At present there are 14 documented trinucleotide repeat disorders that affect humans.

Myotonic dystrophy is one of several known trinucleotide repeat disorders.

Trinucleotide repeat disorders also follow a non-Mendelian pattern of inheritance.

This property results in the characteristic of anticipation seen in trinucleotide repeat disorders.

Trinucleotide repeat disorders are the result of extensive duplication of a single codon.

These mutations, typically short sequences repeated many times, give rise to numerous known diseases including the Trinucleotide repeat disorders.

Some trinucleotide repeats are found in coding regions (see, Trinucleotide repeat disorder).

Trinucleotide repeat disorders generally show genetic anticipation, where their severity increases with each successive generation that inherits them.

Prominent trinucleotide repeat disorders include Fragile X syndrome and Huntington's disease.

HD is one of several trinucleotide repeat disorders which are caused by the length of a repeated section of a gene exceeding a normal range.

It is caused by a trinucleotide repeat disorder in the fragile X mental retardation 1 gene, FMR1.

It is associated with a form of trinucleotide repeat disorder known as "dentatorubral-pallidoluysian atrophy" or "dentatorubropallidoluysian atrophy".

Tandem repeats of trinucleotides are abundant in Dictyostelium, which in humans cause Trinucleotide repeat disorders.

This makes it part of a class of neurodegenerative disorders known as trinucleotide repeat disorders or polyglutamine disorders.

For a complete list see the table under Polyglutamine (PolyQ) Diseases in the article Trinucleotide repeat disorder.

As it involves the repeat of four nucleotides, it is not a trinucleotide repeat disorder, but rather a tetranucleotide repeat disorder.

In a class of autosomal and X-linked dominant diseases known as trinucleotide repeat disorders (for example, Huntington's disease), a molecular mechanism for anticipation has also been demonstrated.

Anticipation is common in trinucleotide repeat disorders such as Huntington's disease and myotonic dystrophy where a dynamic mutation in DNA occurs.

Glutamine-rich polypeptides are important in the amyloidogenesis of Yeast and mammalian prions, as well as Trinucleotide repeat disorders including Huntington's disease.

His work focuses on unusual DNA structures and their role in genomic instability, as well as on dynamic mutations, such as Trinucleotide repeat disorders.

There are at least eight neurodegenerative diseases that are caused by expanded CAG repeats encoding polyglutamine (polyQ) stretches (see: Trinucleotide repeat disorder).

Trinucleotide repeat expansion, also known as triplet repeat expansion, is the DNA mutation responsible for causing any type of disorder categorized as a trinucleotide repeat disorder.

OPMD is an example of a trinucleotide repeat disorder caused by expanding (GCN) to (GCN) at the 5' end of the coding region for PABPN1.

In 2007, he led a team in his lab in the Biological Chemistry, and Computer Sciences and Applied Mathematics Departments at the Weizmann Institute of Science that developed a new disease model to explain the progression of Huntington's Disease and similar trinucleotide repeat disorders.

In 2007, a new disease model was produced to explain the progression of Huntington's Disease and similar trinucleotide repeat disorders, which, in simulations, seems to accurately predict age of onset and the way the disease will progress in an individual, based on the number of repeats of a genetic mutation.