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Verfasst von:Erdinger, Susanne [VerfasserIn]   i
 Amrein, Irmgard [VerfasserIn]   i
 Back, Michaela [VerfasserIn]   i
 Ludewig, Susann [VerfasserIn]   i
 Korte, Martin [VerfasserIn]   i
 Engelhardt, Jakob von [VerfasserIn]   i
 Wolfer, David P. [VerfasserIn]   i
 Müller, Ulrike C. [VerfasserIn]   i
Titel:Lack of APLP1 leads to subtle alterations in neuronal morphology but does not affect learning and memory
Verf.angabe:Susanne Erdinger, Irmgard Amrein, Michaela Back, Susann Ludewig, Martin Korte, Jakob von Engelhardt, David P. Wolfer and Ulrike C. Müller
E-Jahr:2022
Jahr:28 October 2022
Umfang:15 S.
Fussnoten:Gesehen am 19.12.2022
Titel Quelle:Enthalten in: Frontiers in molecular neuroscience
Ort Quelle:Lausanne : Frontiers Research Foundation, 2008
Jahr Quelle:2022
Band/Heft Quelle:15(2022), Artikel-ID 1028836, Seite 1-15
ISSN Quelle:1662-5099
Abstract:The amyloid precursor protein APP plays a crucial role in Alzheimer pathogenesis. Its physiological functions, however, are only beginning to be unraveled. APP belongs to a small gene family, including besides APP the closely related amyloid precursor-like proteins APLP1 and APLP2, that all constitute synaptic adhesion proteins. While APP and APLP2 are ubiquitously expressed, APLP1 is specific for the nervous system. Previous genetic studies, including combined knockouts of several family members, pointed towards a unique role for APLP1, as only APP/APLP1 double knockouts were viable. We now examined brain and neuronal morphology in APLP1 single knockout (KO) animals, that have to date not been studied in detail. Here, we report that APLP1-KO mice show normal spine density in hippocampal CA1 pyramidal cells and subtle alterations in dendritic complexity. Extracellular field recordings revealed normal basal synaptic transmission and no alterations in synaptic plasticity (LTP). Further, behavioral studies revealed in APLP1-KO mice a small deficit in motor function and reduced diurnal locomotor activity, while learning and memory were not affected by the loss of APLP1. In summary, our study indicates that APP family members serve both distinct and overlapping functions that need to be considered for therapeutic treatments of Alzheimer’s disease.
DOI:doi:10.3389/fnmol.2022.1028836
URL:kostenfrei: Volltext: https://doi.org/10.3389/fnmol.2022.1028836
 kostenfrei: Volltext: https://www.frontiersin.org/articles/10.3389/fnmol.2022.1028836
 DOI: https://doi.org/10.3389/fnmol.2022.1028836
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Alzheimer disease
 amyloid precursor like protein
 amyloid precursor protein
 aplp1
 app
 apps-alpha
 behavior
 deficits
 dendritic spines
 family
 generation
 learning
 long-term potentiation
 members
 memory
 mice lacking
 synaptic plasticity
 synaptic plasticity
K10plus-PPN:1827921781
Verknüpfungen:→ Zeitschrift
 
 
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