An enzyme found in the brain could help to preserve cognitive resilience with advancing age, according to research in mice, humans and cells1. Researchers found that high levels of the enzyme are linked to low levels of inflammation in the brains of aged mice. They also showed that the enzyme boosts the growth of neurons in ageing brains.
The findings were reported on 15 October in Nature Neuroscience. The enzyme seems to act “as a compensatory cognitive-resilience mechanism”, says study co-author Amar Sahay, a neuroscientist at Massachusetts General Hospital in Boston. The authors homed in on the enzyme after finding that the gene encoding it suddenly became more active when connections between some of the neurons in the brains of mice were disrupted.
How to avoid dementia — what the science really says To learn more, the scientists genetically altered mice to lack the gene, called Pla2g2f, and looked at what happened as they aged. The researchers saw a surge of inflammation and neuron degradation compared with the brains of unaltered control animals. By contrast, mice that had excess Pla2g2f displayed less inflammation and better-connected neurons in their brains as they got older.
The team also tested the animals’ spatial memory. These results, too, suggested that the enzyme provides protection. Young mice that were lacking Pla2g2f scored lower on the memory tests than did young control mice; older animals with boosted Pla2g2f scored higher on the test than did older control mice.
These findings show that Pla2g2f can be used to shift the trajectory of pathological ageing in mice, Sahay adds. The gene might also have a protective role in humans. The authors analysed two large data sets2,3 compiled by other scientists and found that PLA2G2F activity in the human brain rises with age.
Sahay collaborated with researchers who had collected gene-expression data4 from the brains of deceased human donors. The donors had all undergone cognitive testing before their death. Sahay’s team found that PLA2G2F activity was highest in ‘resilient’ individuals — people whose cognition remained intact even though their brains had deposits of a protein called amyloid-β.
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