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000266787 1001_ $$0P:(DE-2719)9001172$$aViana-da-Silva, Silvia$$b0$$eFirst author$$udzne
000266787 245__ $$aLocalized APP expression results in progressive network dysfunction by disorganizing spike timing.
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000266787 520__ $$aProgressive cognitive decline in Alzheimer's disease could either be caused by a spreading molecular pathology or by an initially focal pathology that causes aberrant neuronal activity in a larger network. To distinguish between these possibilities, we generated a mouse model with expression of mutant human amyloid precursor protein (APP) in only hippocampal CA3 cells. We found that performance in a hippocampus-dependent memory task was impaired in young adult and aged mutant mice. In both age groups, we then recorded from the CA1 region, which receives inputs from APP-expressing CA3 cells. We observed that theta oscillation frequency in CA1 was reduced along with disrupted relative timing of principal cells. Highly localized pathology limited to the presynaptic CA3 cells is thus sufficient to cause aberrant firing patterns in postsynaptic neuronal networks, which indicates that disease progression is not only from spreading pathology but also mediated by progressively advancing physiological dysfunction.
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000266787 650_2 $$2MeSH$$aMice
000266787 650_2 $$2MeSH$$aHumans
000266787 650_2 $$2MeSH$$aAnimals
000266787 650_2 $$2MeSH$$aAged
000266787 650_2 $$2MeSH$$aAmyloid beta-Protein Precursor: genetics
000266787 650_2 $$2MeSH$$aAmyloid beta-Protein Precursor: metabolism
000266787 650_2 $$2MeSH$$aHippocampus: metabolism
000266787 650_2 $$2MeSH$$aNeurons: physiology
000266787 650_2 $$2MeSH$$aAlzheimer Disease: metabolism
000266787 650_2 $$2MeSH$$aSynapses: physiology
000266787 650_2 $$2MeSH$$aMice, Transgenic
000266787 650_7 $$2Other$$aAlzheimer’s disease
000266787 650_7 $$2Other$$aAlzheimer’s disease
000266787 650_7 $$2Other$$aAlzheimer’s disease
000266787 650_7 $$2Other$$aAlzheimer’s disease
000266787 650_7 $$2Other$$aAlzheimer’s disease
000266787 650_7 $$2Other$$aAlzheimer’s disease
000266787 650_7 $$2Other$$aamyloid precursor protein
000266787 650_7 $$2Other$$ahippocampus
000266787 650_7 $$2Other$$aphase precession
000266787 650_7 $$2Other$$aspike timing
000266787 650_7 $$2Other$$atheta oscillations
000266787 650_7 $$2NLM Chemicals$$aAmyloid beta-Protein Precursor
000266787 7001_ $$0P:(DE-2719)9001580$$aHaberl, Matthias$$b1$$udzne
000266787 7001_ $$aGaur, Kshitij$$b2
000266787 7001_ $$0P:(DE-2719)9001322$$aPatel, Rina$$b3$$udzne
000266787 7001_ $$aNarayan, Gautam$$b4
000266787 7001_ $$aLedakis, Max$$b5
000266787 7001_ $$aFu, Maylin L$$b6
000266787 7001_ $$ade Castro Vieira, Miguel$$b7
000266787 7001_ $$aKoo, Edward H$$b8
000266787 7001_ $$aLeutgeb, Jill K$$b9
000266787 7001_ $$aLeutgeb, Stefan$$b10
000266787 773__ $$0PERI:(DE-600)2001944-0$$a10.1016/j.neuron.2023.10.001$$gVol. 112, no. 1, p. 124 - 140.e6$$n1$$p124 - 140.e6$$tNeuron$$v112$$x0896-6273$$y2024
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