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Tau, APP, NCT and BACE1 in lymphocytes through cognitively normal ageing and neuropathology 42
HERRERA-RIVERO,MARISOL; SOTO-CID,ABRAHAM; HERNáNDEZ,MARíA E.; ARANDA-ABREU,GONZALO E..
Although Alzheimer's disease is a brain disorder, a number of peripheral alterations have been found in these patients; however, little is known about how the key genes involved in the pathophysiology express in peripheral cells such as lymphocytes during normal compared to neuropathological ageing. We analysed the expression of tau, of the amyloid precursor protein, of nicastrin and of the β-site APP cleaving enzyme genes by RT-PCR in lymphocytes from a small group of late-onset Alzheimer's disease patients, from aged patients suffering from neuropsychological conditions different from Alzheimer's and from cognitively healthy subjects divided in four groups by age. We also investigated correlations between gene expression and levels of blood pressure,...
Tipo: Info:eu-repo/semantics/article Palavras-chave: Alzheimer's disease; APP; BACE1; Nicastrin; Normal ageing; Risk factors.
Ano: 2013 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652013000401489
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Abeta(1-42) induces abnormal alternative splicing of tau exons 2/3 in NGF-induced PC12 cells 42
LAGUNES,TERESA; HERRERA-RIVERO,MARISOL; HERNÁNDEZ-AGUILAR,MARÍA ELENA; ARANDA-ABREU,GONZALO E..
Protein tau plays a pivotal role in the pathophysiology of Alzheimer's disease, where its hyperphos-phorylation promotes aggregation and microtubule destabilization. Tau undergoes alternative splicing which generates six isoforms in the human brain, due to inclusion/exclusion of exons 2, 3 and 10. Dysregulation of the splicing process of tau exon 10 is sufficient to cause tauopathy and has shown to be influenced by beta-amyloid peptides, but splicing of other exons is less studied. We studied the effects of beta-amyloid(42) in the alternative splicing of tau exons 2/3 and 6, using untreated and Nerve Growth Factor-induced PC12 cells. Beta-amyloid exposure caused formed cell processes to retract in differentiated cells and altered the expression of exons...
Tipo: Info:eu-repo/semantics/article Palavras-chave: Alzheimer's disease; Amyloid peptide; Splicing regulation; Tau isoforms.
Ano: 2014 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652014000401927
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