Telomere shortening in T lymphocytes of older individuals with Down syndrome and dementia

Reduced telomere length in older men with premutation alleles of the fragile X mental retardation 1 gene

“…Moreover, there is growing evidence that telomere shortening may play a causative role in certain age-related human disorders, including heart disease [Samani et al, 2001;Benetos et al, 2004], osteoporosis [Valdes et al, 2007], obesity [Valdes et al, 2005], dyskeratosis congenita [Vulliamy and Dokal, 2007], Alzheimer disease [Panossian et al, 2003], and Down syndrome [Jenkins et al, 2006a]. The recent discovery of UUAGGG-repeat telomeric RNAs may help to better understand the role of the telomere in the above conditions including aging and cancer [Schoeftner and Blasco, 2007].…”

Ageing in individuals with intellectual disability: issues and concerns in Hong Kong

“…28 Apolipoprotein E (APOE) ε4 allele, and high levels of Aβ1-42 peptide have been reported to be associated with the onset of dementia in DS. 29 Mok et al 30 suggested that there are three variants in BACE2 that possibly affect the age of onset of dementia in DS, while Jones et al 31 reported the involvement of PICALM and APOE loci in the process.…”

“…[32][33][34] Telomere shortening Apart from the above-mentioned genes, Jenkins et al 28 reported that the telomeres of chromosomes 21, 1, 2, and 16 are shorter in adults with DS and with either dementia or cognitive impairment compared with the general population. This finding suggests that telomere shortening can be used as a biomarker for inferring dementia.…”

Chapter 4 Alzheimer's Disease in Adults with Down Syndrome

“…However, a few have been investigated. These include measures of the quantity and type of beta amyloid protein found in blood plasma , and telomere size in metaphase and interphase preparations as well as on individual chromosomes (Jenkins, Velinov, Ye, Gu, Pang et al, 2006;Jenkins, Velinov, Ye, Gu, Li et al, 2006).…”

“…Telomere shortening has been linked to Alzheimer's disease in the typically developing population (Panossian et al, 2003), and Jenkins and his colleagues (Jenkins, Velinov, Ye, Gu, Li et al, 2006) hypothesized that a similar association might exist in adults with Down syndrome. Using quantitative telomere protein nucleic acid fluorescent in situ hybridization (FISH) analyses of metaphase and interphase preparations from agematched pairs of participants with Down syndrome with and without dementia, Jenkins observed: (a) shorter telomeres in individuals with dementia, (b) that individual chromosomes 1 and 21 could be used alone and/or in combination to detect telomere shortening (Jenkins, Velinov, Ye, Gu, Pang et al, 2006), (c) that cells from individuals with dementia or MCI had reduced numbers of telomere signals when analyzed using a PNA telomere probe , and (e) shorter telomeres in individuals with MCI (Jenkins et al, 2008 accepted). These preliminary results are encouraging, but the procedure used required samples from each affected case together with his or her matched comparison to be processed simultaneously, and in clinical practice, this circumstance would rarely occur.…”