Neurobiology of Mental Retardation: Fragile X Syndrome In my previous paper I wrote about the subject of the debate fostering nature and how it relates to the dilemma of equality behavior in the brain. In this article I will continue to research on the relationship between genes and neurobiology, but I will focus on specific aspects of this relationship, nervous disorders caused by genetic abnormalities. There are many well studied (not necessarily fully understood) diseases associated with the X chromosome, many of which have neurobiologic roots and behavioral symptoms.
Approximately 30% of cases of mental retardation are caused by genetic factors. Mental retardation may be caused by hereditary genetic abnormalities such as fragile X syndrome. Vulnerable X is a chromosomal abnormality that determines gender and is the most common genetic cause of mental retardation. Single genetic abnormalities, such as phenylketonuria (PKU) and other congenital metabolic abnormalities, may also cause mental retardation if not detected and treated early. It is possible that accidental or mutation in gene development may also cause growth inhibition. An example of such an accident is additional development
Introduction Fragile X syndrome is the most common cause of hereditary mental retardation, with one in about 1,200 men and one in 2,500 men. Men with fragile X syndrome usually have mental retardation and often exhibit distinctive physical features and behaviors. Affected women show a similar, but less severe phenotype. Diagnosis of Fragile X syndrome was based on the expression of folate sensitive fragile site (FRAXA) of Xq 27.3 originally induced in cell culture under folate deficiency conditions. Cytogenetic analysis of metaphase spreads indicated that less than 60% of the most affected individuals had fragile sites. Cytogenetic testing has limitations, especially when it detects the state of the vector exhibiting a high degree of variability between the individual and the laboratory.