Even during healthy aging, we slowly lose our ability to learn and remember new things. Often, cognitive decline is associate with loss of synaptic plasticity—the ability to alter the connections between brain cells. But what causes synaptic connections to become less, well, plastic?
To answer that question, scientists from the University of Luxembourg and the VU University of Amsterdam investigated the molecular basis of memory loss. In particular, they looked at the molecular composition of brain connections in healthy mice of 20 to 100 weeks of age—an age span roughly equivalent to the period between puberty and retirement in humans.
The scientists investigated the temporal profile of the mouse hippocampal synaptic proteome. “Extracellular matrix proteins were the only group of proteins that showed a robust and progressive upregulation over time,” the authors wrote. “This was confirmed by immunoblotting and histochemical analysis, indicating that the increased levels of hippocampal extracellular matrix may limit synaptic plasticity as a potential cause of age-related cognitive decline.”
“Amazingly, there was only one group of four proteins of the extracellular matrix that increased strongly with age. The rest stayed more or less the same,” said Prof. Dr. del Sol Mesa. “The extracellular matrix is a mesh right at the connections between brain cells. A healthy amount of these proteins ensures a balance between stability and flexibility of synapses and is vital for learning and memory.”
Read the full, original story: In aging brain, extracellular scaffolding loses flexibility, memory deficits worsen