What if someone comes to you worried about memory loss, but their memory is actually working relatively well?
That was one of the most compelling clinical lessons from this month’s TruNeura Mastermind, featuring Garland Glenn, DC, PhD and Michelle Eads, MD.
The conversation explored what happens when clinicians look beyond the obvious symptoms of cognitive decline and start asking a different question: What is actually preventing the brain from functioning well?
Look beyond the symptom
Dr. Glenn shared a case that illustrated this beautifully.
A 72-year-old woman came to him convinced she was developing a memory problem. Her CNS Vital Signs testing told a different story. Her memory scores were relatively strong, while other areas, including processing speed and cognitive flexibility, raised more questions.
Her volumetric MRI added another piece to the puzzle.
Rather than showing significant problems in the areas typically associated with memory, the imaging pointed toward dysfunction involving the thalamus and deeper brain structures.
Dr. Glenn described it as a switching and encoding problem.
She could remember information from her past. The challenge was getting new information routed and encoded effectively enough to become a memory.
That distinction matters because it changes what you do next.
Instead of simply treating “memory,” Dr. Glenn uses the assessment data to identify which functional pathways may need support, then builds targeted cognitive exercises around those findings.
The brain can learn new pathways
This is where functional neurology adds another layer to root-cause cognitive care.
Dr. Glenn’s approach combines precision medicine with assessments such as CNS Vital Signs, volumetric MRI and eye movement testing to identify areas of dysfunction. From there, patients can work on targeted drills designed to repeatedly engage specific pathways.
His analogy was simple: if you lose the ability to write with your dominant hand, you can learn to write with the other one.
The goal isn’t simply to understand what isn’t working. It’s to give the nervous system opportunities to build new pathways.
But there’s an important caveat: more isn’t always better.
Dr. Glenn emphasized that a brain struggling with energy production cannot necessarily tolerate long cognitive training sessions. Short, frequent sessions may be more appropriate than pushing through a lengthy workout.
That same principle came up throughout the conversation: cognitive care has to be individualized.
Compliance is part of the clinical picture
Both clinicians also spoke candidly about one of the hardest parts of cognitive care: getting patients to consistently implement what they know they need to do.
Dr. Eads has spent the past decade refining a largely telemedicine-based practice focused exclusively on cognitive health. Her practice has evolved from highly labor-intensive patient education to a more streamlined model that uses education platforms, wearables and simplified resources to help patients stay engaged.
Dr. Glenn has built a larger team around his practice, including a nutritionist, RN and staff dedicated to cognitive exercises.
One of his biggest lessons?
Touch points matter.
Frequent follow-ups, nutrition support, cognitive drills and tools like continuous glucose monitors can create ongoing feedback instead of leaving patients to navigate a complex protocol on their own.
The goal is not simply to give someone a plan. It’s to build a system that helps them actually follow it.
CGM can reveal a different story
Continuous glucose monitoring came up repeatedly throughout the discussion, particularly around sleep.
Dr. Glenn shared a case where a patient was waking around 3 a.m. He initially suspected reactive hypoglycemia. Her CGM showed otherwise.
Her glucose remained relatively stable, followed by a sharp rise.
That observation shifted the clinical thinking toward a different possibility: a stress response and cortisol surge rather than a blood sugar crash.
The discussion opened into a broader conversation about trauma, hypervigilance and disrupted sleep, with several clinicians contributing perspectives on how these patterns can show up in practice.
It was a good reminder that even familiar symptoms can have very different underlying drivers.
Another layer: plasmalogens
Dr. Eads also introduced the group to plasmalogens, a specialized area of cognitive health that she has incorporated into her practice over the past several years.
Plasmalogens are specialized phospholipids found in high concentrations in tissues including the brain. Dr. Eads discussed their role in cellular membranes, oxidative stress, mitochondrial function and neurological health, as well as emerging research into their relationship with cognitive decline.
Her point wasn’t that plasmalogens replace the foundational work of cognitive care.
Rather, they represent another potential layer to investigate as clinicians continue looking for ways to support patients, particularly those with significant symptoms or those focused on prevention.
The bigger takeaway
Perhaps the most important theme from this Mastermind was that cognitive decline cannot be reduced to a single symptom or a single intervention.
Two patients can both say, “I’m having memory problems,” while having very different underlying issues.
One may need deeper investigation into metabolic or inflammatory drivers. Another may need to address sleep, glucose regulation or trauma. Another may have relatively preserved memory but difficulty with processing, switching or encoding.
And another may need to address the brain’s ability to actually use the pathways that remain available.
The more precisely we can understand those differences, the more precisely we can intervene.
That is ultimately what makes this work so exciting: we’re moving beyond asking whether someone is declining and toward asking why, where and what can we do about it?





I really like this way of thinking, it mirrors cardiology so closely: the same symptom or diagnosis can arise from very different biology, and the real clinical work begins when we stop treating the label and start looking for the phenotype.