Aging comes with all sorts of maladies, but one of the most frustrating is the feeling that you are not as sharp as you used to be. Cognitive decline has been previously linked, at least in part, to a dysregulation in the neuronal calcium homeostasis in the hippocampus, which is a brain region essential for learning and memory. One player that keeps in check the proper balance of calcium use is the protein FKBP1b, and, not surprisingly, its amounts are reduced in aging rats and Alzheimer’s suffering patients.
Gant et al. (2015) sought to increase the expression of the FKBP1b protein in the hippocampus, in the hopes that its increase would result in better calcium homeostasis and, as a result, better memory performance in aging rats. They built a virus that carried the gene for making the FKBP1b protein and they injected this directly in the hippocampus. After they waited 5-6 weeks for the gene to be expressed, they tested the rats in the Morris water maze, a test for spatial memory. The old rats that received the injection performed as well as the young rats, and far better than the old rats who didn’t get the injection. Then the researchers made sure that the injection is the one responsible for the results, by checking the levels of the FKBP1b protein in the hippocampus (increased, as per specs), by recording from those neurons (they were awesome), and by imaging the calcium to make sure the balance was restored (ditto).
Reference: Gant, J. C., Chen, K. C., Kadish, I., Blalock, E. M., Thibault, O., Porter, N. M., Landfield, P. W. (29 July 2015). Reversal of Aging-Related Neuronal Ca2+ Dysregulation and Cognitive Impairment by Delivery of a Transgene Encoding FK506-Binding Protein 12.6/1b to the Hippocampus. The Journal of Neuroscience, 35(30):10878 –10887. doi: 10.1523/JNEUROSCI.1248-15.2015. Article + FREE PDF + Journal of Neuroscience cover