SoylentNews

frojack writes:

Neuroplasticity, the ability of the brain, during critical periods of development, to easily change its structure in response to environmental stimuli, declines by adulthood. In humans this happens by age 6. From then on it gets progressively harder to restructure the brain to handle the creation of new synapses.

The Scientist reports on a new study that suggests that this decline is actively caused through out later life by the creation of of a certain protein in the brain. And suppressing that protein allows the brain to regain its neural plasticity.

The brain doesn't actually lose its ability to adapt or make new neural connections, rather that ability is suppressed, activity turned off. The switch has been found to be a paired-immunoglobulin–like receptor B (PirB) protein produced by the brain itself.

The study describes curing Lazy Eye in mice, by covering the "Good Eye". Which is exactly what is done in children. Caught early enough, the brain and visual cortex will adapt to this change in stimuli by building up the fine neuron structures so that the lazy eye will be resume development, and often achieve normal vision.

With the mice, they induced lazy eye intentionally, by covering one eye long enough to cause the brain to "abandon" it.

Later in the mouse's life they introduced an inhibitor to the PirB Protein, removing the suppression of the brain's Neuroplasticity, and then covering the good eye. They saw new functional synapses form, demonstrating that even when PirB is inhibited in a short, one-week time frame, new neuron connections—and recovery from lazy eye—is possible in an adult mouse.

Now Lazy Eye isn't that big of a problem in children if caught early, and lazy eye in mice is even less of a concern, except to the mice.

Rather, the focus of the research is restoring Neuroplasticity to the brain, to handle brain injury or illness later in life. By "turning back the clock" of the brain's developmental cycle, the ability of the brain to adapt itself may be restored long enough to "route around the damage".

Their study has shown that that mice without PirB are partly resistant to memory loss in an Alzheimer’s model. This suggests that maybe the same drug for vision loss could also work for Alzheimer’s disease.

[Title change to correct typo - Ed.]