Overexpression of a protein that regulates calcium homeostasis in hippocampal neurons can safely and effectively reverse and prevent age-related memory impairments in rats while restoring altered gene expression, finds new research published in JNeurosci.
Philip Landfield, John Gant, Eric Blalock and colleagues found that long-term and short-term treatment of aging rats that induces overexpression of FK506-Binding Protein 12.6/1b (FKBP1b) restored the expression of more than 800 genes affected by aging to levels comparable to those of young untreated rats, in addition to improving performance on a water maze task. The restored genes represent a new genomic network that regulates the integrity of neuronal structure in the hippocampus and is targeted by aging. These results suggest that addressing FKBP1b deficiency may represent a new avenue for countering age-related memory loss.
Article: FK506-Binding Protein 12.6/1b, a negative regulator of [Ca2+], rescues memory and restores genomic regulation in the hippocampus of aging rats
Corresponding author: Philip Landfield (University of Kentucky, Lexington, KY, USA), email@example.com
JNeurosci, the Society for Neuroscience's first journal, was launched in 1981 as a means to communicate the findings of the highest quality neuroscience research to the growing field. Today the journal remains committed to publishing cutting-edge neuroscience that will have an immediate and lasting scientific impact while responding to authors' changing publishing needs, representing breadth of the field and diversity in authorship.
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The Society for Neuroscience is the world's largest organization of scientists and physicians devoted to understanding the brain and nervous system. The nonprofit organization, founded in 1969, now has nearly 37,000 members in more than 90 countries and over 130 chapters worldwide.