ArticleGenetics and molecular biology2013
Neural restrictive silencer factor and choline acetyltransferase expression in cerebral tissue of Alzheimer's Disease patients: A pilot study.
Article in Genetics and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- The Dynamic Roles of Repressor Element 1-Silencing Transcription Factor (REST): A Double-Edged Sword in Neural Health and Disease.Molecular neurobiology · 2025Review
- MicroRNA-153-3p targets repressor element 1-silencing transcription factor (REST) and neuronal differentiation: Implications for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- REST Is Not Resting: REST/NRSF in Health and Disease.Biomolecules · 2023Review
- A Mixture ofPlants (Basel, Switzerland) · 2023Article
- Influence of a genetic variant of CHAT gene over the profile of plasma soluble ChAT in Alzheimer disease.Genetics and molecular biology · 2020Article
- RE1-silencing transcription factor controls the acute-to-chronic neuropathic pain transition andThe Journal of biological chemistry · 2018Article
- The Stress-Responding miR-132-3p Shows Evolutionarily Conserved Pathway Interactions.Cellular and molecular neurobiology · 2018Article
- Molecular mechanisms regulating the defects in fragile X syndrome neurons derived from human pluripotent stem cells.Stem cell reports · 2015Article
- ChIP-Seq Data Mining: Remarkable Differences in NRSF/REST Target Genes between Human ESC and ESC-Derived Neurons.Bioinformatics and biology insights · 2013Article
- Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Decreased Choline Acetyltransferase (ChAT) brain level is one of the main biochemical disorders in Alzheimer's Disease (AD). In rodents, recent data show that the CHAT gene can be regulated by a neural restrictive silencer factor (NRSF). The aim of the present work was to evaluate the gene and protein expression of CHAT and NRSF in frontal, temporal, entorhinal and parietal cortices of AD patient brains. Four brains from patients with AD and four brains from subjects without dementia were studied. Cerebral tissues were obtained and processed by the guanidine isothiocyanate method for RNA extraction. CHAT and NRSF gene and protein expression were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. CHAT gene expression levels were 39% lower in AD patients as compared to the control group (p < 0.05, U test). ChAT protein levels were reduced by 17% (p = 0.02, U test). NRSF gene expression levels were 86% higher in the AD group (p = 0.001, U test) as compared to the control group. In the AD subjects, the NRSF protein levels were 57% higher (p > 0.05, U test) than in the control subjects. These findings suggest for the first time that in the brain of AD patients high NRSF protein levels are related to low CHAT gene expression levels.
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