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Cell Press, Current Biology, 20(25), p. R998-R1001, 2015

DOI: 10.1016/j.cub.2015.08.054

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Neuroplasticity: Unexpected Consequences of Early Blindness

Journal article published in 2015 by Micah M. Murray, Pawel J. Matusz ORCID, Amir Amedi
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

Cataracts cause one third of blindness worldwide [1]. Although nowadays cataracts are readily treated surgically (and potentially in the near future even using eye-drops [2]), these techniques are not equally accessible worldwide. The case of Claude Monet, who went blind late in life, illustrates the debilitating consequences of cataracts (Figure 1). Was Monet genetically predisposed to be the originator of impressionism, or was his pioneering role as a painter influenced by a critical period of visual development? What would he have painted if he had been blind during childhood? Disentangling the respective contributions of biological constraints and experience and their neural bases are important challenges for neuroscientists. The visual system has long been used as a model to study this so-called nature–nurture debate: is one born an impressionist master or can this be learnt? Two recent studies [3,4] in Current Biology addressed precisely how early-life blindness reorganises the brain and influences the ability to see again after corrective surgery. Which functions are innate, which require early-life experience, and which can be (re)trained at any time in life?