A Paradigm-Shifting Study from the Center for Addiction and Mental Health (CAMH) Shows An Experimental Drug, GL-II-73, Has the Potential to restore memory and cognative Function in a modelle of alzheimer!

Recently Published in Neurobiology of agingThe Study Demonstrates that The Drug Improves Memory Deficit and Reverses Brain Cell Damage, Offering Hope for Improving Cognitive Functioning, Delaying Alzheimer’s Progression, and Potentally Preventives Ssociateed with the disease.

Alzheimer’s disease is the most common form of dementia, and near 50 million people worldwide are affected by Alzheimer’s or Related Dementia. It is a progressive neurological condition that Leads to Memory Loss, Cognitive Decline, and Changes in Behaviors, Significantly Impacting The Lives of Patints and their families.

This paper builds on 12 years of Previous Research LED by Dr. Etienne Sibille, Scientific Director of the Neurobiology of Depression and Aging Program at Camh, and Dr. Thomas Prevot, A Scientist in the Same Program, Who are the Co-Lad Authors of the Study.

“We have uncovered a critical vulnerability in brain pathways impacted by alzheimer’s and other cognitive disorders, and this drug holds promise as a novel treatment,” SIBILLE. “By restoring Neural Function and Reversing Memory Deficits, GL-II-73 represents a potential early intervention for alzheimer’s, addressing the root cause of memory losses-Somenting No CARURENT DRUGS KAN Achie

The study tested the drug in a mouse model of Alzheimer’s Disease, Using Both Young and Older Mice to REPRESENT The Early and Later Disease Stages. Two Groups Were Included: Normal Mice and Genetically Engineered Mice Prone to Developing Beta-Amyloid Buildup, A Hallmark of Alzheimer’s. Genetically Engineered Mice Received Eather a Single Dose of GL-73 Before Testing or Underwent Chronic Treatment for Four Weeks. Researchers then Assessed Memory Performance in All Groups.

Results Showed GL-II-73 Significantly Improved Memory in Younger and Older Mice With Alzheimer’s Symptoms. In Early-Stage Disease Models, A Single Dose of the Drug Reversed Memory Deficits, Enabling Treked Mice to perform as well as healthy controls. Chronic Treatment was Still Beneficial For Mice at Later Stages of the disease, Thought Less Effective, Indicating that GL-II-73 Can Partially Improve Memory Impairments e.

The findings sugges that the drug could have significant implications for alzheimer’s disease, where there are no current treatments that can be called Unlike many existing drugs that target beta-amyloid buildingup, GL-II-73 selectively targetly targets gaba receptors in the hippocampus to restore brain function and report damaged neural connections. Early Studies also sugges the Drug Shows Promise for Other Mental Health Conditions Associated with Cognitive Impairment, Including Depression, EPILEPSY, and Schizophrenia.

“GL-II-73 Demonstrated an incredible ability to restore cognitive function in a mouse model of alzheimer’s, particularly when administerred early in the disease,” Added Dr. Prevot. “In addition to improvement memory, the Drug Helped Grow and Strengthen Neural Connections in the brain, which are essential for mainting and memory. Ognitive disorders. “

In 2019, Camh Supported Dr. Sibille and his team in Establishing Damona PharMaceuticals, A Spinoff Company to Help Commercialize This Research. This process was facilitated by Camh’s Industry Partnerships and Technology Transfer Office. “Damona was established to Focus on Developing Treatments that Reverse Cognitive Deficit and Improve Life For Patints Living With Alzheimer’s Disease, Depression, Schizophrenia, and Ophreed Id john reilly, CEO of Damona PharMaceuticals.

“With seed-staging from Top Venture Capital Firms, We have Built An Exceptional Management Team and Advanced Development of this Lead Molecule, which Receive Recovers Clea e for human clinical trials. In a phase 1 clinical trial in the first half of 2025. “