Discovery holds promise for pausing age-related cognitive decline
Cognitive decline is, sadly, a normal part of aging. So even for those fortunate enough to avoid developing dementia, functions such as memory recall, processing of information and conceptual reasoning will decline over time.
But scientists at the University of Colorado Anschutz Medical Campus (UC Anchutz) believe they’ve found the mechanism behind age-related cognitive decline, and that it could potentially be combatted with medical intervention.
“The mechanism involves the mis-regulation of a brain protein known as CaMKII which is crucial for memory and learning,” said the study’s co-senior author Ulli Bayer, professor of pharmacology at the UC School of Medicine. “This study directly suggests specific pharmacological treatment strategies.”
By altering this protein in the brains of young mice, the researchers ‘aged’ them to have the same cognition as older animals.
With normal aging, both humans and mice experience the decline in a process known as S-nitrosylation, which involves the modification of certain brain proteins including CaMKII.
As this process slows, memory, learning ability and other executive functions also falter.
“The current study now shows a decrease in this modification of CaMKII is sufficient to cause impairments in synaptic plasticity and in memory that are similar in aging,” Bayer said.
The scientists now believe that therapeutics could be used to maintain nitrosylation function, which could potentially suspend age-related cognitive decline without any other ill effects.
However, treatment would only work for age-related cognitive decline, not for conditions such as Alzheimer’s disease and dementia.
“We know this protein can be targeted,” Bayer said. “And we think it could be done pharmacologically. That is the next logical step.”
The study was published in the journal Science Signaling.