Abstract | BACKGROUND: RESULTS: Here we followed the fate of single dendritic spines in the neocortex of a tauopathy mouse model, expressing human P301S mutated tau, for a period of two weeks. We observed a continuous decrease in spine density during disease progression, which we could ascribe to a diminished fraction of gained spines. Remaining spines were enlarged and elongated, thus providing evidence for morphological reorganization in compensation for synaptic dysfunction. Remarkably, loss of dendritic spines in cortical pyramidal neurons occurred in the absence of neurofibrillary tangles (NFTs). Therefore, we consider prefibrillar tau species as causative for the observed impairment in spine plasticity. CONCLUSIONS: Dendritic spine plasticity and morphology are altered in layer V cortical neurons of P301S tau transgenic mice in vivo. This does not coincide with the detection of hyperphosphorylated tau in dendritic spines.
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Authors | Nadine A Hoffmann, Mario M Dorostkar, Sonja Blumenstock, Michel Goedert, Jochen Herms |
Journal | Acta neuropathologica communications
(Acta Neuropathol Commun)
Vol. 1
Pg. 82
(Dec 17 2013)
ISSN: 2051-5960 [Electronic] England |
PMID | 24344647
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- MAPT protein, human
- tau Proteins
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Topics |
- Animals
- Cerebral Cortex
(pathology, physiopathology)
- Dendritic Spines
(pathology, physiology)
- Disease Models, Animal
- Immunohistochemistry
- Male
- Mice, Transgenic
- Microscopy, Confocal
- Mutation
- Neuronal Plasticity
(physiology)
- Pyramidal Cells
(pathology, physiopathology)
- Tauopathies
(genetics, physiopathology)
- tau Proteins
(genetics, metabolism)
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