Striatal atrophy and dendritic alterations in a knock-in mouse model of Huntington's disease

Highlights ► Here, we show striatal atrophy is already present at 12 months in CAG140 KI mice. ► We also show late-disease-stage (20–26 m) atrophy in white matter in CAG140 KI mice. ► Late-disease-stage KI striatal neurons display extensive morphological degeneration. ► DA input may be altered in la...

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Bibliographic Details
Published in:Brain research bulletin 2012-04, Vol.87 (6), p.571-578
Main Authors: Lerner, Renata P, Trejo Martinez, Luz del Carmen G, Zhu, Chunni, Chesselet, Marie-Françoise, Hickey, Miriam A
Format: Article
Language:English
Subjects:
Age Factors
Analysis of Variance
Animals
Atrophy - etiology
Atrophy - pathology
Brain - pathology
Cell Count
Corpus callosum
Corpus Striatum - pathology
Cortex
Dendrites - pathology
Dendrites - ultrastructure
Disease Models, Animal
Female
Golgi stain
Humans
Huntingtin
Huntingtin Protein
Huntington Disease - complications
Huntington Disease - pathology
Male
Mice
Mice, Transgenic
Nerve Tissue Proteins - genetics
Neurology
Neurons - pathology
Neurons - ultrastructure
Sex Factors
Silver Staining
Stereology
Trinucleotide Repeat Expansion - genetics
Tyrosine 3-Monooxygenase - metabolism
Volume
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Summary:Highlights ► Here, we show striatal atrophy is already present at 12 months in CAG140 KI mice. ► We also show late-disease-stage (20–26 m) atrophy in white matter in CAG140 KI mice. ► Late-disease-stage KI striatal neurons display extensive morphological degeneration. ► DA input may be altered in late-disease-stage KI striatum, as striatal TH is reduced. ► CAG140 KI mice are highly suited for testing neuroprotective therapies.
ISSN:0361-9230
1873-2747
DOI:10.1016/j.brainresbull.2012.01.012