Alzheimer's, Dementia & Mental Health
Flip of a Single Molecular Switch Makes an Old Brain
Yale researchers blocked the function of key gene in old mice, they
reset the old brain to adolescent levels of plasticity
March 6, 2013 - The flip of a single molecular
switch helps create the mature neuronal connections that allow the brain
to bridge the gap between adolescent impressionability and adult
stability. Now Yale School of Medicine researchers have reversed the
process, recreating a youthful brain that facilitated both learning and
healing in the adult mouse.
Scientists have long known that the young and old
brains are very different. Adolescent brains are more malleable or
plastic, which allows them to learn languages more quickly than adults
and speeds recovery from brain injuries. The comparative rigidity of the
adult brain results in part from the function of a single gene that
slows the rapid change in synaptic connections between neurons.
By monitoring the synapses in living mice over
weeks and months, Yale researchers have identified the key genetic
switch for brain maturation a study released March 6 in the journal
The Nogo Receptor 1 gene is required to suppress high levels of
plasticity in the adolescent brain and create the relatively quiescent
levels of plasticity in adulthood. In mice without this gene, juvenile
levels of brain plasticity persist throughout adulthood.
researchers blocked the function of this gene in old mice, they reset
the old brain to adolescent levels of plasticity.
"These are the molecules the brain needs for the
transition from adolescence to adulthood," said Stephen Strittmatter.
Vincent Coates Professor of Neurology, Professor of Neurobiology and
senior author of the paper. "It suggests we can turn back the clock in
the adult brain and recover from trauma the way kids recover."
Rehabilitation after brain injuries like strokes
requires that patients re-learn tasks such as moving a hand. Researchers
found that adult mice lacking Nogo Receptor recovered from injury as
quickly as adolescent mice and mastered new, complex motor tasks more
quickly than adults with the receptor.
"This raises the potential that manipulating Nogo
Receptor in humans might accelerate and magnify rehabilitation after
brain injuries like strokes," said Feras Akbik, Yale doctoral student
who is first author of the study.
Researchers also showed that Nogo Receptor slows
loss of memories. Mice without Nogo receptor lost stressful memories
more quickly, suggesting that manipulating the receptor could help treat
post-traumatic stress disorder.
"We know a lot about the early development of the
brain," Strittmatter said, "But we know amazingly little about what
happens in the brain during late adolescence."
Other Yale authors are: Sarah M. Bhagat, Pujan R.
Patel and William B.J. Cafferty
The study was funded by the National Institutes of
Health. Strittmatter is scientific founder of Axerion Therapeutics,
which is investigating applications of Nogo research to repair spinal
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