Cognitive decline with age is linked to reduced S-nitrosylated proteins in the brain. The protein CaMKII, essential for learning and memory, requires S-nitrosylation for optimal function. Young mice lacking this S-nitrosylation in CaMKII exhibited cognitive impairments akin to older mice, suggesting a mechanism for age-related cognitive decline.
Key takeaways: Decreased nitrosylation of CaMKII causes aging-associated impairments in memory and synaptic plasticity in mice
- Cognitive decline and S-nitrosylated proteins: As individuals age, there’s a noticeable reduction in S-nitrosylated proteins in the brain. These proteins play a pivotal role in maintaining cognitive functions, and their decrease can lead to diminished mental capabilities
- Role of CaMKII in learning and memory: CaMKII is a protein that is central to the processes of learning and memory. For it to function optimally, it requires a modification called S-nitrosylation. Without this modification, its effectiveness in supporting cognitive functions is compromised
- Observations in young mice: In experiments involving mice, young ones that were made deficient in S-nitrosylation of CaMKII exhibited cognitive challenges. These challenges were strikingly similar to what older mice naturally experience, indicating the importance of this protein modification in maintaining cognitive health
The findings suggest that the decline in S-nitrosylation of proteins like CaMKII might be a significant factor contributing to cognitive decline as we age.
Reference: Nicole L. Rumian et al. ,Decreased nitrosylation of CaMKII causes aging-associated impairments in memory and synaptic plasticity in mice.Sci. Signal.16,eade5892(2023).DOI:10.1126/scisignal.ade5892