Drug Unlocks Malleable, Fast-Learning, Child-LIke State In Adult Brain - Neomatica
>The scientists worked in a model animal and disrupted the regular function of a receptor called PirB. The receptor, which is also found in humans, was remov
ed from the visual cortex specifically by either acute shut-down of its gene using genetic engineering tools or repression of its function with a drug. When
the animals were forced to use one eye (thus mimicking "amblyopia", or "lazy eye" in common parlance), the neural circuits of the visual centers of the brain
rewired better to the remaining good eye compared to animals for which the PirB molecule was not suppressed. The results held True in the adult animal, not j
ust during the critical development period when the brain is naturally extremely plastic.
The strategy of disrupting PirB holds True not only for the specific case of lazy eye, but also for other types of neural pathologies, including those that ar
ise from acute injuries such as strokes. Interestingly, the PirB molecule seems to be involved in immunity although it was found, at least in the mouse, to b
e expressed throughout the brain in mice regardless of age. Prior experiments show that the human version, LilrB2, may play a role in Alzheimers disease. S
cientists have found that amyloid beta, a protein that is highly abundant in brains of patients with Alzheimers, binds to the LilrB2 protein. In animal experi
ments the binding leads to loss of synaptic plasticity.
>One challenge remains in the targeting of LilrB2 in humans. Humans have 5 similar variants named LilrB1 through LilrB5. Disruption may be required in more
than one of the proteins.