What’s New in Alzheimer’s Disease Clinical Trials?

Judy Heidebrink, M.D., M.S., Richard D. and Katherine M. O'Connor Research Professor of Neurology at University of Michigan Medical School, and Director, Cognitive Disorders Clinic, University of Michigan - Health

[@Chzmelt]

Great segment, although would have loved to hear about Cassava’s Simufilam. It is set up to be the golden standard of care for Alzheimer’s patients in a few years providing phase 3 trials go well.

[@kci2233]

Cassava sciences’ Simufilam drug is probably the most promising AD drug to date for mild AD Patients. Open label data shows that mild AD patients improve in cognition. Why didn’t you talk about this drug? Please update the video

[@smnb8573]

what about Simufilam?

[@alanrussell4389]

I'm currently in the qualification stages for the AHEAD 3-45 study here in PA. This video has given me a great overview of how to look at all the various studies can be compared and contrasted. Thanks for a great presentation. (FYI - I'm an MSU grad from over 50 years ago.)

[@rudylampas2279]

Let's praise God and the people involved in the research, thanks for all your efforts 🙏

[@Alsatiagent]

Did anyone notice if Lion's Mane was mentioned here? I am unable to view the full session.

[@douglaswatt1582]

Not enough critical engagement with the evidence against the notion that protein aggregates are the only real driver of neurodegeneration. Lots of evidence that this is an oversimplification that has been uncritically accepted. Worth noting that programmed cell death which is presumed to be a principal neurodegenerative mechanism is driven by three factors, mitochondrial dysfunction, endoplasmic reticulum stress response, and the so-called death receptor. And while aggregated protein no doubt has a major role in the endoplasmic reticulum stress response, other recruiters of programmed cell death do not have neat simple relationships to protein aggregation. All of those are in turn modulated by and indeed enter into two-way relationships with inflammation. Inflammation even aside from its interactions with programmed cell death also drives synapse and cell loss via activation of the complement system, and via the destructive effects of pro-inflammatory cytokines. And contrary to the standard party line that inflammation is simply a reaction to aggregated protein, recent evidence shows conclusively the tauopathy is actually spread via pro-inflammatory changes in microglial cells, perhaps mediated by the transcription Factor NFk B.