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.
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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.
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In the early stages of Alzheimer’s disease, patients typically suffer a major loss of the brain connections necessary for memory and information processing. Now, a combination of nutrients that was developed at MIT has shown the potential to improve memory in Alzheimer’s patients by stimulating growth of new brain connections.
In a clinical trial of 225 Alzheimer’s patients, researchers found that a cocktail of three naturally occurring nutrients believed to promote growth of those connections, known as synapses, plus other ingredients (B vitamins, phosopholipids and antioxidants), improved verbal memory in patients with mild Alzheimer’s.
2. But some are disagreeing with the MIT nutrient study –
Anti-Alzheimer’s ‘Cocktail’ Meets With Disdain as Alzheimer’s Experts Worry New Study May Mislead Consumers
Older mice with Alzheimer’s saw deposits in the brain of beta-amyloid, a protein fragment that accumulates in the brain of Alzheimer’s sufferers to form the disease’s signature plaques, erased. They apparently remembered things a bit better too.
Young adult mice with no apparent signs of memory impairment were protected against Alzheimer’s disease after several months of exposure to the mobile phone waves, the study showed.
The memory benefits of phone exposure took months to show up, suggesting that a similar effect in humans would take years.
The researchers conclude that electro-magnetic field exposure could be an effective, non-invasive and drug-free way to prevent and treat Alzheimer’s disease in humans.
Chuanhai Cao, another author of the study, said: “Since production and aggregation of beta-amyloid occurs in traumatic brain injury, particularly in soldiers during war, the therapeutic impact of our findings may extend beyond Alzheimer’s disease.”
A new imaging technique that measures the random motion of water within the brain may prove useful for detecting early signs of Alzheimer’s disease.
The technique, known as diffusion tensor imaging (DTI) or diffusion MRI, is used to assess changes in the white matter regions of the brain.
But it is increasingly clear that DTI can also be used to identify very small structural changes in the gray matter of the brain, which is critical for learning and memory, researcher Giovanni A. Carlesimo, MD, PhD, of Italy’s Tor Vergata University tells WebMD.
In a study published in the Jan. 19 issue of Neurology, Carlesimo and colleagues found that DTI scanning predicted declines in memory performance with more accuracy than traditional MRI.
“This type of brain scan appears to be a better way to measure how healthy the brain is in people who are experiencing memory loss,” Carlesimo says in a news release. “This might help doctors when trying to differentiate between normal aging and diseases like Alzheimer’s.”