CHARLOTTESVILLE, Va. — A new brain sensing tool developed by scientists at the University of Virginia School of Medicine is allowing researchers to observe inter-brain communications in great detail for the first time ever. Consequently, this new technology is providing answers to Alzheimer’s questions that have puzzled scientists and doctors for decades.
Study authors say their new sensor is offering an explanation as to why so many current Alzheimer’s drugs only offer patients limited effectiveness. It’s also giving insight as to why patients usually regress significantly if they stop taking such drugs.
Besides dementia, the research team believes this method will eventually help modern medicine better understand many areas such as depression, autism, sleep disorders, psychiatric conditions, and any number of other neurological diseases. Of course, with greater understanding of the human brain almost assuredly comes new treatment ideas.
“We can now ‘see’ how brain cells communicate in sharp detail in both the healthy and diseased brains,” says lead researcher J. Julius Zhu, PhD, of UVA’s Department of Pharmacology, in a university release.
Using the new device, scientists can observe brain transmissions at both the microscopic and nanoscopic level. Besides offering a biological “sensor,” the new tech also includes two other varieties of “cutting-edge imaging.”
Notably, the device can quantify “neuromodulatory” transmissions. This is important because such transmissions appear across a broad spectrum of brain issues like addiction, sleep disorders, eating disorders, and epilepsy.
What are neuromodulatory transmissions?
These types of transmissions are slower and involve numerous neurons in large regions, as opposed to much faster neuron-to-neuron transmissions.
Interestingly, the new device reveals a “surprising degree of fine control and precision” among neuromodulatory transmissions. According to study authors, this may explain why a popular variety of Alzheimer’s medication, acetylcholinesterase inhibitors, only offer limited relief. These drugs tend to inhibit neuromodulatory communications.
The research team also identified some possible changes in the brain that may be sparked by long-term use of acetylcholinesterase inhibitors. This discovery may explain why many patients regress after ceasing use of these drugs.
“The new method points out Alzheimer’s defects in the unprecedented spatial and temporal resolution, defining the precise targets for medicine,” Zhu concludes.
The study is published in Molecular Psychiatry.