News From Jarred Younger / Neuroinflammation, Pain, and Fatigue Laboratory at UAB, From Aug 2020

Jarred Younger: 077 - Seeing what I see: brain inflammation


ETA AI summary:
Summary: Brain Inflammation Patterns in ME/CFS Patients (Video Transcript)


0:00 — Introduction: Exploring Brain Inflammation Data​

The speaker begins by describing a Sunday research session in the laboratory. They have been analyzing MRI and PET scans from participants with ME/CFS (Myalgic Encephalomyelitis/Chronic Fatigue Syndrome). The images visualize neuroinflammation by using a tracer, 11FPA-714, which binds to activated microglia. Brighter red areas indicate higher inflammatory activity. By examining these scans, the researcher aims to understand where inflammation occurs in the brain and whether it follows specific patterns.


1:52 — Baseline: Healthy Control Example​

The first scan shown is from a healthy control subject. As expected, there is minimal neuroinflammatory activity, with only faint background signals caused by resting microglia. This example serves as a baseline for comparison with ME/CFS patients.


2:18 — Pattern 1: Localized Bilateral Inflammation​

In the first ME/CFS case, the inflammation appears as distinct, symmetrical hot spots in the amygdala and hippocampus—areas crucial for emotion and memory. Additional activity is seen in the periaqueductal gray (PAG), a region involved in pain modulation and anxiety responses. The researcher speculates that this pattern might be linked to symptoms such as anxiety and widespread musculoskeletal pain, similar to fibromyalgia.


3:35 — Pattern 2: Widespread Brain Inflammation​

The second group of ME/CFS scans shows diffuse inflammation throughout the gray matter, meaning nearly all neuron cell bodies exhibit inflammatory activity. Although this inflammation is less intense than in localized cases, its widespread presence might lead to many mild-to-moderate symptoms across cognitive, sensory, and emotional domains. The overall impact may still be significant due to the cumulative burden of numerous symptoms.


5:00 — Pattern 3: Brainstem and Thalamic Involvement​

The third group shows intense inflammation centered in the thalamus, midbrain, pons, and brainstem. This pattern closely resembles results from an earlier ME/CFS PET study by Dr. Nakatomi (over 10 years ago). Even though the inflammation is localized, the affected regions are essential for nearly all brain functions, potentially leading to widespread symptoms and post-exertional malaise (PEM).


6:06 — Reflections and Next Steps​

The researcher emphasizes that these are preliminary observations, not formal hypotheses. Further analysis—linking imaging data with symptom reports and performing statistical testing—may alter the current groupings before publication. The video aims to reveal the messy, iterative process of scientific discovery, rather than the polished final version found in papers.


7:00 — Conclusion: Evidence Supporting the Inflammation Hypothesis​

The preliminary findings support the hypothesis that ME/CFS involves brain inflammation. The researcher plans to continue analyzing data, finish a separate brain lactate paper, and provide future updates as more insights emerge from this ongoing investigation.


 
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He seemed to say "[11F]DPA-714" but based on my limited knowledge (Fluorine-18 and Carbon-11 are radio-isotopes, Fluorine-11 is not?) I'm guessing he meant [18F]DPA-714 or [11C]-PBR28? Or can you mix and match the radio-isotope and the TPSO connecting-part and get [11C]DPA-714?
 
Jarred Younger: 077 - Seeing what I see: brain inflammation


ETA AI summary:

If what Younger presents in this video holds up then this is absolutely huge. But I guess we have to wait for the paper to make any real judgement. He says he's working on a brain lactate one first so might be a while.

I've been quite skeptical about some of his recent statements, but I'm interested to see how this plays out.
 
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