Decreased cyclin dependent kinase in brain of patients with Down Syndrome
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Neurogenesis impairment: An early developmental defect in Down syndrome
2018, Free Radical Biology and MedicineCitation Excerpt :There is evidence that DYRK1A increases G1 duration in a dose-dependent manner and that DYRK1A controls G1 duration by reducing cyclin D1 expression [94]. Consistent with DYRK1A overexpression in DS, cyclin D1 levels are reduced in the frontal lobe of fetuses with DS [103] and in fibroblasts of DS individuals [94]. This evidence suggests that one of the mechanisms underlying the reduced proliferation potency of the DS brain may be the DYRK1A/cyclin D1-dependent precocious exit from the cell cycle.
Trisomy 21 and early brain development
2012, Trends in NeurosciencesCitation Excerpt :Specific changes have been reported for the cell cycle rate and progression in multiple organ systems, which suggests that the altered kinetics of cell production may contribute to many phenotypes. DNA synthesis and doubling times are both slower in DS fibroblasts [27,28] and DS cerebral cortex contains less cyclin-dependent kinase [29], which are indicative of lower replication rates. Recent studies have also shown that proliferation is abnormal in the developing DS forebrain [30] and cerebellum [31].
Elevated apoptosis in pre-mature neurons differentiated from mouse ES cells containing a single human chromosome 21
2002, Biochemical and Biophysical Research CommunicationsApoptosis-associated proteins p53 and APO-1/Fas (CD95) in brains of adult patients with Down syndrome
1999, Neuroscience LettersFive potential reasons for the down syndrome HSCR (DS-HSCR) association: A hypothesis
2012, New Developments in Down Syndrome Research