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Many of those proteins are involved in brain cell signaling at synapses, the tiny gaps between neurons. But in old age, something about these proteins means they don't get broken down as readily and start clogging up synapses.
Support cells called microglia step in to help, pruning clogged synapses to keep neurons firing, but their clean-up efforts may ultimately impair brain cell communication, the researchers surmise. "We didn't set out to understand the synapse specifically, but rather the mechanisms behind the decline in general neuron health and function with age,""We just so happened to arrive at synaptic proteins being particularly vulnerable to slowed breakdown and aggregation." With some 86 billion neurons in the jiggly biological computer between our ears, each communicating with as many as 10,000 other neurons, the brain has more than a quadrillion synapses. These connections are maintained by synaptic proteins, which help neurons grow, direct where synapses form, and regulate the release of Before zeroing in on synapses, the researchers simply wanted to see how protein recycling changes with age in the brain cells of living animals. So they tagged and tracked thousands of proteins in young, middle-aged, and older mice. The team developed a new type of biological tag that's incorporated into proteins as they're built from amino acids. That way, they could see how long proteins lasted before being broken down and recycled. Experiments showed brain cells in mice at the ripe old age of 24 months were unable to recycle proteins as efficiently as their younger counterparts, aged just 4 months. Neurons in old mice took twice as long to recycle neuronal proteins as those in young animals, meaning the spent proteins had more time to accumulate.Mouse brain cells are shown in red, while protein aggregates are shown in green. Brain cells from younger mice, on the left, show much lower rates of protein clumps, or aggregates, compared with brain cells from older mice, on the right. (Aside from cleaning up waste proteins, microglia also prune damaged synapses to help maintain healthy connections between brain cells. "If microglia are taking in synapses' damaged proteins, that could be overwhelming microglia and causing them to become dysfunctional. Overall, it would be a detrimental effect to brain health," Researchers don't know why synaptic proteins are more likely to get tangled up in these clumps than the thousands of other proteins they studied in the mouse brain. But the findings point to a mechanism that joins the dots between synaptic loss and microglial dysfunction, which may be part of the cascade that leads to neurodegenerative diseases in older age."The achievement lies in the technical advance, namely by being able to look at protein degradation and aggregation specifically in neuronal cells," biochemist F. Ulrich Hartl, director of the Max Planck Institute of Biochemistry,Big breakthroughs. Bold ideas. Straight to your inbox.
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