It & Lennie, 2007). It affects about 8%

It is well established that infants over the age of 2 months have goodcolour vision and can easily discriminate between different colours (Thomasson& Teller, 2000). Colour vision and our ability to identify differentcolours in our visual field seems innate, but there are numerous people that exhibitdeficits in this seemingly simple task. Colour blindness refers to a perceptualdeficit that impairs an affected individual’s ability to distinguish betweendifferent colours of the visible spectrum (Solomon & Lennie, 2007). Itaffects about 8% of men and 0.5% of women worldwide. While this condition canbe acquired, it is most commonly inherited, typically through X-linkedrecessive patterns of inheritance as suggested by the higher prevalence ratefor men compared to women (Simunovic, 2009).

One of the first people to publicly explore their colour blindness wasJohn Dalton. In the 1800s, little was known about the visual perception system(Tovée, 1995). At the time, Dalton hypothesized that his inability to distinguishbetween red and green colours was due to a blue tinted vitreous fluid that absorbedlight corresponding to those colours before it could reach his retina (Tovée,1995).

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This was later proven to be false as a dissection performed on of hiseyes after his death revealed that his vitreous fluid had no discolouration(Tovée, 1995). This initial hypothesis, however, paved the way for the use ofmolecular genetics that allowed us not only to understand the root of colourblindness, but also the foundation of normal colour vision perception.Our uncanny ability to perceive the world in colour is mediated byphotoreceptors, called cones, that exist in the retinal layer of our eye. Normalcolour vision, also known as trichromatic vision, involves the activity of threedifferent types of cones; blue, green and red (also referred to as short,medium, and long, respectively (Simunovic, 2009). Each of these different typesof cones express different opsin proteins that absorb photons of light across aspecific range of overlapping wavelengths (Simunovic, 2009). The presence ofdifferent opsin proteins accounts for the spectral sensitivity that each typeof cone displays (Simunovic, 2009).

Blue cones absorb most at 419 nm, green at531 nm and red at 558 nm (Simunovic, 2009). Through phototransduction, light that is absorbed isconverted into an electrical signal and sent along the optic nerve to parts ofthe visual cortex (Simunovic, 2009). There the brain processes the signals received from different cones incomparison to one another, allowing us to perceive specific colours (Simunovic,2009).

Most forms of colour blindness arise when a gene that codes for an opsinprotein suffers deleterious mutations or is deleted (Solomon & Lennie,2007). This can either cause a change in the absorbance of the opsin protein orresult in its loss (Solomon & Lennie, 2007). A moderate form of colourblindness, called anomalous trichromacy, results when all three types of conesintact, but one cone has an altered absorbance (Petrie, 2016). Another form ofcolour blindness, known as dichromacy, results when two types of cones areintact, but one type is completely dysfunctional (Petrie, 2016).

In anomaloustrichromacy and dichromacy, an individual has difficulty distinguishing betweencolours that exist on a specific part of the visible spectrum, depending onwhich cones are affected, while still being able to distinguish between othercolours (Petrie, 2016). The most severe and rarest form of colour blindness, calledmonochromacy, results when one or no functional cones are present (Simunovic,2009). Thus, individuals lack most or all aspects of colour vision and perceivethe world in mainly shades of grey (Simunovic, 2009).

Having a form of colour blindness can be a limitation to the affectedindividual, depending on severity. In terms of day-to-day function, they canhave a hard time differentiating between street lights, often leading toaccidents (Simunovic, 2009). In the long-term, these individuals may beprohibited for pursuing certain careers in which their colour vision deficiencywould pose a threat to themselves or other, such as applying to be a physician (Simunovic,2009).In an effort to make the world more accessible to those who face anydisability, many attempts havebeen made to help colour blind individuals rectify their vision.

Since 2012,Enchroma, a company started by Andrew Schmeder and Don McPherson, has been ableto manufacture corrective lenses that enable those who suffer from red-green colourdeficiencies to see the world more clearly (Lorch & Miah, 2016). Theselenses work by filtering out wavelengths of light that may overlap between redand green cones, ultimately allowing people to differentiate between coloursthey previous visualized to be the same or could not see at all (Lorch , 2016). These glasses, however, are not a perfect solution.

They do notwork for everyone or every form of colour blindness, but nevertheless they arean ingenious start (Lorch & Miah, 2016).            Theoretically, the permanentsolution to fixing colour blindness would be gene therapy. The Neitz lab hasperformed gene therapy on adult squirrel monkeys (Manusco et al., 2009). Thesemonkeys were red-green colour blind due to a missing L-opsin gene (Manusco etal., 2009).

A virus containing a human L-opsin gene was injected in thephotoreceptor layer of their retina (Manusco et al., 2009). To test if theexperiment had been successful, a computerized test consisting of a pattern ofdots, containing a concealed symbol was used (Manusco et al., 2009).

 The treated monkeys were able to respond tothe concealed symbol, despite that the fact that it appeared in a colour thatwas previously invisible to them (Manusco et al., 2009). Many more trials haveto be completed before this can be applied to humans.

There are also ethicalconcerns regarding most forms of colour blindness as not being debilitatingenough for humans to actually undergo such invasive procedures (Manusco et al.,2009). This experiment does, however, highlight the possibility that certaindeficits can be fixed outside of their critical period of development, sinceadult monkeys were able to regain trichromatic vision (Manusco et al., 2009).This could have major implications on solving many other vision deficits. Although colour blindness affects the world an individualperceives, there is a bright future, with many possibilities and a potential cure looming in the horizons.