scholarly journals MyD88 Is Dispensable for Cerebral Amyloidosis and Neuroinflammation in APP/PS1 Transgenic Mice

2014 ◽  
Vol 184 (11) ◽  
pp. 2855-2861 ◽  
Author(s):  
Tara M. Weitz ◽  
David Gate ◽  
Kavon Rezai-Zadeh ◽  
Terrence Town
Keyword(s):  
Transgenic Mice ◽  
Cerebral Amyloidosis

scholarly journals P1-216: SEX-SPECIFIC PERTURBATIONS IN CEREBRAL AMYLOIDOSIS AND MICROGLIA PHENOTYPES IN ANTIBIOTIC-TREATED APPSWE /PS1L166P TRANSGENIC MICE

2019 ◽  
Vol 15 ◽  
pp. P319-P319
Author(s):  
Hemraj B. Dodiya ◽  
Thomas Kuntz ◽  
Shabana M. Shaik ◽  
Caroline Baufeld ◽  
Jeffrey Leibowitz ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Cerebral Amyloidosis

Induced LC degeneration in APP/PS1 transgenic mice accelerates early cerebral amyloidosis and cognitive deficits

2010 ◽  
Vol 57 (4) ◽  
pp. 375-382 ◽  
Author(s):  
Daniel Jardanhazi-Kurutz ◽  
Markus P. Kummer ◽  
Dick Terwel ◽  
Kim Vogel ◽  
Thomas Dyrks ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Cognitive Deficits ◽  
Cerebral Amyloidosis

scholarly journals Haplodeficiency ofCathepsin Ddoes not affect cerebral amyloidosis and autophagy in APP/PS1 transgenic mice

2017 ◽  
Vol 142 (2) ◽  
pp. 297-304 ◽  
Author(s):  
Shaowu Cheng ◽  
Willayat Y. Wani ◽  
David A. Hottman ◽  
Angela Jeong ◽  
Dongfeng Cao ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Cerebral Amyloidosis

BACE1 and Mutated Presenilin-1 Differently Modulate Aβ40 and Aβ42 Levels and Cerebral Amyloidosis in APPDutch Transgenic Mice

2007 ◽  
Vol 4 (2-3) ◽  
pp. 127-135 ◽  
Author(s):  
Martin C. Herzig ◽  
Paolo Paganetti ◽  
Matthias Staufenbiel ◽  
Mathias Jucker
Keyword(s):  
Transgenic Mice ◽  
Presenilin 1 ◽  
Cerebral Amyloidosis

Restricted diffusion in the brain of transgenic mice with cerebral amyloidosis

2004 ◽  
Vol 20 (3) ◽  
pp. 811-817 ◽  
Author(s):  
Thomas Mueggler ◽  
Melanie Meyer-Luehmann ◽  
Martin Rausch ◽  
Matthias Staufenbiel ◽  
Mathias Jucker ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Restricted Diffusion ◽  
Cerebral Amyloidosis ◽  
The Brain

BACE/APPV717F Double-Transgenic Mice Develop Cerebral Amyloidosis and Inflammation

2005 ◽  
Vol 2 (6) ◽  
pp. 284-298 ◽  
Author(s):  
Laurence Ozmen ◽  
Marie Woolley ◽  
Anita Albientz ◽  
Marie-Therese Miss ◽  
Peter Nelboeck ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Cerebral Amyloidosis ◽  
Double Transgenic Mice

Mechanism and pathogenesis of cerebral amyloidosis in APP transgenic mice

2000 ◽  
Vol 21 ◽  
pp. 71
Author(s):  
M. Jucker ◽  
A. Phinney ◽  
L. Bondolfi ◽  
D. Winkler ◽  
M. Tolnay ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Cerebral Amyloidosis

scholarly journals Tauopathy in theAPPswe/PS1ΔE9mouse model of familial Alzheimer’s disease

2018 ◽  
Author(s):  
Athanasios Metaxas ◽  
Camilla Thygesen ◽  
Stefan J. Kempf ◽  
Marco Anzalone ◽  
Ramanan Vaitheeswaran ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mice ◽  
Experimental Models ◽  
Mouse Tissue ◽  
Murine Models ◽  
Littermate Control ◽  
Cerebral Amyloidosis ◽  
Necessary And Sufficient ◽  
Tau Aggregation

AbstractDespite compelling evidence that the accumulation of amyloid-beta (Aβ) promotes cortical MAPT (tau) aggregation in familial and idiopathic Alzheimer’s disease (AD), murine models of cerebral amyloidosis are not considered to develop tau-associated pathology. The absence of neurofibrillary lesions in amyloidosis mice remains a challenge for the amyloidocentric paradigm of AD pathogenesis. It has resulted in the generation of transgenic mice harboring mutations in theirtaugene, which may be inappropriate for studying a disease with no knownTAUmutations, such as AD. Here, we have usedAPPswe/PS1ΔE9mice to show that tau pathology can develop spontaneously in murine models of familial AD. Tauopathy was abundant around Aβ deposits, with Gallyas- and thioflavin-S-positive perinuclear inclusions accumulating in theAPPswe/PS1ΔE9cortex by 18 months of age. Age-dependent increases in Gallyas signal correlated positively with binding levels of the paired helical filament (PHF) ligand [18F]Flortaucipir, in all brain areas examined. Sarkosyl-insoluble PHFs were visualized by electron microscopy. Tandem mass tag proteomics identified sequences of hyperphosphorylated tau in transgenic mice, along with signs of RNA missplicing, ribosomal dysregulation and disturbed energy metabolism. Human frontal gyrus tissue was used to validate these findings, revealing primarily quantitative differences between the tauopathy observed in AD patient vs. transgenic mouse tissue. Levels oftaumRNA were not different betweenAPPswe/PS1ΔE9and littermate control animals. As physiological levels of endogenous, ‘wild-type’ tau aggregate secondarily to Aβ in transgenic mice, this study demonstrates that amyloidosis is both necessary and sufficient to drive tauopathy in experimental models of familial AD.

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