Home > Publications Database > Localized APP expression results in progressive network dysfunction by disorganizing spike timing. > print

001     266787
005     20240808170119.0
024 7 _ |a pmc:PMC10877582
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024 7 _ |a 10.1016/j.neuron.2023.10.001
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024 7 _ |a pmid:37909036
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024 7 _ |a 0896-6273
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024 7 _ |a 1097-4199
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037 _ _ |a DZNE-2024-00045
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Viana-da-Silva, Silvia
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245 _ _ |a Localized APP expression results in progressive network dysfunction by disorganizing spike timing.
260 _ _ |a New York, NY
|c 2024
|b Elsevier
336 7 _ |a article
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520 _ _ |a Progressive 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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650 _ 2 |a Mice
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650 _ 2 |a Humans
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650 _ 2 |a Animals
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650 _ 2 |a Aged
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650 _ 2 |a Amyloid beta-Protein Precursor: genetics
|2 MeSH
650 _ 2 |a Amyloid beta-Protein Precursor: metabolism
|2 MeSH
650 _ 2 |a Hippocampus: metabolism
|2 MeSH
650 _ 2 |a Neurons: physiology
|2 MeSH
650 _ 2 |a Alzheimer Disease: metabolism
|2 MeSH
650 _ 2 |a Synapses: physiology
|2 MeSH
650 _ 2 |a Mice, Transgenic
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650 _ 7 |a Alzheimer’s disease
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650 _ 7 |a Alzheimer’s disease
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650 _ 7 |a Alzheimer’s disease
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650 _ 7 |a Alzheimer’s disease
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650 _ 7 |a Alzheimer’s disease
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650 _ 7 |a Alzheimer’s disease
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650 _ 7 |a amyloid precursor protein
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650 _ 7 |a hippocampus
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650 _ 7 |a phase precession
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650 _ 7 |a spike timing
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650 _ 7 |a theta oscillations
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650 _ 7 |a Amyloid beta-Protein Precursor
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700 1 _ |a Haberl, Matthias
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700 1 _ |a Gaur, Kshitij
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700 1 _ |a Patel, Rina
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700 1 _ |a Narayan, Gautam
|b 4
700 1 _ |a Ledakis, Max
|b 5
700 1 _ |a Fu, Maylin L
|b 6
700 1 _ |a de Castro Vieira, Miguel
|b 7
700 1 _ |a Koo, Edward H
|b 8
700 1 _ |a Leutgeb, Jill K
|b 9
700 1 _ |a Leutgeb, Stefan
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773 _ _ |a 10.1016/j.neuron.2023.10.001
|g Vol. 112, no. 1, p. 124 - 140.e6
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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