A hallmark of Parkinson’s disease is the buildup of Lewy bodies—misfolded clumps of the protein known as alpha-synuclein. Long before Lewy bodies form, alpha-synuclein can interfere with neurons’ ability to transport proteins and other cargo along their axons to the synapses. When present at high levels, alpha-synuclein binds too tightly to structures inside the axon, creating the cellular equivalent of traffic jams. These disruptions may even help set the stage for the later accumulation of Lewy bodies in the brain.

Now, University at Buffalo researchers have identified a way to reduce these traffic jams and restore flow—by altering how alpha-synuclein interacts with another Parkinson’s-related protein known as leucine-rich repeat kinase 2 (LRRK2).

In a study published last month, the researchers increased levels of specific mutant forms of LRRK2 in fruit fly larvae. They found that one mutation had a downstream effect on alpha-synuclein, limiting its ability to bind to cargo and disrupt axonal transport. The research is published in the journal Frontiers in Molecular Neuroscience.

I still vividly remember the first time we observed neurons responding not to audible sound, but to concentrated, precisely calibrated ultrasonic pulses. On the screen in front of us, calcium signals from brain cells began to rise and fall in little waves. It was less about forcing the brain to adapt and more about listening to the brain and responding subtly.

Understanding how neurons interact and how neurological conditions like Parkinson’s disease affect this communication has been the focus of my study for many years. Calcium, a small ion that functions as a potent messenger inside cells, is at the center of this communication.

Neurons struggle to survive, connect, and operate correctly when calcium transmission is disrupted. Our team began to wonder if we might safely modify this fundamental signaling function without requiring invasive operations or drugs.

A new type of brain implant may have implications for both brain research and future treatments of neurological diseases such as epilepsy. Researchers from DTU, the University of Copenhagen, University College London, and other institutions have developed a long, needle-thin brain electrode with channels—a so-called microfluidic Axialtrode (mAxialtrode), named for its ability to distribute functional interfaces along the length of the implant, enabling both neural signal recording and precisely targeted medication delivery across different brain regions. The research results have been published in Advanced Science.

The technology has primarily been developed for basic research into the brain. It can help researchers better understand how signals move across brain layers, for example in epilepsy, memory, or decision-making. In the longer term, the researchers point out that the mAxialtrode may be important for treatment—for example, in targeted drug delivery combined with electrical or light-based stimulation of specific areas of the brain.

Postdoc Kunyang Sui, who led the development of the mAxialtrode concept together with Associate Professor Christos Markos, emphasizes that it has made it possible to combine several functions in a single implant which makes brain research less invasive and more precise.