A5001922762- Alzheimer's disease research and treatments
- Neuroscience and Neuropharmacology Research
- Genetics and Neurodevelopmental Disorders
- Barrier Structure and Function Studies
- Nuclear Receptors and Signaling
- Advanced Neuroimaging Techniques and Applications
- Neurogenesis and neuroplasticity mechanisms
- Cancer-related Molecular Pathways
- Ubiquitin and proteasome pathways
- Cholinesterase and Neurodegenerative Diseases
- Neuroinflammation and Neurodegeneration Mechanisms
- Signaling Pathways in Disease
- Connexins and lens biology
Heidelberg University
2018-2023
University of Kaiserslautern
2016
Zero to Three
2016
Article16 April 2018free access Source DataTransparent process Distinct in vivo roles of secreted APP ectodomain variants APPsα and APPsβ regulation spine density, synaptic plasticity, cognition Max C Richter Institute Pharmacy Molecular Biotechnology (IPMB), Ruprecht-Karls University Heidelberg, Germany Search for more papers by this author Susann Ludewig Zoological Institute, Division Cellular Neurobiology, TU Braunschweig, Alex Winschel Department Biology, Neurophysiology und Neurosensory...
The physiological role of the amyloid-precursor protein (APP) is insufficiently understood. Recent work has implicated APP in regulation synaptic plasticity. Substantial evidence exists for a and its secreted ectodomain APPsα Hebbian Here, we addressed relevance homeostatic plasticity using organotypic tissue cultures prepared from <i>APP</i><sup>−/−</sup> mice both sexes. In absence APP, dentate granule cells failed to strengthen their excitatory synapses homeostatically. Homeostatic...
Astrocytes form large gap junctional networks that contribute to ion and neurotransmitter homeostasis. concentrate in the lateral superior olive (LSO), a prominent auditory brainstem center. Compared LSO, astrocyte density is lower region dorsal LSO (dLSO) internuclear space between paraolivary nucleus (SPN). We questioned whether exhibit certain properties reflect precise neuronal arrangement. Employing whole‐cell patch‐clamp concomitant injection of junction‐permeable tracer, we analyzed...
The Tau protein can be phosphorylated by numerous kinases. In Alzheimer’s disease (AD) hyperphosphorylated species accumulate as neurofibrillary tangles that constitute a major hallmark of AD. AD is further characterized extracellular Aβ plaques, derived from the β-amyloid precursor APP. Whereas produced amyloidogenic APP processing, processing along competing non-amyloidogenic pathway results in secretion neurotrophic and synaptotrophic APPsα. Recently, we demonstrated APPsα has therapeutic...
Alzheimer9s disease (AD) is histopathologically characterized by Aβ plaques and the accumulation of hyperphosphorylated Tau species, latter also constituting key hallmarks primary tauopathies. Whereas produced amyloidogenic APP processing, processing along competing nonamyloidogenic pathway results in secretion neurotrophic synaptotrophic APPsα. Recently, we demonstrated that APPsα has therapeutic effects transgenic AD model mice rescues Aβ-dependent impairments. Here, examined potential to...
Significance Ca 2+ dysfunction is correlated to the progression of Alzheimer’s disease; mechanistic insight into physiological role amyloid precursor protein (APP) for homeostasis still missing. We demonstrate that loss APP and its homolog APLP2, but not APLP2 alone, impairs handling synaptic plasticity because altered function endoplasmic reticulum stores caused by expression SERCA-ATPase as well store-operated channel–associated proteins Stim1 Stim2. Long-term APPsα ectodomain restored...
ABSTRACT The physiological role of the amyloid-precursor protein (APP) is insufficiently understood. Recent work has implicated APP in regulation synaptic plasticity. Substantial evidence exists for a and its secreted ectodomain APPsα Hebbian Here, we addressed relevance homeostatic plasticity using organotypic tissue cultures −/− mice. In absence APP, dentate granule cells failed to strengthen their excitatory synapses homeostatically. Homeostatic rescued by amyloid-β (Aβ) not APPsα, it...
A large body of evidence indicates a neuroprotective and neurotrophic function for APPs⍺ not only in vitro, but also when expressed by AAV vectors vivo such as APP/PS1 transgenic AD model mice with Aβ-induced pathology. Previously, we could show that rescued deficits synaptic plasticity spine density reduced plaque deposition. Thus, it is crucial to test more general applicability treatment assess whether beneficial tau-induced