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New Publication Identifies Key Proteins Involved in Amyloid Oligomer Binding and Supports Mechanism of CT1812

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Cognition Therapeutics, Inc. (NASDAQ: CGTX) announced new findings that provide insight into the biology of Alzheimer's disease. The research, conducted by collaborators at the University of Edinburgh, revealed the role of the σ-2 receptor in regulating Aβ oligomer binding. The study utilized high-resolution microscopy techniques to analyze protein-protein interactions in brain samples from individuals with Alzheimer's disease. The results indicate that Aβ oligomers are proximate to certain receptor proteins on the synapse surface, which may form a complex. Additionally, the study confirmed that CT1812, Cognition's lead product candidate, causes the removal of Aβ oligomers from synapses, offering a potential new mechanism to fight Alzheimer's disease progression.
Positive
  • Insight into the role of the σ-2 receptor in regulating Aβ oligomer binding
  • High-resolution microscopy techniques used to analyze protein-protein interactions in Alzheimer's brain samples
  • Confirmation that CT1812 causes the removal of Aβ oligomers from synapses, potentially offering a new mechanism to fight Alzheimer's disease progression
Negative
  • None.

Insights

The recent publication from the University of Edinburgh provides scientific validation for the therapeutic approach of Cognition Therapeutics, Inc. in targeting the σ-2 receptor to combat Alzheimer's disease. The data suggesting that the company's lead drug, CT1812, can displace Aβ oligomers from synapses offers a promising avenue for Alzheimer’s treatment, which has historically been a challenging area with limited success. The ability to disrupt the binding of Aβ oligomers, which are implicated in synaptic damage and disease progression, could represent a significant advancement in the field.

From a research perspective, the use of advanced imaging techniques like FRET and array tomography to observe protein interactions at the synaptic level is a notable development. It enhances our understanding of the disease's pathology and provides a more detailed map for drug developers to target. The results also reinforce the importance of synaptic protection in the management of neurodegenerative diseases.

For investors, these findings could signal a positive outlook for Cognition Therapeutics' drug pipeline and its potential market impact. However, it is essential to consider the long development timelines and regulatory hurdles inherent in bringing a new drug to market, especially in the complex field of neurodegenerative diseases.

The announcement of scientific findings supporting Cognition Therapeutics' treatment approach may have positive implications for the company's valuation and investor confidence. The Alzheimer's disease market is projected to be substantial, given the increasing prevalence of the disease and the lack of effective treatments. A drug like CT1812 that offers a novel mechanism of action could capture significant market share if clinical trials continue to yield positive results.

Investors should note the potential for increased R&D costs as the company progresses through clinical trials, which could impact short-term financials. However, the long-term potential for revenue generation in a successful scenario could offset these concerns. It is also critical to monitor the competitive landscape, as other companies are also actively seeking to develop treatments for Alzheimer's disease.

Further, partnerships or interest from larger pharmaceutical companies could arise, influenced by these findings, which may provide additional funding or strategic support for Cognition Therapeutics. Such developments could lead to stock price movements and warrant close attention from the investment community.

The recent findings are likely to resonate within the pharmaceutical industry, particularly among companies focused on neurodegenerative disorders. The Alzheimer's treatment market is highly competitive and innovations that offer potential disease-modifying effects are closely watched.

Market dynamics for Alzheimer's treatments are driven by demographic trends, such as aging populations in many developed countries, which increase the urgency for effective therapies. This research could position Cognition Therapeutics as a key player in the Alzheimer's space if subsequent clinical trials are successful. Market analysts will be interested in assessing how these scientific developments might translate into market share and pricing strategies for CT1812, considering the high unmet need in Alzheimer's disease treatment.

Moreover, the company's stock market performance could be influenced by investor perception of the drug's potential, which may be bolstered by this research. It is crucial to analyze how this news is received by the market and whether it leads to a reevaluation of the company's growth prospects.

NEW YORK, Feb. 06, 2024 (GLOBE NEWSWIRE) -- Cognition Therapeutics, Inc. (NASDAQ: CGTX), a clinical stage company developing drugs that treat neurodegenerative disorders, announced that collaborators at the University of Edinburgh, Scotland published findings in the journal, Acta Neuropathologica, (doi: 10.1007/s00401-023-02679-6) that provide new insight into the biology of Alzheimer’s disease that is consistent with our understanding of the role the σ-2 receptor has in regulating Aβ oligomer binding. 

Using a combination of two high-resolution microscopy techniques: array tomography and Förster resonance energy transfer (FRET), Professor Tara Spires-Jones and colleagues at the UK Dementia Research Institute at University of Edinburgh’s Centre for Discovery Brain Sciences analyzed protein-protein interactions in over 1 million individual synapses in brain samples from people who had died with Alzheimer’s disease. Results detected TMEM97, a protein component of the σ-2 receptor complex, in close proximity to cellular prion protein (PrPc) on Alzheimer’s brain synapses. In addition, results found that Aβ oligomers were proximate to both PrPc, which has been shown to bind Aβ oligomers in neuronal cultures, as well as to TMEM97. These findings support the hypothesis that these receptor proteins may form a complex on the synapse surface with Aβ oligomers binding to one or both proteins. 

“Losing synaptic connections in the brain contributes to Alzheimer’s disease symptoms,” explained Professor Spires-Jones. “Previous work indicated that Aβ oligomers damage synapses, but until now it was not possible to know which proteins bind toxic forms of Aβ in human synapses. Combining FRET and array tomography imaging overcomes the limits of traditional microscopy and lets us determine whether proteins are close enough to interact in human brain samples. In simplest terms, while we had previous evidence that certain proteins existed in the same cellular neighborhood, we couldn’t precisely determine until now which houses were next to one another. Our findings help clarify the specific interactions between Aβ oligomers and synaptic receptors, which we hope will provide valuable information for drug developers.” 

Professor Spires-Jones' work also confirmed that in the presence of CT1812, Cognition’s lead product candidate, Aβ oligomers are displaced from the oligomer receptor, a discovery echoed in the SNAP study, which was published in May 2023 in Translational Neurodegeneration. In Professor Spires-Jones' study using an Alzheimer's mouse model, a FRET signal was observed between TMEM97 and Aβ oligomers in synapses, which could occur if oligomers were bound to TMEM97 or to PrPc, the putative oligomer binding site. Importantly, this FRET signal is reduced in CT1812-treated mice, suggesting that CT1812 caused the release of Aβ oligomers from their binding site and prevented them from re-binding.  

“Professor Spires-Jones' most recent work showing that CT1812 causes the removal of Aβ oligomers from synapses is an important confirmation of the mechanism initially proposed in the two seminal PLoS One papers authored by Cognition’s founding scientists,” explained Anthony Caggiano, MD, PhD, Cognition's CMO and head of R&D. "We believe these findings build on our clinical evidence that targeting the σ-2 receptor with CT1812 may offer a distinct and relevant new mechanism to fight Alzheimer’s disease progression by protecting synapses from the damaging effects of Aβ oligomers.” 

About Cognition Therapeutics, Inc. 
Cognition Therapeutics, Inc. is a clinical-stage biopharmaceutical company engaged in the discovery and development of innovative, small molecule therapeutics targeting age-related degenerative disorders of the central nervous system and retina. We are currently investigating our lead candidate CT1812 in clinical programs in Alzheimer’s disease, dementia with Lewy bodies (DLB) and dry age-related macular degeneration (dry AMD). We believe CT1812 and our pipeline of σ-2 receptor modulators can regulate pathways that are impaired in these diseases. We believe that targeting the σ-2 receptor with CT1812 represents a mechanism functionally distinct from other current approaches in clinical development for the treatment of degenerative diseases. More about Cognition Therapeutics and its pipeline can be found at https://cogrx.com. 

Forward Looking Statements  
This press release contains forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995. All statements contained in this press release, other than statements of historical facts or statements that relate to present facts or current conditions, including but not limited to, statements regarding our product candidates, including CT1812, and any expected or implied benefits or results, including that initial clinical results observed with respect to CT1812 will be replicated in later trials and our clinical development plans, including statements regarding our clinical studies of CT1812 and any analyses of the results therefrom, are forward-looking statements. These statements, including statements relating to the timing and expected results of our clinical trials, involve known and unknown risks, uncertainties and other important factors that may cause our actual results, performance, or achievements to be materially different from any future results, performance, or achievements expressed or implied by the forward-looking statements. In some cases, you can identify forward-looking statements by terms such as “may,” might,” “will,” “should,” “expect,” “plan,” “aim,” “seek,” “anticipate,” “could,” “intend,” “target,” “project,” “contemplate,” “believe,” “estimate,” “predict,” “forecast,” “potential” or “continue” or the negative of these terms or other similar expressions. We have based these forward-looking statements largely on our current expectations and projections about future events and financial trends that we believe may affect our business, financial condition, and results of operations. These forward-looking statements speak only as of the date of this press release and are subject to a number of risks, uncertainties and assumptions, some of which cannot be predicted or quantified and some of which are beyond our control. Factors that may cause actual results to differ materially from current expectations include, but are not limited to: competition; our ability to secure new (and retain existing) grant funding; our ability to grow and manage growth, maintain relationships with suppliers and retain our management and key employees; our ability to successfully advance our current and future product candidates through development activities, preclinical studies and clinical trials and costs related thereto; uncertainties inherent in the results of preliminary data, pre-clinical studies and earlier-stage clinical trials being predictive of the results of early or later-stage clinical trials; the timing, scope and likelihood of regulatory filings and approvals, including regulatory approval of our product candidates; changes in applicable laws or regulations; the possibility that the we may be adversely affected by other economic, business or competitive factors, including ongoing economic uncertainty; our estimates of expenses and profitability; the evolution of the markets in which we compete; our ability to implement our strategic initiatives and continue to innovate our existing products; our ability to defend our intellectual property; the impact of the COVID-19 pandemic on our business, supply chain and labor force; and the risks and uncertainties described more fully in the “Risk Factors” section of our annual and quarterly reports filed with the Securities & Exchange Commission and are available at www.sec.gov. These risks are not exhaustive and we face both known and unknown risks. You should not rely on these forward-looking statements as predictions of future events. The events and circumstances reflected in our forward-looking statements may not be achieved or occur, and actual results could differ materially from those projected in the forward-looking statements. Moreover, we operate in a dynamic industry and economy. New risk factors and uncertainties may emerge from time to time, and it is not possible for management to predict all risk factors and uncertainties that we may face. Except as required by applicable law, we do not plan to publicly update or revise any forward-looking statements contained herein, whether as a result of any new information, future events, changed circumstances or otherwise.  

Contact Information:   
Cognition Therapeutics, Inc.    
info@cogrx.com  
Casey McDonald (media)  
Tiberend Strategic Advisors, Inc.     
cmcdonald@tiberend.com  
Mike Moyer (investors) 
LifeSci Advisors 
mmoyer@lifesciadvisors.com  

 

FAQ

What is the ticker symbol for Cognition Therapeutics, Inc.?

The ticker symbol for Cognition Therapeutics, Inc. is CGTX.

What new findings were announced by Cognition Therapeutics, Inc.?

Cognition Therapeutics, Inc. announced new findings that provide insight into the biology of Alzheimer's disease.

What is the role of the σ-2 receptor in Alzheimer's disease?

The role of the σ-2 receptor in regulating Aβ oligomer binding in Alzheimer's disease was revealed in the study.

What is the lead product candidate of Cognition Therapeutics, Inc.?

CT1812 is the lead product candidate of Cognition Therapeutics, Inc.

What did the study confirm about CT1812?

The study confirmed that CT1812 causes the removal of Aβ oligomers from synapses, potentially offering a new mechanism to fight Alzheimer's disease progression.

Cognition Therapeutics, Inc.

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