Common brain signalling in Parkinson’s and Alzheimer’s could unlock new treatments

A study has identified a shared brain-signalling mechanism in Parkinson’s and Alzheimer’s diseases, revealing a possible common cause behind their neurodegenerative symptoms.

Researchers discovered a molecular pathway that disrupts communication between brain cells in both conditions, improving understanding of how their symptoms are produced.

The disruption occurs at synapses — junctions between nerve cells where electrical signals are transmitted.

The team investigated how disease-related protein buildup interferes with communication between brain cells and found a pathway that impairs synaptic vesicle recycling — the process by which small sacs called vesicles store and release neurotransmitters, the brain’s chemical messengers.

Scientists from the Okinawa Institute of Science and Technology (OIST) identified how this process breaks down in both diseases.

First author Dr Dimitar Dimitrov of OIST’s Synapse Biology Unit said: “Synapses are communication hubs in the brain involved in different neuronal circuits controlling different functions.

“Therefore, protein accumulation in synapses of one neuronal circuit may impact memory, while in another it may impair motor control.

“This helps to explain how a shared mechanism of synaptic dysfunction can lead to the distinct symptoms of both Alzheimer’s and Parkinson’s diseases.”

Brain cells rely on neurotransmitters to send signals between one another.

These chemical messengers are stored in vesicles that fuse with cell membranes to release their contents into the synaptic cleft — the gap between cells — before being retrieved, refilled, and reused to sustain normal signalling.

The researchers identified a molecular cascade that interrupts this retrieval process, disrupting normal brain function.

“When disease-related proteins accumulate in brain cells, they cause over-production of protein filaments called microtubules, which are normally essential for cell structure and function,” explained Dr Dimitrov.

“When over-produced, these microtubules trap a protein called dynamin, which is responsible for the retrieval of emptied vesicles from cell membranes, playing a crucial role in vesicle recycling.

“With less dynamin available, vesicle retrieval and recycling slow, thereby interrupting signalling and communication between brain cells.”

By revealing this shared mechanism, the findings highlight several potential drug discovery targets.

OIST professor emeritus Tomoyuki Takahashi said:”Preventing disease-related protein accumulation, stopping microtubule over-production, or disrupting microtubule-dynamin bindings — our new mechanism identifies three potential therapeutic targets common across Parkinson’s and Alzheimer’s disease.

“”Research like this is important to develop new treatments that ease the impact of these diseases on patients, families, and society as a whole.”