1. Your gut is its own nervous system
Most of us grow up thinking we have one nervous system. Professor Ke opened the session by pointing out there are actually three.
The central nervous system — your brain and spinal cord. The peripheral nervous system, the nerves branching out through your body. And the enteric nervous system, a vast network of nerve cells lining your entire digestive tract.
Here's the part that surprised a lot of attendees: everything inside your gut is technically outside your body. That tube running from your mouth to the other end is separated from your bloodstream, organs, and nervous system by a single layer of cells — the gut wall, or epithelial barrier.
That wall, as Professor Ke explained, is the gatekeeper. It decides what gets absorbed into your body and what doesn't. Which makes it, quietly, one of the most important structures you've probably never thought much about.
2. When that wall breaks down, the brain pays the price
The gut wall is held together by what researchers call tight junctions. When the gut becomes chronically inflamed through poor diet, toxin exposure, or microbial imbalance, those junctions loosen. Gaps form. And things that were never meant to enter the bloodstream start leaking through.
This is where a protein called alpha-synuclein enters the picture.
Alpha-synuclein proteins are naturally occurring and play an important role in nerve signalling. But under conditions of inflammation and oxidative stress, they can misfold and clump together. Research cited in the session, including the foundational work of Heiko Braak, published in 2003, has proposed that these aggregates may travel from the gut via the Vagus nerve, cross the blood–brain barrier, and trigger neuroinflammation in the brain.
When that happens, the brain's own immune cells — called microglia — mount a response. The problem, as Professor Ke described it, is when that response can't be switched off. Chronic neuroinflammation, not the initial immune response, is where the damage is done.
This remains an active and evolving area of research. But it's one of the most discussed and scrutinised models in Parkinson's science right now and for good reason.
3. Not all Parkinson's starts in the same place
Building on Braak's work, researchers, most notably Per Borghammer and his team at Aarhus University in Denmark, have proposed a distinction between two subtypes of Parkinson's that the webinar explored in some depth.
Body-first Parkinson's is thought to originate in the enteric nervous system before spreading upward to the brain. In the research literature, this subtype has been associated with early symptoms like constipation and REM sleep behaviour disorder, often appearing a decade or more before motor symptoms and a formal diagnosis.
Brain-first Parkinson's is proposed to begin in the olfactory bulb, just behind the nose, and spread downward toward the gut. Sleep disturbance is notably less prevalent in this group.
Of every 10 people with Parkinson's, roughly one carries a known genetic marker like the LRRK2 gene. The subtype framework applies to the remaining majority — though as the panel was clear to note, this research is ongoing, and the picture continues to develop.
4. Light therapy and the gut: What we're investigating
In collaboration with University of Leeds, we're funding in vitro research to explore whether near-infrared photobiomodulation has a meaningful effect on gut barrier function and the microbiome. Postgraduate Researcher, Niamh Corry who was on the webinar panel, walked us through the two models she's using to run two parallel experiments at Leeds to investigate this.
The first uses CACO-2 cells, a well-established gut barrier model derived from human colon cells, inflamed with LPS, a bacterial component associated with gut dysbiosis. After treating with SYMBYX near-infrared LEDs, Niamh measures changes in inflammatory markers, permeability, and ATP — the energy currency of the mitochondria. The thinking, as she explained it, is that the light may be acting like a battery charger for the cells, stimulating energy output and potentially kickstarting repair.
The second uses something called the MiGut — a miniaturised colon model at the University of Leeds that circulates real faecal samples through three vessels representing different sections of the human colon. Before and after light treatment, changes in the microbiome and metabolites are measured.
This is early-stage, in vitro study science. No clinical claims are being made based on this work. What it will do is start to explore the mechanism of action and help identify the most promising biomarkers to carry forward into the Newcastle University clinical study — 90 participants, 20 weeks of photobiomodulation versus placebo, with blood and faecal samples taken at baseline, six months, and one year.
