Cognition presents proteomic data on CT1812 in altering underlying AD

Cognition Therapeutics presented results of a meta-analysis from the first cohort, SHINE-A, of 24 participants in the Phase 2 SHINE and the complete dataset from the Phase 1b SPARC studies in adults with mild-to-moderate Alzheimer’s disease who were treated with either CT1812 or placebo. Treatment with CT1812 was associated with statistically significant and directionally positive effects on key proteins and corresponding Alzheimer’s disease pathways. These included: Synapse health, Neuroinflammation and amyloid-ss, Ass, biology. These robust biomarker findings point towards a prominent effect of CT1812 in altering underlying disease processes active in Alzheimer’s disease progression. Of particular note, CT1812 had a significant impact on CSF levels of clusterin, CLU , which has been identified as a genetic risk factor for Alzheimer’s disease and is a mediator of amyloid toxicity. In addition, CT1812 treatment resulted in a significant shift in levels of prion protein , a major constituent of the Ass oligomer receptor complex and the receptor component to which Ass oligomers bind. The biomarker findings summarized in the poster further strengthen our understanding of CT1812’s effect on Ass oligomer-driven neurotoxicity. "Combining the proteomic data from two trials that enrolled participants with mild-to-moderate disease and who were similarly treated with CT1812 allowed for a statistically robust analysis of cerebrospinal fluid samples," explained Mary Hamby, Ph.D., VP of research at Cognition Therapeutics. "We and our collaborators at Emory University were particularly interested in the change in levels of PRPN. This is consistent with other clinical and preclinical data, showing that modulation of the sigma-2 receptor results in displacement of oligomers from their target receptor on neurons." A comparative analysis of the overlap between the SHINE and SPARC datasets revealed 28 biomarkers that were significantly altered as a result of treatment with CT1812, 11 of which are priority biomarkers of Alzheimer’s biology. Subsequent unbiased pathway analysis mapped these biomarkers to specific brain networks and biological pathways, indicating a clear role for these proteins in synaptic function, neuroinflammation and Ass biology.