Alzheimer’s Disease

Age-related Buildup of Toxic Proteins

Alzheimer’s disease is believed to be caused, in part, by the age-related buildup of proteins including amyloid beta (Aβ).

Under normal conditions, these proteins are removed from the brain before they accumulate and aggregate into more toxic forms, called oligomers. When this function is disrupted, the formation of toxic oligomers can lead to neurodegenerative disorders such as Alzheimer’s disease. These toxic oligomers bind to synapses and cause a cascade of damage resulting eventually in the loss of neurons and cognitive dysfunction.

A Unique Approach to Treating Alzheimer’s Disease

In Alzheimer’s disease, evidence suggests that Aβ oligomers are toxic to synapses in the brain. When oligomers bind to neurons, they damage synapses, which are the points of communication between neurons. Over time, the recurring damage to synapses leads to loss of neurons and cognitive decline.

Many efforts in drug development for Alzheimer’s disease have focused on removing Aβ plaques that have accumulated from the brain. We believe that preventing Aβ oligomers from binding to the synapse, where their toxic effects initiate damage, is a promising neuroprotective approach acting earlier in the amyloid cascade.

Cognition Therapeutics isdeveloping CT1812, an oral, brain-penetrant, small molecule therapeutic, which has been shown to protect neurons and synapses by preventing the binding of toxic oligomers. We believe that the results of our clinical trials demonstrate that CT1812 acts as a neuroprotective agent both by shielding neurons and synapses from oligomer binding and by preventing oligomers from attaching to synapses in the first place. CT1812 may help mitigate the neurotoxic effects, slowing cognitive decline and progression of Alzheimer’s disease. 

CT1812: A Team Player

CT1812 has the potential to work in synergy with recently approved monoclonal antibody treatments. Due to its unique mechanism of action and favorable safety profile, CT1812 has the potential to complement treatments that remove plaques or impact other disease mechanisms by playing the vital role of synaptic protector.

Watch our mechanism of action video to learn more. »

SEQUEL COG0202 study:
  • Assessed disease-modification as a function of synapse function as measured by qualitative EEG.
  • Topline results showed improvements in global measures of brain activity.
  • For more information, please visit clinicatrials.gov and reference NCT04735536.
  • Background information on qEEG and a summary of topline results maybe found here.
SNAP COG0104 study:
  • Assessed target engagement vis-a-vis displacement of Aβ oligomers.
  • For more information, please visit clinicaltrials.gov and reference NCT03522129.
SPARC COG0105 study:
  • Assessed disease-modification as a measure of synapse density with PET imaging.
  • For more information, please visit clinicaltrials.gov and reference NCT03493282.
Phase 1b/2a COG0102 study:
  • CT1812 was generally safe and tolerated in patients with mild-to-moderate Alzheimer’s disease.
  • All adverse events were mild or moderate; there were no serious adverse events.
  • CT1812 achieved CSF concentrations greater than 80 percent estimated brain receptor occupancy, a level previously demonstrated in preclinical studies to be the minimum efficacious dose.
  • Protein biomarkers associated with Alzheimer’s disease changed differentially in CT1812-treated vs. placebo patients.
  • For more information, please visit clinicaltrials.gov and reference NCT02907567.
SHINE COG0201 study:
  • Enrollment complete: 153 adults with mild-to-moderate Alzheimer’s disease have been randomized to receive one of two doses of CT1812 or placebo.
  • Top-line results from Part A (n=24) showed a slowing of cognitive decline in favor of CT1812.
  • Treatment-emergent adverse events were well balanced across all treatment groups in Part A.
  • For more information, please visit clinicatrials.gov and reference NCT03507790.
START COG0203 study:
  • Phase 2 study in early Alzheimer’s disease in collaboration with the Alzheimer’s Clinical Trials Consortium (ACTC).
  • Target enrollment: 540
  • Supported by a $81 million grant from the National Institute on Aging (NIA) of the National Institutes of Health (NIH).
  • For more information, please visit start-study.org or clinicatrials.gov and reference NCT05531656.
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Cognition Therapeutics assumes no responsibility for the content of third-party website. Neither does Cognition control, endorse or guarantee any aspect of your use of third-party sites. We encourage you to read and evaluate terms of use, privacy and other policies of the destination site as they may differ from Cognition’s policies.

You are now leaving the Cognition Therapeutics website

Cognition Therapeutics assumes no responsibility for the content of third-party website. Neither does Cognition control, endorse or guarantee any aspect of your use of third-party sites. We encourage you to read and evaluate terms of use, privacy and other policies of the destination site as they may differ from Cognition’s policies.

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Cognition Therapeutics assumes no responsibility for the content of third-party website. Neither does Cognition control, endorse or guarantee any aspect of your use of third-party sites. We encourage you to read and evaluate terms of use, privacy and other policies of the destination site as they may differ from Cognition’s policies.

You are now leaving the Cognition Therapeutics website

Cognition Therapeutics assumes no responsibility for the content of third-party website. Neither does Cognition control, endorse or guarantee any aspect of your use of third-party sites. We encourage you to read and evaluate terms of use, privacy and other policies of the destination site as they may differ from Cognition’s policies.