Amyloid β induces interneuron-specific changes in the hippocampus of APPNL-F mice

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by cognitive decline and amyloid-beta (Aβ) depositions generated by the proteolysis of amyloid precursor protein (APP) in the brain. In APPNL-F mice, APP gene was humanized and contains two familial AD mutations, and APP-unl...

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Veröffentlicht in:	PloS one 2020, Vol.15 (5), p.e0233700-e0233700
Hauptverfasser:	Sos, Katalin E, Mayer, Márton I, Takács, Virág T, Major, Abel, Bardóczi, Zsuzsanna, Beres, Barnabas M, Szeles, Tamás, Saito, Takashi, Saido, Takaomi C, Mody, István, Freund, Tamás F, Nyiri, Gábor
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer Disease - genetics Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amyloid beta-Peptides - genetics Amyloid beta-Peptides - metabolism Amyloid precursor protein Amyloidosis Animal cognition Animal models Animals Axons Axons - metabolism Axons - pathology Biology and Life Sciences Brain Cognitive ability Dementia Electron microscopy Excitability Experiments Hippocampus Hippocampus - metabolism Hippocampus - pathology Humans Immunohistochemistry Inflammation Interneurons Interneurons - metabolism Interneurons - pathology Laboratories Medical research Medicine Medicine and Health Sciences Memory Memory, Short-Term Mice Mice, Transgenic Mutation Nerve Net - metabolism Nerve Net - pathology Neurobiology Neurodegenerative diseases Neurons Neurosciences Parvalbumin Peptide Fragments - genetics Peptide Fragments - metabolism Perineuronal nets Photovoltaic cells Proteins Proteolysis Pyramidal Cells - metabolism Pyramidal Cells - pathology Receptors, GABA-A - genetics Receptors, GABA-A - metabolism Research and Analysis Methods Scanning electron microscopy Senile plaques Short term memory Somatostatin Synapses Transgenic animals γ-Aminobutyric acid A receptors
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