Expression of LDOC1 mRNA in leucocytes of patients with Down’s syndrome

Down’s syndrome (DS), or trisomy 21, results from an extra chromosome 21 which is due to failure of normal chromosomal segregation during meiosis. Individuals with trisomy 21 can develop premature ageing and some traits of Alzheimer disease at an earlier age than subjects without trisomy 21 (Wisniewski et al. 1985). These individuals were thought to experience a neurodegenerative process because of the presence of an extra copy of the amyloid precursor protein (APP) gene located on chromosome 21, but this hypothesis has not been entirely confirmed by the literature (Elsayed and Elsayed 2009; Arriagada et al. 2010). Several studies have amply demonstrated that genes related to apoptosis play a crucial role in neurodegenerative diseases, indeed apoptotic pathways appear to play a causal role in neurodegenerative processes and in cancer proliferation (Engidawork and Lubec 2001; Gulesserian et al. 2001; Seidl et al. 2001; Yoo et al. 2001; Engidawork and Lubec 2001; Fromage and Anglade 2002; Lubec and Engidawork 2002). The cancer process is favoured when the apoptotic surveillance is, for any reason (Hu and Kavanagh 2003), decreased; conversely, when the apoptotic process is some what encouraged, neurodegenerative processes, such as those related to Alzheimer disease, will be prevailing (Elmore 2007). The leucine zipper, downregulated in cancer 1 (LDOC1) gene, was mapped on chromosome X at q27 and consists of only one exon (OMIM 300402). The Xq27 region is