University of Colorado Anschutz Medical Campus scientists have potentially uncovered a mechanism behind age-related cognitive decline .

 

This mechanism involves a brain protein called CaMKII, crucial for learning and memory. 

The researchers found that aging, in both mice and humans, leads to a decrease in S-nitrosylation, a modification of specific brain proteins including CaMKII. This decrease in CaMKII modification, according to the study, is sufficient to cause impairments in synaptic plasticity and memory similar to those seen in aging. 

This discovery, published in the journal Science Signaling, suggests potential pharmacological treatment strategies that could maintain nitrosylation function and potentially delay or prevent normal age-related cognitive decline. However, it is important to note that this research focuses on normal age-related cognitive decline and not on conditions like Alzheimer's disease and dementia. 

Another study by the CU Anschutz Medical Campus, published in the journal Nature, found that a key process for learning and memory (long-term potentiation or LTP) depends on the structural, not enzymatic, functions of CaMKII. This finding is significant because it opens the door to using a new class of inhibitors that target only the enzymatic activity of CaMKII, potentially offering new therapies for Alzheimer's and other brain diseases without debilitating side effects.