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10.1111/acel.12873 http://scihub22266oqcxt.onion/10.1111/acel.12873 30488653/?report=reader!6351836!30488653     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Aging+Cell 2019 ; 18 (1): e12873 Nephropedia Template TP {{tp|p=30488653|t=2019. Temporal and regional progression of Alzheimer s disease-like pathology in 3xTg-AD mice |pdf=|usr=}}{{30488653}} gab.com Text Temporal and regional progression of Alzheimer s disease-like pathology in 3xTg-AD mice JO: Aging Cell http://www.kidney.de/pget.php?&tw=1&pmid=30488653 #FOAvip Accumulation of amyloid-beta (Abeta) and fibrillary tangles, as well as neuroinflammation and memory loss, are hallmarks of Alzheimer's disease (AD). After almost 15 years from their generation, 3xTg-AD mice are still one of the most used transgenic models of AD. Converging evidence indicates that the phenotype of 3xTg-AD mice has shifted over the years and contradicting reports about onset of pathology or cognitive deficits are apparent in the literature. Here, we assessed Abeta and tau load, neuroinflammation, and cognitive changes in 2-, 6-, 12-, and 20-month-old female 3xTg-AD and nontransgenic (NonTg) mice. We found that ~80% of the mice analyzed had Abeta plaques in the caudal hippocampus at 6 months of age, while 100% of them had Abeta plaques in the hippocampus at 12 months of age. Cortical Abeta plaques were first detected at 12 months of age, including in the entorhinal cortex. Phosphorylated Tau at Ser202/Thr205 and Ser422 was apparent in the hippocampus of 100% of 6-month-old mice, while only 50% of mice showed tau phosphorylation at Thr212/Ser214 at this age. Neuroinflammation was first evident in 6-month-old mice and increased as a function of age. These neuropathological changes were clearly associated with progressive cognitive decline, which was first apparent at 6 months of age and became significantly worse as the mice aged. These data indicate a consistent and predictable progression of the AD-like pathology in female 3xTg-AD mice, and will facilitate the design of future studies using these mice. Twit Text FOAVip Temporal and regional progression of Alzheimer s disease-like pathology in 3xTg-AD mice ????Aging Cell http://www.kidney.de/pget.php?&tw=1&pmid=30488653 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30488653 #FOAvip English Wikipedia <ref>{{Cite pmid|30488653}}</ref> Temporal and regional progression of Alzheimer s disease-like pathology in 3xTg-AD mice #MMPMID30488653 Belfiore R; Rodin A; Ferreira E; Velazquez R; Branca C; Caccamo A; Oddo S Aging Cell 2019[Feb]; 18 (1): e12873 PMID30488653show ga Accumulation of amyloid-beta (Abeta) and fibrillary tangles, as well as neuroinflammation and memory loss, are hallmarks of Alzheimer's disease (AD). After almost 15 years from their generation, 3xTg-AD mice are still one of the most used transgenic models of AD. Converging evidence indicates that the phenotype of 3xTg-AD mice has shifted over the years and contradicting reports about onset of pathology or cognitive deficits are apparent in the literature. Here, we assessed Abeta and tau load, neuroinflammation, and cognitive changes in 2-, 6-, 12-, and 20-month-old female 3xTg-AD and nontransgenic (NonTg) mice. We found that ~80% of the mice analyzed had Abeta plaques in the caudal hippocampus at 6 months of age, while 100% of them had Abeta plaques in the hippocampus at 12 months of age. Cortical Abeta plaques were first detected at 12 months of age, including in the entorhinal cortex. Phosphorylated Tau at Ser202/Thr205 and Ser422 was apparent in the hippocampus of 100% of 6-month-old mice, while only 50% of mice showed tau phosphorylation at Thr212/Ser214 at this age. Neuroinflammation was first evident in 6-month-old mice and increased as a function of age. These neuropathological changes were clearly associated with progressive cognitive decline, which was first apparent at 6 months of age and became significantly worse as the mice aged. These data indicate a consistent and predictable progression of the AD-like pathology in female 3xTg-AD mice, and will facilitate the design of future studies using these mice. |*Disease Progression[MESH] |Aging/pathology[MESH] |Alzheimer Disease/complications/*pathology/physiopathology[MESH] |Amyloid beta-Peptides/metabolism[MESH] |Animals[MESH] |Gliosis/pathology[MESH] |Hippocampus/metabolism/pathology[MESH] |Memory Disorders/complications/physiopathology[MESH] |Mice, Inbred C57BL[MESH] |Mice, Transgenic[MESH] |Microglia/pathology[MESH] |Phosphorylation[MESH] |Plaque, Amyloid/pathology[MESH] |Time Factors[MESH]Temporal and regional progression of Alzheimer s disease-like patholog(epmc).pdf DeepDyve Pubget Overpricing