How Otx2 Could Lead to Advanced TBI Recovery
Researchers and scientists are constantly exploring new possibilities aimed at developing a cure or “rebuilding” treatment for traumatic brain injury victims and other patients suffering from similar neurological disorders. In recent years, neuroscience has successfully identified a key factor that triggers the brain’s ability to learn.
For years, medical science has worked to understand the conditions which enable advanced learning (plasticity) in a young child’s brain. Think about it, infants quickly learn simple habits and become familiar with parents and siblings long before they are able to form words. Relatively, small children can also learn one or more languages strictly through immersion and day to day routine, without the use of logic, memory cards, written passages, or language exercises. Children even learn tense, grammar and sentence structure through daily routine alone. So why is replicating or “tapping into” this same learning process next to impossible for adults?
Triggering Plasticity – Telling the Brain to Begin Learning
DNA that develops during the embryonic phase in humans and most animals pre-establishes certain control mechanisms for auditory and visual stimulation. In 2008, neuroscientists at Boston Children’s Hospital identified a protein that appears to trigger learning (plasticity) in the young brain. Lead researcher, Takao Hensch, PhD, identified a protein called Otx2. Otx2 causes a key type of cell (parvalbumin cells) in the cortex to mature and initiates critical learning periods and stages – the windows during which the brain makes new connections and can literally rewire itself.
This is the process enabling toddlers and young children to learn at natural, yet exponential rates. The cortex is saturated with Otx2 and plasticity operates at max capacity, processing stimuli and wiring the brain more quickly in life’s early years than will ever be possible later in life. However, the learning window is limited. Otx2 initiates a chain reaction which culminates by closing off the “elevated” learning process. After a fixed time interval (months, years) inhibitory circuits activate and essentially “lock in” the information, ending the period of elevated plasticity.
Where does Otx2 come from? Will more Otx2 reactivate the adult brain?
Otx2 is a cell protein developed and stored in the retina. Researchers have linked visual development to the timed release of Otx2. In rats, once babies’ eyes are fully open, Otx2 is released from the retina and travels to the cortex. Hensch’s study observed baby rats reared in total darkness. Though their eyes had opened, no Otx2 had been sent to the cortex. In essence, visual maturity in mammals and humans triggers the release of Otx2. When the eyes are developed enough to process external stimuli, the signal of Otx2 tells the brain to begin learning.
Researchers can isolate Otx2 and deliver it directly to the cortex. However, current knowledge has not yet enabled the brain plasticity process to be reactivated successfully. This natural development in young mice (and humans) incorporates a complete process. In other words, the natural conditions which activate Otx2 have already created a counter-mechanism to terminate learning after a fixed period of time. One does not exist without the other.
Natural inhibitors are created at the same time and “balance out” the equation of rapid learning in the young brain. An optimized neurochemical environment must exist inclusive of both variables. Only under a correct balance of conditions will Otx2 stimulate parvalbumin cells to maturity. Injecting random Otx2 into the cortex (alone) will not yield the desired results.
More research is needed, but scientists like Hensch have been working to identify the equation’s other factors in hopes of optimizing the other variables required to successfully reactivate the “child-like” learning pattern in the brain.
Hopes for Otx2 in Treating TBI and Beyond
The identification of Otx2 is a huge step forward in understanding (and perhaps reactivating) the brain’s ability to learn. Hensch and his Boston colleagues hope that this research might one day lead to expedited recovery in traumatic brain injury patients. Even if scientists discover how to successfully create new brain cells, activating them properly will be necessary. If a TBI patient could be successfully placed back into a neurological state of child-like plasticity, the time and process of relearning basic functions could be drastically reduced and improved.
Hensch’s discovery sets the stage for tremendous advances in healing science. Hensch further elaborated on the study’s accomplishments in stating:
“Otx2 itself could be a carrier for factors you’d want to deliver to the brain, like eye drops for brain disorders such as schizophrenia, in which parvalbumin cells don’t properly mature. Launching a critical period might also help people recover from stroke or brain injury, or learn languages or musical instruments as easily as young children…other sensory organs may also send similar signals to the brain as they mature, triggering critical periods for hearing, smell, etc.”
References:
Children’s Hospital Boston
