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

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

One of the first people to publicly explore their colour blindness was
John Dalton. In the 1800s, little was known about the visual perception system
(Tovée, 1995). At the time, Dalton hypothesized that his inability to distinguish
between red and green colours was due to a blue tinted vitreous fluid that absorbed
light corresponding to those colours before it could reach his retina (Tovée,
1995). This was later proven to be false as a dissection performed on of his
eyes after his death revealed that his vitreous fluid had no discolouration
(Tovée, 1995). This initial hypothesis, however, paved the way for the use of
molecular genetics that allowed us not only to understand the root of colour
blindness, but also the foundation of normal colour vision perception.

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Our uncanny ability to perceive the world in colour is mediated by
photoreceptors, called cones, that exist in the retinal layer of our eye. Normal
colour vision, also known as trichromatic vision, involves the activity of three
different types of cones; blue, green and red (also referred to as short,
medium, and long, respectively (Simunovic, 2009). Each of these different types
of cones express different opsin proteins that absorb photons of light across a
specific range of overlapping wavelengths (Simunovic, 2009). The presence of
different opsin proteins accounts for the spectral sensitivity that each type
of cone displays (Simunovic, 2009). Blue cones absorb most at 419 nm, green at
531 nm and red at 558 nm (Simunovic, 2009). Through phototransduction, light that is absorbed is
converted into an electrical signal and sent along the optic nerve to parts of
the visual cortex (Simunovic, 2009). There the brain processes the signals received from different cones in
comparison to one another, allowing us to perceive specific colours (Simunovic,
2009).

Most forms of colour blindness arise when a gene that codes for an opsin
protein suffers deleterious mutations or is deleted (Solomon & Lennie,
2007). This can either cause a change in the absorbance of the opsin protein or
result in its loss (Solomon & Lennie, 2007). A moderate form of colour
blindness, called anomalous trichromacy, results when all three types of cones
intact, but one cone has an altered absorbance (Petrie, 2016). Another form of
colour blindness, known as dichromacy, results when two types of cones are
intact, but one type is completely dysfunctional (Petrie, 2016). In anomalous
trichromacy and dichromacy, an individual has difficulty distinguishing between
colours that exist on a specific part of the visible spectrum, depending on
which cones are affected, while still being able to distinguish between other
colours (Petrie, 2016). The most severe and rarest form of colour blindness, called
monochromacy, results when one or no functional cones are present (Simunovic,
2009). Thus, individuals lack most or all aspects of colour vision and perceive
the world in mainly shades of grey (Simunovic, 2009).

Having a form of colour blindness can be a limitation to the affected
individual, depending on severity. In terms of day-to-day function, they can
have a hard time differentiating between street lights, often leading to
accidents (Simunovic, 2009). In the long-term, these individuals may be
prohibited for pursuing certain careers in which their colour vision deficiency
would 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 any
disability, many

attempts have
been made to help colour blind individuals rectify their vision. Since 2012,
Enchroma, a company started by Andrew Schmeder and Don McPherson, has been able
to manufacture corrective lenses that enable those who suffer from red-green colour
deficiencies to see the world more clearly (Lorch & Miah, 2016). These
lenses work by filtering out wavelengths of light that may overlap between red
and green cones, ultimately allowing people to differentiate between colours
they previous visualized to be the same or could not see at all (Lorch &
Miah, 2016). These glasses, however, are not a perfect solution. They do not
work for everyone or every form of colour blindness, but nevertheless they are
an ingenious start (Lorch & Miah, 2016).

            Theoretically, the permanent
solution to fixing colour blindness would be gene therapy. The Neitz lab has
performed gene therapy on adult squirrel monkeys (Manusco et al., 2009). These
monkeys were red-green colour blind due to a missing L-opsin gene (Manusco et
al., 2009). A virus containing a human L-opsin gene was injected in the
photoreceptor layer of their retina (Manusco et al., 2009). To test if the
experiment had been successful, a computerized test consisting of a pattern of
dots, containing a concealed symbol was used (Manusco et al., 2009).  The treated monkeys were able to respond to
the concealed symbol, despite that the fact that it appeared in a colour that
was previously invisible to them (Manusco et al., 2009). Many more trials have
to be completed before this can be applied to humans. There are also ethical
concerns regarding most forms of colour blindness as not being debilitating
enough for humans to actually undergo such invasive procedures (Manusco et al.,
2009). This experiment does, however, highlight the possibility that certain
deficits can be fixed outside of their critical period of development, since
adult 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 individual
perceives, there is a bright future, with many

possibilities and a potential cure looming in the horizons.