000285639 001__ 285639
000285639 005__ 20260313163512.0
000285639 037__ $$aDZNE-2026-00278
000285639 1001_ $$0P:(DE-2719)2810906$$aXie, Kan$$b0$$udzne
000285639 245__ $$aDataset: Over-expression of human mutated APP transgene in the mouse brain induces differential gene expression profiles depending on the age of exposure
000285639 260__ $$bGene Expression Omnibus$$c2026
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000285639 520__ $$aAlzheimer's disease (AD) is the most prevalent neurodegenerative disorder causing about two third of all dementia cases in the elderly. Although AD pathological features have been intensively examined in numerous scientific studies employing invertebrate and vertebrate model organisms, the exact underlying mechanisms remain poorly understood. Extracellular accumulation of amyloid beta (Aβ) peptides represents a pathological hallmark of AD and it has been considered as the initiation point of AD by the popular amyloid hypothesis. In the current study, we aim to address whether expression of a mutated APP transgene (APPSweInd) would provoke differential neurological outcomes depending on the age of exposure in mice. Towards this end, we employed a tetracycline-based inducible genetic system to target APPSweInd transgene expression to defined age intervals initiated at adulthood, i.e., between 6-18 months (= mid-aged group) and 12-24 months (= aged group). Surprisingly, over-expression of mutant APP reduced the transcriptional levels of genes embedded in the cholinergic network exclusively in the aged mouse brain, while gene expression profiles related to inflammatory activation and exacerbated gliosis were shared between age groups. Hence, our data support the notion that AD pathology may rely on a disruption of the cholinergic system that is triggered through an altered response of the aged brain towards toxic Aβ aggregates.
000285639 536__ $$0G:(DE-HGF)POF4-352$$a352 - Disease Mechanisms (POF4-352)$$cPOF4-352$$fPOF IV$$x0
000285639 7001_ $$0P:(DE-2719)2431567$$aRyan, Devon$$b1
000285639 7001_ $$0P:(DE-2719)2810547$$aBonn, Stefan$$b2
000285639 7001_ $$0P:(DE-2719)2289209$$aEhninger, Dan$$b3$$udzne
000285639 7870_ $$0DZNE-2026-00120$$aXie, Kan et.al.$$dLondon : BioMed Central, 2026$$iRelatedTo$$r$$tSelective vulnerability of the aging cholinergic system to amyloid pathology revealed by induced APP overexpression.
000285639 8564_ $$uhttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE271806
000285639 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2810906$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b0$$kDZNE
000285639 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2289209$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b3$$kDZNE
000285639 9131_ $$0G:(DE-HGF)POF4-352$$1G:(DE-HGF)POF4-350$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lNeurodegenerative Diseases$$vDisease Mechanisms$$x0
000285639 9201_ $$0I:(DE-2719)1013005$$kAG Ehninger$$lTranslational Biogerontology$$x0
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