Posted on 8 October 2019
A new study finds that changes in presynaptic calcium signalling contributes to the decline in cognitive function, such as memory and learning, during ageing.
The hippocampus is a key region of the brain involved in learning and memory. As we age, there is not any extensive cell death or gross neuropathological changes in the hippocampus, as is observed with age-related neurodegenerative conditions such as Alzheimer’s. Instead the loss of cognitive function is caused by more subtle changes in synaptic properties.
So what are synapses? Synapses are specialised junctions where neurons communicate with each other or with target cells, usually by releasing a chemical transmitter. This study focused on presynaptic cells, the ones releasing neurotransmitters, and investigates whether changes in presynaptic calcium signalling contributes to age-related cognitive decline.
The researchers used a mouse line (SyG37) that has been engineered to express a calcium-sensing fluorescent protein, which allows the measurement of calcium signals based on fluorescence levels. Analysis suggests that in the hippocampus there is a general increase in baseline presynaptic calcium levels with age, even after compensating for changes in calcium-sensor expression levels. This suggests that during ageing, the ability of neurons to maintain calcium homeostasis is lost, leading to an overall change in calcium signalling.
Interestingly, experimentally decreasing the extracellular calcium concentration causes the presynaptic terminals of aged animals to behave more like younger ones. This suggests a potential avenue to delay or mitigate the loss of cognitive function with age, if the findings of this study can be replicated in humans.