Washington, July 9 (ANI): A compound, called P7C3, could restore the capacity to form new memories in aging rats, likely by improving the survival of newborn neurons in the brain's memory hub, revealed scientists at University of Texas Southwestern Medical Center, Dallas.
The research has turned up clues to a neuroprotective mechanism that could lead to a treatment for Alzheimer's disease.
"This neuroprotective compound, called P7C3, holds special promise because of its medication-friendly properties. It can be taken orally, crosses the blood-brain barrier with long-lasting effects, and is safely tolerated by mice during many stages of development," explained Dr. Steven McKnight, who co-led the research with Dr. Andrew Pieper.
"This striking demonstration of a treatment that stems age-related cognitive decline in living animals points the way to potential development of the first cures that will address the core illness process in Alzheimer's disease," said NIMH Director Dr. Thomas Insel.
Physical activity, social, or other enriching experiences promote neurogenesis - the birth and maturation of new neurons.
Newborn hippocampus neurons fare much worse in aging-related disorders like Alzheimer's, marked by runaway cell death.
In hopes of finding compounds that might protect such vulnerable neurons during this process, the researchers tested more than 1000 small molecules in living mice.
One of the compounds, designated P7C3, corrected deficits in the brains of adult mice engineered to lack a gene required for the survival of newborn neurons in the hippocampus.
Giving P7C3 to the mice reduced programmed death of newborn cells - normalizing stunted growth of branch-like neuronal extensions and thickening an abnormally thin layer of cells by 40 percent.
Among clues to the mechanism by which P7C3 works, the researchers discovered that it protects the integrity of machinery for maintaining a cell's energy level.
The researchers pinpointed a derivative of P7C3, called A20, which is even more protective than the parent compound.
They also produced evidence suggesting that two other neuroprotective compounds eyed as possible Alzheimer's cures may work through the same mechanism as P7C3.
The A20 derivative proved 300 times more potent than one of these compounds currently in clinical trials for Alzheimer's disease.
This suggested that even more potent neuroprotective agents could potentially be discovered using the same methods.
Following up on these leads, the researchers are now searching for the molecular target of P7C3 - key to discovering the underlying neuroprotective mechanism.
The study has been published in the journal Cell. (ANI)
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