NeuroSense Therapeutics, a late-clinical-stage biotechnology company developing therapies for severe neurodegenerative diseases, has announced positive biomarker findings from its Phase 2 proof-of-concept RoAD (NST-AD-001) clinical trial evaluating PrimeC in patients with Alzheimer’s disease.

The randomised, double-blind, placebo-controlled study enrolled eight participants, who received either PrimeC or a placebo. Three participants completed the full 12-month follow-up, during which Cerebrospinal Fluid (CSF) and plasma samples were collected at multiple time points for biomarker analysis.

The results showed changes in several biomarkers associated with Alzheimer’s disease, including total tau, phosphorylated tau and the amyloid-beta 42/40 ratio. Researchers also observed changes in biomarkers linked to other neurodegenerative disorders, including alpha-synuclein and TAR DNA-binding protein 43 (TDP-43), proteins commonly associated with Parkinson’s disease, dementia with Lewy bodies and amyotrophic lateral sclerosis (ALS). Additional changes were recorded in biomarkers related to oxidative stress, inflammation and protein homeostasis, all of which are implicated in neurodegeneration.

According to NeuroSense, the findings are consistent with PrimeC’s proposed multi-target mechanism of action and mirror biomarker responses previously observed in the company’s ALS programme, suggesting the therapy may engage shared biological pathways across multiple neurodegenerative diseases.

The biomarker data also builds on previously reported safety results from the RoAD study, in which PrimeC demonstrated a favourable safety and tolerability profile, with no serious adverse events or unexpected safety signals reported during the trial.

Commenting on the findings, Alon Ben-Noon, Co-Founder and Chief Executive Officer of NeuroSense, said the study provides encouraging evidence that the biological mechanisms targeted by PrimeC in ALS may also be relevant in Alzheimer’s disease. He noted that while the study involved a limited number of participants and remains exploratory, the consistency of biomarker signals across different neurodegenerative diseases strengthens confidence in the therapy’s underlying approach and will help guide the design of larger, adequately powered clinical studies.

Prof. Steven E. Arnold, Professor of Neurology at Harvard Medical School and a member of NeuroSense’s Scientific Advisory Board, said Alzheimer’s disease is driven by multiple interacting pathological processes, making single-target therapies less effective. He added that the initial biomarker findings suggest broad effects on protein regulation that align with PrimeC’s proposed mechanism of action. However, he stressed that the preliminary findings require confirmation in larger, well-controlled trials to determine whether the observed biological changes can translate into meaningful clinical benefits for patients with Alzheimer’s disease.