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000136446 0247_ $$2doi$$a10.1016/j.bios.2011.12.026
000136446 0247_ $$2pmid$$apmid:22221799
000136446 0247_ $$2ISSN$$a0956-5663
000136446 0247_ $$2ISSN$$a1873-4235
000136446 037__ $$aDZNE-2020-02768
000136446 041__ $$aEnglish
000136446 082__ $$a610
000136446 1001_ $$aJahnke, Heinz-Georg$$b0
000136446 245__ $$aImpedance spectroscopy based measurement system for quantitative and label-free real-time monitoring of tauopathy in hippocampal slice cultures.
000136446 260__ $$aAmsterdam [u.a.]$$bElsevier Science$$c2012
000136446 264_1 $$2Crossref$$3print$$bElsevier BV$$c2012-02-01
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000136446 520__ $$aAlzheimer's disease (AD) and other tauopathies comprise death of cell bodies, synapses and neurites but there is surprising little knowledge of the temporal sequence and the causal relationships among these events. Here, we present a novel biosensoric approach to monitor retrograde neurite degeneration before cell death occurs. We induced tau hyperphosphorylation in organotypic hippocampal slice cultures (OHSC) and applied marker-independent real-time electrical impedance spectroscopy (EIS) for cellular real-time pathology monitoring. Using this approach, we were able to define two distinct phases of neurite degeneration, first a rapid swelling of axonal processes that manifests itself in relative impedance above control levels followed by a slower phase of collapse and subsequent fragmentation indicated by decreased relative impedance below control levels. Initial axon swelling is strictly dose-dependent and swelling intensity correlates with second phase impedance decrease implicating a causative link between both degenerative mechanisms. Moreover, suppressing tau hyperphosphorylation by kinase inhibition nearly prevented both phases of axon degeneration. Our findings demonstrate that the temporal sequence of tau-triggered neurite degeneration can be directly visualized by EIS-based, non-invasive and label-free monitoring. We therefore suggest this approach as a powerful extension of high content applications to study mechanisms of neurite degeneration and to exploit therapeutic options against AD and tau-related disorders.
000136446 536__ $$0G:(DE-HGF)POF3-342$$a342 - Disease Mechanisms and Model Systems (POF3-342)$$cPOF3-342$$fPOF III$$x0
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000136446 650_7 $$2NLM Chemicals$$aCarbazoles
000136446 650_7 $$2NLM Chemicals$$aEnzyme Inhibitors
000136446 650_7 $$2NLM Chemicals$$aSRN 003-556
000136446 650_7 $$2NLM Chemicals$$atau Proteins
000136446 650_2 $$2MeSH$$aAnimals
000136446 650_2 $$2MeSH$$aBiosensing Techniques: instrumentation
000136446 650_2 $$2MeSH$$aCarbazoles: pharmacology
000136446 650_2 $$2MeSH$$aCells, Cultured
000136446 650_2 $$2MeSH$$aDielectric Spectroscopy: instrumentation
000136446 650_2 $$2MeSH$$aEnzyme Inhibitors: pharmacology
000136446 650_2 $$2MeSH$$aEquipment Design
000136446 650_2 $$2MeSH$$aHippocampus: cytology
000136446 650_2 $$2MeSH$$aNeurites: drug effects
000136446 650_2 $$2MeSH$$aNeurites: pathology
000136446 650_2 $$2MeSH$$aRats
000136446 650_2 $$2MeSH$$aRats, Sprague-Dawley
000136446 650_2 $$2MeSH$$aTauopathies: drug therapy
000136446 650_2 $$2MeSH$$aTauopathies: pathology
000136446 650_2 $$2MeSH$$atau Proteins: antagonists & inhibitors
000136446 7001_ $$aBraesigk, Annett$$b1
000136446 7001_ $$0P:(DE-2719)9000424$$aMack, Till G A$$b2$$udzne
000136446 7001_ $$aPönick, Sarah$$b3
000136446 7001_ $$0P:(DE-2719)9000420$$aStriggow, Frank$$b4$$udzne
000136446 7001_ $$0P:(DE-HGF)0$$aRobitzki, Andrea A$$b5$$eCorresponding author
000136446 77318 $$2Crossref$$3journal-article$$a10.1016/j.bios.2011.12.026$$b : Elsevier BV, 2012-02-01$$n1$$p250-258$$tBiosensors and Bioelectronics$$v32$$x0956-5663$$y2012
000136446 773__ $$0PERI:(DE-600)1496379-6$$a10.1016/j.bios.2011.12.026$$gVol. 32, no. 1, p. 250 - 258$$n1$$p250-258$$q32:1<250 - 258$$tBiosensors and bioelectronics$$v32$$x0956-5663$$y2012
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000136446 9141_ $$y2012
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