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Body + BrainBody & Brain

Single Gene May Dramatically Reverse Age-Related Mental Decline

With people living longer than ever, can science give us a means to defy age, and keep our minds intact?

ByTiffany DillNOVA NextNOVA Next
With people living longer than ever, can science give us a means to defy age, and keep our neurons and dendrites in good shape?

Our brains are marvelous memory machines. Repeated use of a specific brain circuit—reminiscing about your favorite pet, solving puzzles, or practicing the violin—encourages new circuits to stay with us for life. When we neglect to engage them, our circuits—and encoded memories—can wither into oblivion (reinforcing the old adage, “use it or lose it”).

And yet, even when we take strides to keep our minds sharp, we don’t always have a say in the matter. As we age, our mental capacity to learn and retain information is at risk to deteriorate rapidly with age.

Age-related mental decline doesn’t interfere with a person’s daily life to the extent of dementia, but it does compromise social interactions and can turn once-trivial mental tasks into unexpected bouts of frustration.

With people living longer than ever, can science give us a means to defy age, and keep our minds intact?

To do this, we need to understand our brains and how age augments them. In extreme cases, such as Alzheimer’s, cell by-products physically accumulate and clog neural pathways, creating a blockade in normal circuits. However, normal brain-aging changes are much more nuanced—several years ago, Phillip Landfield and his group of researchers at the University of Kentucky noticed old brain cells retain unusually high levels of calcium—one of several key ions in brain circuits.

Taking a closer look, the scientists discovered a coinciding deficiency: a protein called FPBP1b was drastically low when compared with youthful brains.

Attempting to reverse these age-related deficits, Landfield and his group injected elderly mice with a virus engineered for cranking-up FKBP1b protein levels in their brains. These mice were then challenged with a memory-intensive exercise: navigating a water maze and learning where a hidden platform exists.

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Much to their surprise, the mice not only outperformed their age-matched counterparts, but their neurons had drastically reverted back to more youthful characteristics. Examining the brain cells at a molecular level, some 800 genes unexpectedly began reverting back to “young brain” levels. With so many punctuated changes arising from a single protein, FKBP1b (and calcium levels it controls) is much more relevant to mental aging than previously thought.

Many of the augmented genes were tied to important brain cells activities, such as rewiring connections and transmitting electrical signals. However, inflammation signatures were unchanged throughout the regenerative process, prompting scientists to pause and question how much inflammation impacts aging (currently a hot topic in the realm of brain research).

Obviously, much more work is required to develop a medicinal equivalent to the “fountain of youth,” but this study is an encouraging first-step. It opens the door for understanding how certain key proteins, such as FKBP1b, keep our minds sharp as we venture into retirement.

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