The extra genetic material present in<unk>  results in overexpression of a portion of the 310 genes located on chromosome 21. This overexpression has been estimated at around 50%, due to the third copy of the chromosome present. Some research has suggested the<unk>  critical region is located at bands 21q22.1–q22.3, with this area including genes for the amyloid precursor protein, superoxide dismutase, and likely the ETS2 proto oncogene. Other research, however, has not confirmed these findings. MicroRNAs are also proposed to be involved. The dementia that occurs in<unk>  is due to an excess of amyloid beta peptide produced in the brain and is similar to Alzheimer's disease, which also involves amyloid beta build-up. Amyloid beta is processed from amyloid precursor protein, the gene for which is located on chromosome 21. Senile plaques and neurofibrillary tangles are present in nearly all by 35 years of age, though dementia may not be present. Those with<unk>  also lack a normal number of lymphocytes and produce less antibodies which contributes to their increased risk of infection. Epigenetics<unk>  is associated with an increased risk of many chronic diseases that are typically associated with older age such as Alzheimer's disease. The accelerated aging suggest that trisomy 21 increases the biological age of tissues, but molecular evidence for this hypothesis is sparse. According to a biomarker of tissue age known as epigenetic clock, trisomy 21 increases the age of blood and brain tissue (on average by 6.6 years).
Down syndrome
Alzheimer's disease
Baboon syndrome
Apert syndrome
Ring chromosome 14 syndrome
Ring chromosome 20 syndrome
TORCH syndrome
Williams syndrome