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Scientists at the University of Colorado Anschutz Medical Campus believe they have found the primary mechanism underlying cognitive decline associated with normal aging.
“The mechanism involves the misregulation of a brain protein known as CaMKII, which is crucial for memory and learning,” said the study’s co-senior author Ulli Bayer, Ph.D., professor of pharmacology at the University of Colorado School of Medicine. “This study directly suggests specific pharmacological treatment strategies.”
The findings were published in the journal Science Signaling today.
Using animal models, researchers discovered that changing the CaMKII brain protein generated cognitive consequences similar to those seen with natural aging.
According to Bayer, aging in mice and humans both decreases a process known as S-nitrosylation, which is the modification of certain brain proteins such as CaMKII.
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.
Nitric oxide levels in the body decrease as we age. According to the study, this diminishes nitrosylation, which reduces memory and learning ability.
According to Bayer, the new discovery paves the path for the development of medications and other therapeutic approaches that could restore the protein’s nitrosylation. He claims that this opens the door of curing or delaying natural cognitive decline for an undetermined period of time.
He emphasized that this would only work in normal age-related cognitive decline, not in 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.”
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