Treating CNS disorders by targeting the cellular damage response mechanism​​s

Targeting Key Cellular Response Mechanisms to Fight Neurodegenerative Diseases

Neurodegenerative diseases like Alzheimer’s disease, Parkinson’s disease, dementia with Lewy bodies, age-related macular degeneration and Huntington’s disease involve different regions of the central nervous system yet they share key defects in cellular pathways. By selectively modulating a central cellular damage response pathway, Cognition’s drug candidates stop the toxic effects of age-related damage on brains cells that lead to neurodegeneration. By facilitating the normal function of this pathway, neurons in the brain and eye may function normally and avoid the effects of neurodegeneration.

Areas of Focus

Alzheimer's Disease

Alzheimer’s diseases and other neurodegenerative disorders are characterized by an age-related build-up of toxic proteins in the brain, which bind to receptors and disrupt key cellular processes. Cognition Therapeutics’ lead candidate, CT1812, is designed to displace toxic protein oligomers on neurons and allow the damage response mechanisms to return the cell to normal function.


A number of eye diseases, including dry AMD and geographic atrophy (GA), a more advanced form of the disease, are characterized by oxidative stress and an age-related buildup of toxic proteins that cause damage to retinal cells. CT1812 may remove these toxic proteins and restore downstream processes.

Other Neurological Disorders

The age-related buildup of stressors such as oligomeric forms of proteins (Aβ, α-synuclein, huntingtin), reactive oxygen species and inflammatory agents drive many neurodegenerative diseases. We hypothesize that our our candidates have disease-modifying effects on a number of neurodegenerative and neuro-ophthalmic conditions.

Meet the Leadership Team​

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

Cognition’s Unique Approach​

Cognition’s biological discovery platform, through which CT1812 was identified, is based on unbiased phenotypic screens in the target cell population of mature primary neurons.