Despite a massive global research effort, many basics of Alzheimer’s disease onset remain elusive. This has hampered development of treatments effective during the earliest stages of the disease, when prevention is most likely.
But 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, which will be published Friday, Jan. 8, in the peer-reviewed 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.
Researchers have known for years that a substance called amyloid-beta gums up brain cells when it becomes too concentrated, because it forms damaging deposits on the cells known as plaques. These prevent normal electrical signal generation in the cells, eventually killing them. That drives the memory loss and other problems that plague Alzheimer’s sufferers.
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.
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