The alzheimer’s drug candidates reverse broader aging, In a mouse model of Alzheimer’s disease, tested drug candidates, known as CMS121 and J147, improve memory and delay the degeneration of brain cells.
Researchers have now shown how this compound can also delay aging in healthy old mice by blocking the damage to brain cells that occur during aging and by tracking the values of certain molecules back to those seen in younger brains.
These drug candidates may be useful for the treatment of a wider range of diseases and show new pathways that link normal aging with Alzheimer’s disease.
Age is the biggest risk factor for Alzheimer’s disease over the age of 65 years. The risk of developing the disease doubles every five years. But, at the molecular level, scientists are not sure what happens in the brain to aging that contributes to Alzheimer’s disease.
The contribution of unwanted processes related to age to disease has ignored in the discovery of drugs for Alzheimer’s disease.
Before, researchers have developed CMS121 and J147, variants of active herbal ingredients with healing properties. Both compounds are positive because of their ability to keep neurons alive when exposed to a form of cellular stress associated with aging and Alzheimer’s disease.
Since then, researchers have used drug candidates to treat Alzheimer’s disease in animal models of the disease. But, experiments that show exactly how compounds work show that they target molecular pathways that are also important for longevity and aging.
The animals given to one of the drug candidates not only perform better in mice memory tests that have not yet received treatment but also differences in the brain at the cellular and molecular level.
The expression of genes related to mitochondria called cellular energy-producing structures maintained by CMS121 and J147 as we age.
Research in humans has shown that mitochondrial function disrupted by aging and deteriorating due to Alzheimer’s disease.
They also hope to use the new results to encourage the development of new Alzheimer’s drugs. Overcoming other molecules through the acetyl-CoA pathway can help treat the disease they suspect.
“We have used various animal models to study how these neuroprotective pathways regulate certain molecular aspects of mitochondrial biology and their effects on aging and Alzheimer’s disease,” the researchers said.