Scientists at the University of Colorado Anschutz Medical Campus have discovered what they believe to be the central mechanism behind cognitive decline associated with normal aging.
Ulli Bayer, PhD, professor of pharmacology at the University of Colorado School of Medicine, said:
“The mechanism involves the mis-regulation of a brain protein known as CaMKII which is crucial for memory and learning. This study directly suggests specific pharmacological treatment strategies.”
The study was published today in the journal `Science Signaling.’
Researchers using mouse models have discovered that changing the CaMKII brain protein has similar cognitive effects to those that occur naturally during aging.
Bayer explained that both mice and humans experience a reduction in a process called S-nitrosylation, which modifies specific brain proteins including CaMKII, as they age.
Bayer said,
“This study shows that a decrease in the modification of CaMKII is enough to cause impairments in synaptic plasticity and memory that are similar to those observed in aging.”
The study suggests that normal aging decreases the amount of nitric oxide in the body, which in turn reduces nitrosylation, leading to memory and learning difficulties.
Bayer believes that this new research could lead to the development of drugs and other therapeutic interventions that could restore normal nitrosylation of the protein, potentially delaying normal cognitive decline for an unknown period of time.
He also noted that this approach would not be effective in treating the cognitive decline seen in Alzheimer’s disease and dementia, which are not related to normal aging.
“We know this protein can be targeted. And we think it could be done pharmacologically. That is the next logical step.”
