Literature DB >> 2955849

Sparing of acetylcholinesterase-containing striatal neurons in Huntington's disease.

R J Ferrante, M F Beal, N W Kowall, E P Richardson, J B Martin.   

Abstract

The present study demonstrates that large aspiny neurons, containing the enzyme acetylcholinesterase (AChE), are relatively preserved in the caudate nucleus and putamen in Huntington's disease (HD). Although histochemical evidence indicates that AChE and choline acetyltransferase (ChAT) co-localize within the same striatal neurons, measurements of ChAT activity showed significant reductions in enzyme activity, as others have reported. Reduced ChAT activity in the presence of presence of persistent AChE-positive neurons may be a consequence of loss of synaptic terminals resulting from the death of spiny neurons. The selectivity of neuronal sparing in HD may be related to the patterns of synaptic contact or a paucity of excitatory amino acid receptors on striatal aspiny neurons.

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Year:  1987        PMID: 2955849     DOI: 10.1016/0006-8993(87)90694-9

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


  43 in total

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4.  Large neostriatal neurons in humans and their possible role in neuronal networks.

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5.  Striatal neuronal loss correlates with clinical motor impairment in Huntington's disease.

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Review 6.  Functional Differences Between Direct and Indirect Striatal Output Pathways in Huntington's Disease.

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Review 7.  Cause or compensation?-Altered neuronal Ca2+ handling in Huntington's disease.

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8.  TrkB receptor controls striatal formation by regulating the number of newborn striatal neurons.

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9.  AAV vector-mediated RNAi of mutant huntingtin expression is neuroprotective in a novel genetic rat model of Huntington's disease.

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10.  Regionally selective atrophy of subcortical structures in prodromal HD as revealed by statistical shape analysis.

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Journal:  Hum Brain Mapp       Date:  2012-12-20       Impact factor: 5.038

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