A novel approach to synaptic protection and restoration in Alzheimer’s disease

Alzheimer’s Disease: A Societal Tsunami

Alzheimer’s disease is a progressive, uniformly fatal neurodegenerative disorder, affecting more than 5.7 million people in the US alone, a number expected to reach 16 million by 2050. Alzheimer’s disease is the sixth leading cause of death in the US and is the only leading cause of death currently without a means to prevent, cure or slow the disease. Patients suffering in the later stages of Alzheimer’s disease require nearly full-time care, resulting in a significant societal and economic burden, with direct healthcare costs estimated to be in excess of $290 billion annually in 2019. Without the development of new medicines for Alzheimer’s disease, this societal and economic burden is anticipated to quadruple by 2050.

Synaptic Protection and Restoration with Elayta™

Cognition Therapeutics’ lead candidate, Elayta™, is a novel first-in-class, orally available small molecule that in early clinical studies has shown the potential to reduce synaptic damage in Alzheimer’s patients.

Genetic evidence and scientific consensus points to a specific protein, amyloid beta (Aβ), as the underlying cause of Alzheimer’s disease, with the oligomeric form being the most synaptotoxic. Unlike previous attempts to address Aβ, Elayta does not target or directly interact with any form of the protein or its precursors. Rather, Elayta binds to the sigma-2 receptor complex, a key regulator of the oligomer binding site. Elayta’s interaction with sigma-2 results in the displacement of Aβ oligomers from their receptor targets on the synapse.

Cognition is the first company focused solely on stopping the synaptic binding and signaling of soluble Aβ oligomers through the use of small molecule receptor antagonists like Elayta.

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Cognition Therapeutics’ leadership team has deep experience in the development and marketing of novel therapeutics.
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Cognition’s Unique Approach​

Cognition’s proprietary biological discovery platform, through which Elayta was identified, is based on unbiased phenotypic screens in the target cell population of mature primary neurons.