The other day we reported about an algae found in nature that makes people stupid. Now we find out that scientists may have discovered a way to make you smart, by reverting the brain to a “plastic” child-like state.
The Independent UK reports…
Researchers at Stanford University experimented by interfering with PirB, a protein expressed in animal brain cells that allows skills to be recalled but which also hampers the ability to learn new skills, and realised they could disrupt the receptor’s regular function, allowing the brain to make faster connections.
By doing so, Professor Carla Shatz and her colleagues, Dr. David Bochner and Richard Sapp, found that their test subjects – animals – were better able to adapt to using only one eye, compared to animals that did not have the PirB molecule supressed.
In repressing the protein to a “plastic” state – which is a technical term that implies the ability to adapt to new conditions – Professor Shatz saw that at least one part of the brain became more malleable and could more easily recover from damage, rewire itself and learn new skills – in effect making a person smarter.
Neuroplasticity, which occurs in the brain under two primary conditions, describes how experiences reorganise neural pathways in the brain – or what happens when we learn something new (like a skill) or memorise information.
This happens over an individual’s lifetime, but is usually set off during normal brain development as a child; or as an adaptive mechanism to compensate for a lost function (like the loss of an eye); or to maximise the remaining functions in the wake of a serious brain injury.
The PirB molecule, which is also found in humans, and which is thought to stabilise neural connections, was removed from the visual cortex specifically by either acute shut-down of its gene using genetic engineering tools or by repressing its function with a drug.
The study, first reported on Neomatica, is important not only for its therapeutic implications but also for the developing field of brain and cognition-enhancing drugs.
The animal experiment mimicked the effects of lazy eye, or “amblyopia”, but the results could also be applied to acute injuries, such as strokes.
Previous experiments have also shown that the human version of PirB, known as LilrB2, may play a part in Alzheimer’s disease after scientists discovered that a protein (amyloid beta) which is commonly found in the brains of Alzheimer patients, binds itself to the LilrB2 protein.
There is a final hurdle: humans possess five similar variants named LilB2 through LilB5 and in order to achieve success, scientists may need to work out how to disruption more than one of the proteins.
Scientists better hurry on getting this to market.