of very low amyloid-beta concentrations on healthy cells in an effort to mimic the earlier stages of Alzheimer's. The results were shocking.
The UCF team found that over time, though there are no outward signs of damage, exposure to moderate amyloid-beta concentrations somehow prevents electrical signals from traveling normally through the cells. Because the effect is seen in otherwise healthy cells, Hickman believes the team may have uncovered a critical process in the progression of Alzheimer's that could occur before a person shows any known signs of brain impairment.
"What we're claiming is that before you have any behavioral clues, these electrical transmission problems may be occurring," he says.
If this proves true, then the team has opened a promising potential path to an Alzheimer's treatment that could block the onset of the mild cognitive impairment associated with early Alzheimer's. In contrast, all currently available treatments manage symptoms of Alzheimer's after they first appear -- when it is likely too late for prevention.
Kucku Varghese, a former graduate student in the Hickman lab now at the University of Florida, first demonstrated amyloid-beta's effects at low concentrations on healthy cells using a common cell research method that is laborious and unsuitable for long-term experiments. But the Hickman team quickly moved to more advanced experiments using microelectrode arrays (MEA) to study the new finding. MEA studies use cultures of neurons on plates embedded with tiny electrodes that can send and measure electrical signals through nearby cells without damaging them, allowing extended experimentation.
Hickman hopes to use MEAs and other tools to pinpoint the physiological and chemical changes within the brain cells that cause the loss of signal generation in healthy cells. Mechanisms responsible for the changes could offer potential targets for drugs, which pharmaceutical companies could search for using the MEA techniques demonstrated, and the mechanisms might provide a measurable target for early diagnosis of Alzheimer's.
"We're trying to find a marker that will lead to detection and treatment while slowing down Alzheimer's progression and can really make a difference by delaying or even preventing onset of the disease," says Hickman.