FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2697000055> ?p ?o ?g. }

• W2697000055 endingPage "88" @default.
• W2697000055 startingPage "76" @default.
• W2697000055 abstract "The intellectual disability that characterizes Down syndrome (DS) is primarily caused by prenatal changes in central nervous system growth and differentiation. However, in later life stages, the cognitive abilities of DS individuals progressively decline due to accelerated aging and the development of Alzheimer's disease (AD) neuropathology. The AD neuropathology in DS has been related to the overexpression of several genes encoded by Hsa21 including DYRK1A (dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1A), which encodes a protein kinase that performs crucial functions in the regulation of multiple signaling pathways that contribute to normal brain development and adult brain physiology. Studies performed in vitro and in vivo in animal models overexpressing this gene have demonstrated that the DYRK1A gene also plays a crucial role in several neurodegenerative processes found in DS. The Ts65Dn (TS) mouse bears a partial triplication of several Hsa21 orthologous genes, including Dyrk1A, and replicates many DS-like abnormalities, including age-dependent cognitive decline, cholinergic neuron degeneration, increased levels of APP and Aβ, and tau hyperphosphorylation. To use a more direct approach to evaluate the role of the gene dosage of Dyrk1A on the neurodegenerative profile of this model, TS mice were crossed with Dyrk1A KO mice to obtain mice with a triplication of a segment of Mmu16 that includes this gene, mice that are trisomic for the same genes but only carry two copies of Dyrk1A, euploid mice with a normal Dyrk1A dosage, and CO animals with a single copy of Dyrk1A. Normalizing the gene dosage of Dyrk1A in the TS mouse rescued the density of senescent cells in the cingulate cortex, hippocampus and septum, prevented cholinergic neuron degeneration, and reduced App expression in the hippocampus, Aβ load in the cortex and hippocampus, the expression of phosphorylated tau at the Ser202 residue in the hippocampus and cerebellum and the levels of total tau in the cortex, hippocampus and cerebellum. Thus, the present study provides further support for the role of the Dyrk1A gene in several AD-like phenotypes found in TS mice and indicates that this gene could be a therapeutic target to treat AD in DS." @default.
• W2697000055 created "2017-06-30" @default.
• W2697000055 creator A5000769621 @default.
• W2697000055 creator A5012504202 @default.
• W2697000055 creator A5039196986 @default.
• W2697000055 creator A5073199380 @default.
• W2697000055 creator A5073397339 @default.
• W2697000055 date "2017-10-01" @default.
• W2697000055 modified "2023-10-16" @default.
• W2697000055 title "Normalizing the gene dosage of Dyrk1A in a mouse model of Down syndrome rescues several Alzheimer's disease phenotypes" @default.
• W2697000055 cites W1487193077 @default.
• W2697000055 cites W1504060840 @default.
• W2697000055 cites W1520284233 @default.
• W2697000055 cites W1560980386 @default.
• W2697000055 cites W1575120918 @default.
• W2697000055 cites W1608240838 @default.
• W2697000055 cites W1773591497 @default.
• W2697000055 cites W1775749144 @default.
• W2697000055 cites W1829879414 @default.
• W2697000055 cites W1831651395 @default.
• W2697000055 cites W1943985293 @default.
• W2697000055 cites W1957658076 @default.
• W2697000055 cites W1964927978 @default.
• W2697000055 cites W1968937229 @default.
• W2697000055 cites W1969979382 @default.
• W2697000055 cites W1971319272 @default.
• W2697000055 cites W1972160270 @default.
• W2697000055 cites W1972456354 @default.
• W2697000055 cites W1972812487 @default.
• W2697000055 cites W1974368272 @default.
• W2697000055 cites W1977002082 @default.
• W2697000055 cites W1980729492 @default.
• W2697000055 cites W1983829653 @default.
• W2697000055 cites W1985792428 @default.
• W2697000055 cites W1986457432 @default.
• W2697000055 cites W1986503994 @default.
• W2697000055 cites W1986609940 @default.
• W2697000055 cites W1992834359 @default.
• W2697000055 cites W1994573232 @default.
• W2697000055 cites W1994765456 @default.
• W2697000055 cites W1997271339 @default.
• W2697000055 cites W1998533302 @default.
• W2697000055 cites W1998665897 @default.
• W2697000055 cites W1999536106 @default.
• W2697000055 cites W2000157849 @default.
• W2697000055 cites W2001831314 @default.
• W2697000055 cites W2007079584 @default.
• W2697000055 cites W2007551204 @default.
• W2697000055 cites W2009705032 @default.
• W2697000055 cites W2011253324 @default.
• W2697000055 cites W2017976401 @default.
• W2697000055 cites W2019036379 @default.
• W2697000055 cites W2020471775 @default.
• W2697000055 cites W2022532556 @default.
• W2697000055 cites W2023370651 @default.
• W2697000055 cites W2025883141 @default.
• W2697000055 cites W2026745182 @default.
• W2697000055 cites W2027588113 @default.
• W2697000055 cites W2030938592 @default.
• W2697000055 cites W2034706078 @default.
• W2697000055 cites W2035923900 @default.
• W2697000055 cites W2040114944 @default.
• W2697000055 cites W2040150222 @default.
• W2697000055 cites W2043333250 @default.
• W2697000055 cites W2044872202 @default.
• W2697000055 cites W2047514208 @default.
• W2697000055 cites W2051603499 @default.
• W2697000055 cites W2051685982 @default.
• W2697000055 cites W2055453151 @default.
• W2697000055 cites W2056745213 @default.
• W2697000055 cites W2056990175 @default.
• W2697000055 cites W2058570072 @default.
• W2697000055 cites W2058968970 @default.
• W2697000055 cites W2069389312 @default.
• W2697000055 cites W2073374252 @default.
• W2697000055 cites W2073724760 @default.
• W2697000055 cites W2083514064 @default.
• W2697000055 cites W2084963741 @default.
• W2697000055 cites W2091678070 @default.
• W2697000055 cites W2094489923 @default.
• W2697000055 cites W2096963202 @default.
• W2697000055 cites W2103440561 @default.
• W2697000055 cites W2106538371 @default.
• W2697000055 cites W2108506483 @default.
• W2697000055 cites W2108741722 @default.
• W2697000055 cites W2109466393 @default.
• W2697000055 cites W2110608677 @default.
• W2697000055 cites W2110646442 @default.
• W2697000055 cites W2116147604 @default.
• W2697000055 cites W2116247013 @default.
• W2697000055 cites W2118000416 @default.
• W2697000055 cites W2121754948 @default.
• W2697000055 cites W2123984379 @default.
• W2697000055 cites W2125851351 @default.
• W2697000055 cites W2128527424 @default.
• W2697000055 cites W2128532993 @default.
• W2697000055 cites W2134774579 @default.
• W2697000055 cites W2136855986 @default.

• next