Amblyopia is a central nervous system disease caused by the abnormal development of the visual cortex of the brain during a critical period of visual development (generally referred to as children before the age of seven). Usually occurs in a single eye, because the eyesight of one eye (poor eye) is significantly weaker than the other eye (skin eye), children will use more healthy eyes and give up using poor eyes. This preference leads to more control of the healthy eye in the brain's visual center while giving up the response to the poor eye (this phenomenon is called eye-advantage plasticity), which ultimately leads to permanent loss of monocular vision.

Amblyopia that develops in childhood will persist in adulthood, but you will find that most patients with amblyopia do not have organic lesions. Therefore, amblyopia is not blind, but cerebral blindness. 1-5% of people worldwide are affected by amblyopia, but there is currently no effective treatment for amblyopia.

Recently, researchers from the University of California, Irvine and the University of Maryland, College Park, respectively, discovered the molecular mechanisms that control the formation of amblyopia. They found that neuregulin-1 (Neuregulin-1 or NRG1) regulates the neural plasticity of the visual cortex by acting on the ErbB4 receptor on the surface of small albumin-positive inhibitory neurons in the visual cortex of the brain. The protein is most strongly expressed during critical periods of development and weakens in adulthood. This change in expression intensity over time coincides with the critical period of neuroplasticity, suggesting that it is likely to be an important molecular switch that opens and closes critical periods.

Moreover, in the mouse model at the early stage of amblyopia, the expression level of neuregulin-1 in the visual cortex was significantly reduced relative to the control group, resulting in the occurrence of dominant plasticity of the eye, eventually forming amblyopia. More importantly, exogenous injection of neuregulin-1 successfully inhibited the development and formation of amblyopia in childhood. In addition, inhibition of neuregulin-1 activity in adulthood can reopen a critical period of visual development similar to that of juveniles.

The results of the above studies were published on October 5th in Neuron (Sun et al., 2016; correspondent Xiangmin Xu) and The Journal of Neuroscience (Gu et al., 2016; Corresponding author Elizabeth M. Quinlan).

This finding means that humans are expected to completely suppress its development and deterioration at the beginning of the formation of amblyopia in childhood, thus preventing permanent visual defects. In addition, the critical period of reopening visual development in adulthood is expected to correct the already formed visual defects caused by amblyopia.

Not only that, but the findings will also have a profound impact on the treatment of other diseases associated with neurodevelopment. For example, scientists have found that neuregulin-1 is closely related to the development of schizophrenia and is one of the most sensitive susceptibility proteins to schizophrenia. Moreover, recent research shows that schizophrenia mostly begins in adolescence and is a neurological disease closely related to brain development. Therefore, the study of neuregulin-1 mediated cellular signaling and its function will be equally important for the treatment of schizophrenia.

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