Down syndrome, one of the most common genetic causes of mental retardation associated with genetic factors, occurs in approximately 1.2 per 1000 live births, is typically caused by a nondisjunction of the 21st chromosome during meiosis resulting in a complete trisomy genotype, although atypical forms occur occasionally. Adults with Down syndrome have benefited from the advances in public health practices that have resulted in a dramatic extension in life expectancy. However, Down syndrome is still characterized by increased mortality rates during later stages of life. Causes of higher mortality rates later in life may be due to a number of factors, two of which are an increased risk for Alzheimer~s disease and an apparent tendency toward premature aging. Aging processes among adults with Down syndrome have been of interest for over 100 years because of the occurrence of the signs and symptoms of Alzheimer~s disease in the population. Indeed, brain tissue of virtually all adults with Down syndrome over 35 to 40 years of age displays significant accumulations of amyloid plaques, historically considered to be a hallmark of Alzheimer's disease neuropathology presumably due to the triplication and over expression of the gene for beta-amyloid precursor protein located on chromosome 21. The genotypic and phenotypic characteristics of the """"""""oldest old"""""""" (i.e., 65 and older) adult population with mental retardation due to Down syndrome will be compared to those of their younger peers (also with Down syndrome) in order to identify genetic risk factors associated with survival and the cognitive declines associated with dementia of the Alzheimer~s-type. We have been able to identify a group of 100 people with Down syndrome 65 years of age or older. Investigation of this unique group of individualist will allow us to characterize the phenotype of the ~oldest old~ with Down syndrome and identify genetic and health status factors that are associated with extended survival and successful aging on one hand and the development of DAT on the other.
| Jenkins, Edmund C; Ye, Lingling; Krinsky-McHale, Sharon J et al. (2016) Telomere longitudinal shortening as a biomarker for dementia status of adults with Down syndrome. Am J Med Genet B Neuropsychiatr Genet 171B:169-74 |
| Jenkins, Edmund C; Ye, Lingling; Velinov, Milen et al. (2012) Mild cognitive impairment identified in older individuals with Down syndrome by reduced telomere signal numbers and shorter telomeres measured in microns. Am J Med Genet B Neuropsychiatr Genet 159B:598-604 |
| Jenkins, Edmund C; Ye, Lingling; Silverman, Wayne P (2012) Does the cryogenic freezing process cause shorter telomeres? Cryobiology 65:72-3 |
| Jenkins, Edmund C; Ye, Lingling; Gu, Hong et al. (2010) Shorter telomeres may indicate dementia status in older individuals with Down syndrome. Neurobiol Aging 31:765-71 |
| Prasher, V P; Sajith, S G; Mehta, P et al. (2010) Plasma beta-amyloid and duration of Alzheimer's disease in adults with Down syndrome. Int J Geriatr Psychiatry 25:202-7 |
| Schupf, N; Zigman, W B; Tang, M-X et al. (2010) Change in plasma Aýý peptides and onset of dementia in adults with Down syndrome. Neurology 75:1639-44 |
| Schupf, Nicole; Lee, Joseph H; Wei, Michelle et al. (2008) Estrogen receptor-alpha variants increase risk of Alzheimer's disease in women with Down syndrome. Dement Geriatr Cogn Disord 25:476-82 |
| Urv, Tiina K; Zigman, Warren B; Silverman, Wayne (2008) Maladaptive behaviors related to dementia status in adults with Down syndrome. Am J Ment Retard 113:73-86 |
| Jenkins, Edmund C; Ye, Lingling; Gu, Hong et al. (2008) Increased ""absence"" of telomeres may indicate Alzheimer's disease/dementia status in older individuals with Down syndrome. Neurosci Lett 440:340-3 |
| Zigman, Warren B; Devenny, Darlynne A; Krinsky-McHale, Sharon J et al. (2008) Alzheimer's Disease in Adults with Down Syndrome. Int Rev Res Ment Retard 36:103-145 |
Showing the most recent 10 out of 26 publications
