Dendritic BC200 RNA in aging and in Alzheimer's disease

Small untranslated BC1 and BC200 RNAs are translational regulators that are selectively targeted to somatodendritic domains of neurons. They are thought to operate as modulators of local protein synthesis in postsynaptic dendritic microdomains, in a capacity in which they would contribute to the mai...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2007-06, Vol.104 (25), p.10679-10684
Main Authors: Mus, El, Hof, Patrick R, Tiedge, Henri
Format: Article
Language:English
Subjects:
Aged
Aged, 80 and over
Aging
Alzheimer Disease - genetics
Alzheimer's disease
Alzheimers disease
Biological Sciences
Brain
Calibration
Case-Control Studies
Cerebral Cortex - metabolism
Datasets
Dementia
Dendrites - chemistry
Gene Expression Regulation
Geriatric psychology
Hippocampus
Humans
In Situ Hybridization
Medical schools
Middle Aged
Nervous system diseases
Neurology
Neurons
Neurosciences
Ribonucleic acid
RNA
RNA Probes
RNA, Ribosomal - metabolism
RNA, Untranslated - genetics
RNA, Untranslated - metabolism
Tissue samples
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Summary:Small untranslated BC1 and BC200 RNAs are translational regulators that are selectively targeted to somatodendritic domains of neurons. They are thought to operate as modulators of local protein synthesis in postsynaptic dendritic microdomains, in a capacity in which they would contribute to the maintenance of long-term synaptic plasticity. Because plasticity failure has been proposed to be a starting point for the neurodegenerative changes that are seen in Alzheimer's disease (AD), we asked whether somatodendritic levels of human BC200 RNA are deregulated in AD brains. We found that in normal aging, BC200 levels in cortical areas were reduced by >60% between the ages of 49 and 86. In contrast, BC200 RNA was significantly up-regulated in AD brains, in comparison with age-matched normal brains. This up-regulation in AD was specific to brain areas that are involved in the disease. Relative BC200 levels in those areas increased in parallel with the progression of AD, as reflected by Clinical Dementia Rating scores. In more advanced stages of the disease, BC200 RNA often assumed a clustered perikaryal localization, indicating that dendritic loss is accompanied by somatic overexpression. Mislocalization and overexpression of BC200 RNA may be reactive-compensatory to, or causative of, synaptodendritic deterioration in AD neurons.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.0701532104