Yet another, and not my last, installment of research reports from Neuro 2023, the PSP and CBD International Research Symposium held a month ago in London. Please note that many of these reports have not yet been peer-reviewed at a journal.

:: A review of speech therapy records compared various devices to improve communication in people with PSP with severe speech deficits.  In 37 patients, the most successful were large print for reading and a stylus or keyguard (photo) for typing.  As the combination of deficits in motor, cognitive and eye movement control progressed, even these methods lost most of their initial utility.  This study demonstrates the need for better devices to assist in communication by those with advanced PSP.  (CML Foy et al, Sussex Community NHS Foundation Trust, North Chailey, East Sussex, UK)

:: As you’re all aware, two similar anti-tau monoclonal antibodies tested a few years ago failed to slow PSP progression.  However, the trials provided valuable data on the course of the disease over a 12-month period for the middle-stage patients with PSP-Richardson’s syndrome whom the trials enrolled.  The most recent such analysis of the trial for AbbVie’s tilavonemab showed that the patients with greatest language deficits were the ones who progressed most quickly over the ensuing year.  The study measured language in a variety of ways, including naming pictures, following written instructions, writing a dictated sentence, and quickly generating words of a specified category. These results could be of use in understanding the mode of disease spread in PSP, in designing future disease-slowing trials and in counseling patients in routine care. (Indira García-Cordero, et al, University of Toronto, Canada)   

:: A study compared the ongoing production (technically called “expression”) of tau molecules in neurons and glial cells in autopsied PSP brain tissue, correlating the results with the presence of tau aggregates, the pathologic hallmark of PSP.  It found continued tau production in cells with existing tau aggregates.  In fact, in oligodendroglia, where the PSP process probably starts, production was greatest in those cells with the most aggregates.  These findings argue against the theory that existing tau aggregates exert their toxic effect by shutting down normal tau production.  Another conclusion is that the abnormal tau in oligodendroglia doesn’t just come from adjacent neurons, but also (or exclusively) from within the oligos themselves. The results have implications for design of new PSP-slowing drugs. (Shelley Forrest et al, Macquarie University, Sydney, Australia; and University of Toronto, Canada)

:: The Pharma company Amylyx has announced details of their upcoming trial of AMX0035, an orally administered combination of sodium phenylbutyrate and taurursodiol.  It has already shown modest success in ALS in slowing symptom progression and in Alzheimer’s disease at the level of spinal fluid chemistry.  The 600-patient trial in PSP is scheduled to start in December 2023 in 200 centers in Europe, Japan and North America.  The benefit will be measured by comparing the placebo and active-drug groups with regard to rate of progression in the PSP Rating Scale over a one-year period.  Amylyx has not yet posted contact information for prospective participants.   (Disclosure, I’m a consultant for Amylyx and one of the 16 authors of this presentation at Neuro 2023.  The lead author is Günter Höglinger, Ludwig Maximilian University, Munich, Germany.)