Experimental drug shows promise in restoring memory in Alzheimer’s model

A paradigm shift survey from the Center for Addiction and Mental Health (CAMH) shows an experimental medicine, GL-II-73, has the potential to restore memory and cognitive function in a mouse model of Alzheimer’s disease. Recently published in Neurobiology of agingThe study shows that the drug improves memory shortages and reverses brain cell damage, offers hope for improving cognitive functioning, postponing the progression of Alzheimer’s and possibly preventing some of the brain damage from associated with the disease.

Alzheimer’s disease is the most common form of dementia and nearly 50 million people worldwide are affected by Alzheimer’s or related dementia. It is a progressive neurological disorder that leads to memory loss, cognitive decline and changes in behavior, which significantly influences the lives of patients and their families.

This article builds on 12 years earlier research led by Dr. Etienne Sibille, scientific director of the Neurobiology of Depression and Aging Program in Camh, and Dr. Thomas Prevot, scientist in the same program, who are the Co-Lead authors of the authors study. “We have exposed a critical vulnerability in brain paths that are affected by Alzheimer’s and other cognitive impairment, and this medicine has promised as a new treatment,” Dr. Sibille. “By restoring the neural function and the reversal of memory shortages, GL-II-73 represents a potential early intervention for Alzheimer’s, with regard to the main cause of memory loss-ik that cannot reach current medicines.”

The study tested the medicine in a mouse model of Alzheimer’s disease, with the help of both young and older mice to display the early and later illness phases. Two groups were admitted: normal mice and genetically manipulated mice that are susceptible to the development of beta-amyloid structure, a characteristic of Alzheimer’s. Genetically manipulated mice received either a single dose of GL-II-73 before testing for four weeks or underwent a chronic treatment. Researchers then assessed memory performance in all groups.

Results showed GL-II-73 considerably improved memory in younger and older mice with the symptoms of Alzheimer’s. At an early stage of disease models, a single dose of the drug shortages reversed, so that treated mice can be carried out, as well as healthy checks. Chronic treatment was still beneficial for mice in later stages of the disease, although less effective, indicating that GL-II-73 can partially improve memory disorders, even after a significant cognitive decline.

The findings suggest that the drug could have important implications for Alzheimer’s disease, where there are no current treatments that can fully delay or reverse the cognitive decline. Unlike many existing drugs that focus on beta-amyloid structure, GL-II-73 focuses selectively on GABA receptors in the Hippocampus to restore brain function and restore damaged neural connections. Early studies also suggest that the drug shows promise for other mental disorders associated with cognitive impairment, including depression, epilepsy and schizophrenia.

GL-II-73 showed an incredible ability to restore the cognitive function in a mouse model of Alzheimer’s, especially when it is administered early in the disease. In addition to improving memory, the drug has helped to grow and strengthen neural connections in the brain, which are essential for maintaining learning and memory. This can be a crucial step forward for the treatment of Alzheimer’s and other cognitive disorders. “

Dr. Thomas Prevot, scientist, neurobiology of depression and aging program at CAMH

In 2019, Camh supported Dr. Sibille and his team in establishing Damona Pharmaceuticals, a spin -off company to help commercialize this research. This process was facilitated by Camh’s industrial partnerships and technology transfer office. “Damona was founded to concentrate on developing treatments that reversed cognitive shortages and improve life for patients living with Alzheimer’s disease, depression, schizophrenia and other brain disorders,” said John Reilly, CEO of Damona Pharmaceuticals. “With Seed phase financing from top business capital companies, we have built an exceptional management team and advanced development of this main molecule, which recently received the tailoring of the US Food and Drug Administration (FDA) for clinical tests for people. We look forward to registering patients in A phase 1 clinical study in the first half of 2025. ”

Financing for the study was provided by the Weston Brain Institute.