coding region, CAG codes for glutamine (Q), so CAG repeats result in an expanded polyglutamine tract. These diseases are commonly referred to as polyglutamine (or polyQ) diseases. The repeated codons in the remaining disorders do not code for glutamine, and these can be classified as non-polyQ or non-coding trinucleotide repeat disorders. Polyglutamine (PolyQ) diseases Non-coding trinucleotide repeat disorders Symptoms and signs , ten neurological and neuromuscular disorders were known to be caused by an increased number of CAG repeats. Although these diseases share the same repeated codon (CAG) and some symptoms, the repeats are found in different, unrelated genes. Except for the CAG repeat expansion in the 5' UTR of PPP2R2B in SCA12, the expanded CAG repeats are translated into an uninterrupted sequence of glutamine residues, forming a polyQ tract, and the accumulation of polyQ proteins damages key cellular functions such as the ubiquitin-proteasome system. A common symptom of polyQ diseases is the progressive degeneration of nerve cells, usually affecting people later in life. However different polyQ-containing proteins damage different subsets of neurons, leading to different symptoms. The non-polyQ diseases or non-coding trinucleotide repeat disorders do not share any specific symptoms and are unlike the PolyQ diseases. In some of these diseases, such as Fragile X syndrome, the pathology is caused by lack of the normal function of the protein encoded by the affected gene. In others, such as Myotonic Dystrophy Type 1, the pathology is caused by a change in protein expression or function mediated through changes in the messenger RNA produced by the expression of the affected gene. In yet others, the pathology is caused by toxic assemblies of RNA in the nuclei of cells. Genetics Trinucleotide repeat disorders generally show genetic anticipation: their severity increases with each successive generation that inherits them. This is likely explained by the addition of CAG repeats in the affected gene as the gene is transmitted from parent to child. For example, Huntington's disease occurs when there are more than 35 CAG repeats on the gene coding for the protein HTT. A parent with 35 repeats would be considered normal and would not exhibit any symptoms of the disease. However, that parent's offspring would be at an increased risk of developing Huntington's compared to the general population, as it would take only the addition of one more CAG codon to cause the production of mHTT (mutant HTT), the protein responsible for disease.