Cognition Therapeutics KOL Event Provided Platform for Valuable Discussion of Current Therapeutic Options and Need for Additional Options to Treat Alzheimer’s Disease

PURCHASE, N.Y., April 22, 2024 (GLOBE NEWSWIRE) -- Cognition Therapeutics, Inc., (the “Company” or “Cognition”) (NASDAQ: CGTX), a clinical stage company developing drugs that treat neurodegenerative disorders, provided a recap of the virtual KOL event hosted on April 12, 2024 featuring Martin J. Sadowski, MD, PhD, DSci of the NYU School of Medicine; Anton Porsteinsson, MD of the University of Rochester Alzheimer's Disease Care, Research and Education Program; and Everard (Jort) Vijverberg, MD, PhD of the Alzheimer Center Amsterdam and Neuroscience Amsterdam.

“The KOL roundtable we conducted featured a panel of Alzheimer’s disease expert clinicians and researchers who highlighted the need to find Alzheimer’s disease treatments that are less burdensome for patients and their care partners,” said Lisa Ricciardi, Cognition’s president and CEO. “They reinforced the importance of removing toxic oligomers as an important step in slowing the progress of Alzheimer’s disease and highlighted the need for new treatment modalities to use alone or in conjunction with the currently approved treatments.”

The KOLs shared their perspectives on the currently approved immunotherapies for early Alzheimer’s disease, including perception of their effectiveness in targeting plaque, impact of amyloid related imaging abnormalities (ARIA) on commercial uptake, and the clinical meaningfulness of the reported changes in disease progression. Dr. Sadowski explained that “removal of the plaques in patients with Alzheimer’s disease ... changes things a lot, but it's not enough.” He continued, suggesting that improved outcomes from beta amyloid (Aβ) antibodies may be achievable, but “we would need to have some other agents that can be given in tandem with beta amyloid therapies or as a sequel to beta amyloid therapies.”

Dr. Porsteinsson agreed, noting “a pretty remarkable clearance of Aβ plaques with [the currently approved therapies].” However, he explained, "even if the humanized monoclonal antibodies targeting beta amyloid plaques become well established, they won't meet the need of all patients with early symptomatic Alzheimer's disease.”

In addition to the direct engagement of Aβ plaque, other processes that were discussed in the KOL event were neurodegeneration, neuroinflammation and neuro-regeneration, which are biological processes associated with Alzheimer’s disease progression. In order to improve upon the outcomes observed with monoclonal antibody monotherapy, options may include drugs that address these secondary biological processes, which are driven by toxic aggregated Aβ oligomers, oxidative stress and inflammation. Dr. Porsteinsson pointed to one such candidate, Cognition’s CT1812, which he observed displaces “oligomers or prevents them from binding to neurons, clears them to the cerebrospinal fluid and through that prevents the synaptic toxicity and ... the impact on neuronal function. In fact, in preclinical models of Alzheimer's disease, it was able to restore cognitive deficits.”