This week on the Evolution of Medicine podcast, and last week in the TruNeura Mastermind, we welcomed Nikki Schultek. I came away from those conversations thinking about a question that has been at the heart of my work for years:
How do we organize practitioners so that we can learn faster together?
Nikki is a co-founder of the Alzheimer’s Pathobiome Initiative, which brings researchers from different institutions and disciplines together to investigate the role of microbes in Alzheimer’s and other brain diseases. Some are studying herpesviruses. Others are investigating bacteria such as Chlamydia pneumoniae, or the possible involvement of other organisms. Her work creates a place for those researchers to compare findings and develop better ways of investigating a complicated question.
That matters because the pathobiome hypothesis asks us to consider more than a single organism. It asks how communities of microbes, and their interactions with the person carrying them, might contribute to disease. If different combinations matter in different people, we need a way to make sense of that variation.
Watch my conversation with Nikki Schultek about the Alzheimer’s Pathobiome Initiative and what this emerging research could mean for brain medicine.
As I listened to Nikki, I kept coming back to the clinical opportunity. Alongside the researchers investigating these mechanisms, we have practitioners seeing people with cognitive decline every day. How can we help them identify potential contributors, make better decisions, and record what happens in a way that other clinicians can learn from?
To me, that is one of the most promising ways to move this work forward. It is also a big part of what we are building at TruNeura.
We now have 70 clinics in the community. These practitioners bring different backgrounds and different experiences to the same challenge. Some have worked with cognitive decline for years. Others are starting to take on these cases and discovering how much there is to learn from colleagues who have already been doing the work.
You could see that in Dr. Burke’s Ask Me Anything this week. Many of the questions came directly out of Nikki’s session the week before. Practitioners discussed screening tests, lab interpretation, and treatment strategies. It was another example of the ongoing clinical learning discussed in The 20 Years Before Diagnosis.
Dr. Burke’s background in environmental medicine is particularly relevant here. Her approach to cognitive decline developed through looking at the wider picture of a person’s health, including exposures that might otherwise go unexplored. Precision brain medicine has grown as practitioners from functional medicine, environmental medicine, and other disciplines have brought their experience into the same conversation.
When clinicians begin evaluating patients more broadly, some are surprised by findings that prompt further investigation of infections, tick-borne illness, or mold exposure. Those observations deserve attention. They also require careful interpretation: evidence of past exposure is not the same as an active infection, and a positive test does not establish what is driving someone’s cognitive decline. Mycotoxins are toxins produced by fungi, rather than microbes themselves, so the environmental questions overlap with the pathobiome discussion without being identical to it.
The opportunity is to get better at making those distinctions together. Which tests are appropriate for this patient’s history? What does a result actually tell us? Does it change the treatment plan? And, over time, does addressing a well-supported finding make a measurable difference?
This is where organized clinical data becomes so valuable. Our decision support tool helps practitioners organize findings and consider next steps. When clinicians also document what they do and track outcomes consistently, we create the possibility of learning across cases. As the community grows from hundreds of patients toward thousands, the quality and consistency of that information will matter as much as the volume.
We have shared cases on this Substack in which patients improved during care that included addressing mold exposure. Those experiences are part of why I am so interested in this work. They also raise questions worth investigating properly. What else changed during treatment? How was improvement measured? Did it last? Were there similar patients who did not improve?
If we only share our best stories, we miss much of the learning. We need to understand the patients who stay the same, the ones who get worse, and the treatments that cause problems as well as the cases that encourage us. That means recording a baseline, following cognition and daily function over time, and documenting treatments and other changes carefully enough that the results can be interpreted.
The research from Rudy Tanzi and his colleagues gives this discussion another dimension. Their 2016 study of amyloid-beta’s antimicrobial activity found protective effects against infection in experimental models. A subsequent 2018 study examining herpes viruses explored how amyloid-beta could bind and entrap viruses, with infection accelerating amyloid deposition in those models.
That raises a fascinating possibility: some of the amyloid accumulation we associate with Alzheimer’s may begin as part of a protective response. It does not mean amyloid is harmless, or that infection explains every case. It also does not establish that elevated p-tau is protective; that is a separate question. But it gives us a reason to ask what might be provoking the response, alongside studying the damage that follows.
If that hypothesis proves relevant in a subset of patients, we need to understand how to identify them and whether treating the underlying contributor changes their trajectory. A community of clinicians collecting comparable information could help identify the patterns most worth investigating.
Clinical observations alone will not settle those questions. People receiving multimodal care may change their sleep, diet, medications, and activity at the same time as they address an infection or exposure. We need researchers and controlled studies to help separate those effects. But well-documented clinical experience can give researchers better questions to test, while research gives clinicians better questions to ask of the patient in front of them.
That relationship is what excites me. Nikki is bringing researchers together across disciplines. Through TruNeura, we are bringing clinicians together who want to understand the complexity of cognitive decline and become more effective at caring for the people experiencing it. There is an enormous opportunity for those efforts to inform each other.
For years, I have argued that community is essential to the evolution of medicine. Here, that becomes very practical. A practitioner encounters something unfamiliar, brings it to the group, learns from a colleague, and follows the patient over time. With appropriate consent, privacy protections, and a consistent way of recording outcomes, those experiences can contribute to a much larger body of learning.
If you want your patient cases to contribute to that understanding, tracking outcomes has to become part of the work. Your clinical experience becomes more useful to others when they can understand what you found, why you acted, and what happened afterward.
We would love for you to be part of that community. If you are a clinician who wants to develop your skills in precision brain medicine, learn alongside colleagues, and help us ask better questions about what drives cognitive decline, book a TruNeura demo.
This feels like the journey of a lifetime. I am grateful that we get to bring practitioners together to play a part in it, alongside the researchers working to understand these mechanisms and the patients and families who give the work its urgency.
