Thinking out loud

I’m making a list of clinical topics to be covered in CurePSP’s next annual scientific conference.  That task made me think carefully about what’s important to clinicians seeking to stay current on PSP and CBD.  So, I thought I’d share that list with you all, for what it’s worth.  Keep in mind that the laboratory research end of things will be a separate list.

  • Clinical spectrum and its pathology
  • Clinical aspects of genetics and epigenetics
  • Fluid biomarkers             
  • PET biomarkers
  • MRI biomarkers
  • Clinical outcome measures (rating scales, wearables, eye movement, gait measures, etc)
  • Gene therapy
  • Tau-directed drug trials
  • Mitochondria-directed drug trials
  • Gait retraining
  • Current best practices in symptomatic care

2 thoughts on “Thinking out loud

  1. Hello Dr. Golbe,

    Do you think p-tau198 is a promising biomarker for 4-repeat tauopathies like PSP?

    Here’s the article:
    https://www.insideprecisionmedicine.com/topics/patient-care/neurological-disorders/tau-biomarker-in-alzheimers-disease-may-aid-earlier-diagnosis/

    And scientific paper (abstract only; unfortunately don’t have access to full text): https://pubs.acs.org/doi/full/10.1021/acschemneuro.2c00342

    If p-tau198 is a new biomarker that we think can identify/diagnose 4 repeat tauopathies, would this be something used in CSF, blood, or imaging (or all)?

    Many thanks

    • Hi. When I saw that paper, I was very excited for the Alzheimer’s community, as this may become good way to differentiate AD from PSP, CBD and Pick’s disease, as well as non-neurological controls. We assume that Parkinson’s, MSA and dementia with Lewy bodies would also give negative results, as they’re not even tauopathies. But this research used autopsied brain tissue, so they’d have to see if it works in blood or spinal fluid from a living person. Unfortunately, the marker wouldn’t work for PSP, except to differentiate it from AD, which isn’t much of an issue in practice. Bottom line is that the test wouldn’t be able to differentiate PSP from the diseases that can mimic it during life, or from people with no neurological disease.

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