Tadalafil reduces some plasma neurodegeneration biomarkers in type 2 diabetes patients

This was a post-hoc analysis of a 6-week, single-center randomized controlled trial conducted at Sahlgrenska University Hospital. The study included 15 individuals with type 2 diabetes who were randomized to receive either the PDE-5 inhibitor tadalafil or a placebo. The analysis focused on plasma biomarkers associated with Alzheimer's disease pathology.

Compared to placebo, 6 weeks of tadalafil treatment was associated with reductions in plasma amyloid-β 40, amyloid-β 42, and glial fibrillary acidic protein (GFAP). The amyloid-β 42/40 ratio, phosphorylated tau217 (p-tau217), neurofilament light protein (NfL), and growth/differentiation factor 15 (GDF-15) showed no significant reduction. No effect sizes, absolute numbers, or p-values/confidence intervals for these changes were reported.

Safety and tolerability data were not reported for this post-hoc analysis. Key limitations include its nature as a post-hoc analysis, a very small sample size of 15 participants, the use of biomarker outcomes only, and a short follow-up period of 6 weeks. The clinical significance of these plasma biomarker changes is unknown.

This analysis generates a hypothesis that tadalafil may influence certain plasma biomarkers of neurodegeneration in people with type 2 diabetes. The findings are preliminary and do not demonstrate clinical efficacy for Alzheimer's disease. Further research is needed to confirm these observations and understand their potential relevance.