The cone complement contains the types of cones (or their opsins) expressed by an individual. Causes
Color vision deficiencies can be classified as inherited or acquired. Inherited: inherited or congenital/genetic color vision deficiencies are most commonly caused by mutations of the  genes encoding opsin proteins. However, several other genes can also lead to less common and/or more severe forms of color blindness. Acquired: color blindness that is not present at birth, may be caused by chronic illness, accidents, medication, chemical exposure or simply normal ageing processes. Genetics
Color blindness is typically an inherited genetic disorder. The most common forms of colorblindness are associated with the Photopsin genes, but the mapping of the human genome has shown there are many causative mutations that dont directly affect the opsins. Mutations capable of causing color blindness originate from at least 19 different chromosomes and 56 different genes (as shown online at the Online Mendelian Inheritance in Man [OMIM]). Genetics of red–green color blindness
By far the most common form of colorblindness is congenital red–green colorblindness (Daltonism), which includes protanopia/protanomaly and deuteranopia/deuteranomaly. These conditions are mediated by the OPN1LW and OPN1MW genes, respectively, both on the X chromosome. Protanopia and Deuteranopia (Dichromacy) could be caused by either a missing gene, or a mutation that renders the protein fully non-functional. Protanomaly and Deuteranomaly are caused by a mutation of the genes that causes the spectral sensitivity of the associated opsin proteins to shift towards the other.
Aromatic L-amino acid decarboxylase deficiency is a rare genetic disorder caused by mutations in the DDC gene, which encodes an enzyme called aromatic L-amino acid decarboxylase. Signs and symptoms
Babies with severe aromatic L-amino acid decarboxylase deficiency usually present during the first few months of life. Symptoms can include:

Hypotonia (floppiness)
Developmental delay
Oculogyric crises
Difficulty with initiating and controlling movements
Dystonia and dyskinesia
Gastointestinal dysmotility which can present at as vomiting, gastro-oesophageal reflux, diarrhoea and/or constipation
Autonomic symptoms including difficulties controlling temperature and blood sugar, excessive sweating and nasal congestionSome people may develop cerebral folate deficiency, because O-methylation of the excessive amounts of L-Dopa can deplete methyl donors such as S-adenosyl methionine and levomefolic acid. This deviation can be detected by measuring the levels of levomefolic acid in the cerebrospinal fluid, and can be corrected by folinic acid. Genetics
Aromatic L-amino acid decarboxylase deficiency is an autosomal recessive condition, meaning an individual needs to have two faulty copies of the DDC gene in order to be affected. Usually, one copy is inherited from each parent. Pathophysiology
The aromatic L-amino acid decarboxylase deficiency enzyme is involved in the synthesis of dopamine and serotonin, both of which are important neurotransmitters. Diagnosis
Once there is a clinical suspicion of the diagnosis, neurotransmitters can be analysed in cerebrospinal fluid from a lumbar puncture. If these show the pattern of abnormalities typical for aromatic L-amino acid decarboxylase deficiency, the diagnosis can be confirmed by genetic testing and/or measurement of enzyme activity.