Neurogenesis In The R6/2 Mouse Model Of Huntington'S Disease Is Impaired At The Level Of Neurod1
(2011) In Neuroscience 173. p.76-81- Abstract
- Adult neurogenesis is impaired in the hippocampus of transgenic R6 mouse models of Huntington's disease (HD). The phenotypes of R6 transgenic mice mimic several symptoms and signs of the disease (Li et al., 2005). They exhibit neurological and endocrine changes resembling some symptoms seen in humans. The reduction in neurogenesis is only apparent in the dentate gyrus as the number of newborn neurons in the subventricular zone, and olfactory bulb, is normal in R6 mice. The mechanism(s) underlying the reduction in hippocampal neurogenesis is still not fully understood. Here we show that the number of neuroblasts, but not granule neuron progenitors, is greatly reduced in 11-week old transgenic mice compared with wild-type (WT) controls. We... (More)
- Adult neurogenesis is impaired in the hippocampus of transgenic R6 mouse models of Huntington's disease (HD). The phenotypes of R6 transgenic mice mimic several symptoms and signs of the disease (Li et al., 2005). They exhibit neurological and endocrine changes resembling some symptoms seen in humans. The reduction in neurogenesis is only apparent in the dentate gyrus as the number of newborn neurons in the subventricular zone, and olfactory bulb, is normal in R6 mice. The mechanism(s) underlying the reduction in hippocampal neurogenesis is still not fully understood. Here we show that the number of neuroblasts, but not granule neuron progenitors, is greatly reduced in 11-week old transgenic mice compared with wild-type (WT) controls. We demonstrate that NeuroD1 expression is reduced in the hippocampus. This is coupled to a decreased expression of downstream markers doublecortin and calretinin in maturing neurons. Taken together, our results suggest that mutant huntingtin (Htt) causes alterations of proteins expression in hippocampal progenitors, which might contribute to cognitive deficits in Huntington's disease. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1790685
- author
- Fedele, Valentina LU ; Roybon, Laurent LU ; Nordström, Ulrika LU ; Li, Jia-Yi LU and Brundin, Patrik LU
- organization
- publishing date
- 2011
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- huntingtin, hippocampus, neuroblasts, transcriptional dysregulation, transgenic mice
- in
- Neuroscience
- volume
- 173
- pages
- 76 - 81
- publisher
- Elsevier
- external identifiers
-
- wos:000286487000006
- scopus:78650677351
- ISSN
- 1873-7544
- DOI
- 10.1016/j.neuroscience.2010.08.022
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Neuronal Survival (013212041), Neural Plasticity and Repair (013210080)
- id
- b6ba6f80-6526-470b-9a76-2f9945db6c73 (old id 1790685)
- date added to LUP
- 2016-04-01 11:09:03
- date last changed
- 2022-04-20 17:28:13
@article{b6ba6f80-6526-470b-9a76-2f9945db6c73, abstract = {{Adult neurogenesis is impaired in the hippocampus of transgenic R6 mouse models of Huntington's disease (HD). The phenotypes of R6 transgenic mice mimic several symptoms and signs of the disease (Li et al., 2005). They exhibit neurological and endocrine changes resembling some symptoms seen in humans. The reduction in neurogenesis is only apparent in the dentate gyrus as the number of newborn neurons in the subventricular zone, and olfactory bulb, is normal in R6 mice. The mechanism(s) underlying the reduction in hippocampal neurogenesis is still not fully understood. Here we show that the number of neuroblasts, but not granule neuron progenitors, is greatly reduced in 11-week old transgenic mice compared with wild-type (WT) controls. We demonstrate that NeuroD1 expression is reduced in the hippocampus. This is coupled to a decreased expression of downstream markers doublecortin and calretinin in maturing neurons. Taken together, our results suggest that mutant huntingtin (Htt) causes alterations of proteins expression in hippocampal progenitors, which might contribute to cognitive deficits in Huntington's disease. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.}}, author = {{Fedele, Valentina and Roybon, Laurent and Nordström, Ulrika and Li, Jia-Yi and Brundin, Patrik}}, issn = {{1873-7544}}, keywords = {{huntingtin; hippocampus; neuroblasts; transcriptional dysregulation; transgenic mice}}, language = {{eng}}, pages = {{76--81}}, publisher = {{Elsevier}}, series = {{Neuroscience}}, title = {{Neurogenesis In The R6/2 Mouse Model Of Huntington'S Disease Is Impaired At The Level Of Neurod1}}, url = {{http://dx.doi.org/10.1016/j.neuroscience.2010.08.022}}, doi = {{10.1016/j.neuroscience.2010.08.022}}, volume = {{173}}, year = {{2011}}, }