Document Detail


Role of Presenilin1 in Structural Plasticity of Cortical Dendritic Spines in vivo.
MedLine Citation:
PMID:  21951279     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Mutations in presenilins are the major cause of familial Alzheimer's disease (FAD), leading to impairments of memory and synaptic plasticity followed by age-dependent neurodegeneration. Presenilins are the catalytic subunits of γ-secretase, which itself is critically involved in the processing of amyloid precursor protein (APP) to release neurotoxic amyloidβ (Aβ). Besides Aβ generation, there is growing evidence that presenilins play an essential role in the formation and maintenance of synapses. To further elucidate the effect of presenilin1 (PS1) on synapses, we performed longitudinal in vivo two-photon imaging of dendritic spines in the somatosensory cortex of transgenic mice overexpressing either human wildtype PS1 (hPS1) or the FAD-mutated variant A246E (FAD-PS1). Interestingly, the consequences of transgene expression were different in two subtypes of cortical dendrites. On apical layer 5 dendrites we found an enhanced spine density in both hPS1 and FAD-PS1, whereas on basal layer 3 dendrites only overexpression of FAD-PS1 increased the spine density. Time-lapse imaging revealed no differences in kinetically distinct classes of dendritic spines nor was the shape of spines affected. While γ-secretase dependent processing of synapse-relevant proteins seemed to be unaltered, higher expression levels of ryanodine receptors suggest a modified Ca(2+) homeostasis in PS1 overexpressing mice. On the other hand, the conditional depletion of PS1 in single cortical neurons had no observable impact on dendritic spines. In consequence our results favor the view that PS1 influences dendritic spine plasticity in a gain-of-function but γ-secretase independent manner.
Authors:
Christian Ke Jung; Martin Fuhrmann; Kamran Honarnejad; Fred Van Leuven; Jochen Herms
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-9-27
Journal Detail:
Title:  Journal of neurochemistry     Volume:  -     ISSN:  1471-4159     ISO Abbreviation:  -     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-9-28     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Journal of Neurochemistry © 2011 International Society for Neurochemistry.
Affiliation:
Center for Neuropathology and Prion Research, Laboratory of Experimental Neuropathology, Ludwig-Maximilian-University; Feodor-Lynen-Str. 23, 81377 Munich, Germany German Center for Neurodegenerative Diseases; Ludwig-Erhard-Allee 2, 53175 Bonn, Germany Experimental Genetics Group, KULeuven-Campus Gasthuisberg; O&N I Herestraat 49 - box 602, 3000 Leuven, Belgium.
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