The time window for the brain to
develop optimal connections is relatively short-lived and usually occurs prior
to adulthood.
However, according to a study
published in Science Translational Medicine, it appears neuroplasticity can
be restarted in the visual cortex. Blocking the activity of a single protein resulted in growth of new
neural synapses.
BRAIN PLASTICITY USE IT OR LOSE IT - NEW HOPE
“There is a lot of interest in
the ‘critical period’ of development when the brain is plastic and undergoes a
lot of changes and learning,” said Christiaan
Levelt, who studies the biology of visual plasticity at the
Netherlands Institute for Neuroscience in Amsterdam. “This study shows that, in an adult animal you can re-open
this critical period window and get enhanced plasticity.”
“At its heart, this is about
understanding why it gets harder to learn new things as we get older and
whether this is something that we can reverse if we knew the right molecules to
target, by either adding them back or by suppressing them,” said study author
David Bochner.
Bochner, his Stanford advisor Carla Shatz, and their colleagues took a different approach. Previous research
discovered that paired-immunoglobulin–like
receptor B (PirB) protein–works to halt the plasticity of the visual cortex.
In this study, researchers
disrupted PirB function—either genetically or biochemically—and 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.
"What is really surprising was the creation of new synapses in the adult brain. We didn't expect to see such a start result," said Shatz.
In mammals, the visual system
fully develops after birth when the visual cortex of the brain learns to
process input from the eyes. If vision in one eye is diminished, the other eye
makes stronger neuronal connections in a larger portion of the visual cortex
while the neurons relaying information from the poor-seeing eye all but shut
down, a condition called amblyopia, or lazy eye.
“This is an example of the
use-it-or-lose-it principle,” said Shatz. The condition can be repaired during
a critical period of development—up to about four weeks after birth in mice and
age six in humans—by closing the good eye and allowing the impaired one to work
on its own.
Levelt notes that understanding
and reactivating the capacity for brain plasticity throughout life could help
treat victims of brain trauma or those with neurodevelopment disorders. Elizabeth Quinlan, who studies amblyopia and synaptic
plasticity in the adult visual system at the University of Maryland, agrees.
“Reactivated plasticity could be
harnessed to promote recovery of damaged sensory input, and to promote learning
in disabled and healthy brains,” she said. “PirB is a potential target for
therapeutic interventions in humans, especially if antagonists of PirB are
developed that could cross the blood brain barrier, and be targeted to specific
cortical regions or synapses.”
Shatz would next like to measure eyesight
in the mice with amblyopia depleted of PirB to directly understand the extent
of the recovery of visual function and whether acutely eliminating PirB can
have a lasting effect on neuronal plasticity. The team would also like to one
day develop a pill version of the PirB inhibitor, Shatz said.
The lab has also shown 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,” Shatz said.
“No one yet knows how to tap into the brain’s inherent ability to make
connections, but it’s something exciting to try to understand.”
Source: Neural Plasticity Research
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