Despite decades of gene-centric approaches, the molecular mechanisms underlying these diseases remain widely elusive. Neurodegenerative diseases (NDs), including the most prevalent Alzheimer's disease and Parkinson disease, share common pathological features. Pearson correlation coefficient for each gene is depicted below the name of each gene. Statistical significance (P value threshold 0.05) for anti-Alu greater than control (depicted as asterisk, n = 3/group, unpaired directional t-test, error bars represent standard deviation from the mean). Based on the r and P value, genes were classified into four categories: (i) NS, non-significant for P value > 0.05, (ii) no correlation or weak correlation (r ≤ 0.05), (iii) significant (P 0.5) or only weakly/not correlated (right, r < 0.5).
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Statistical test is based on Pearson's product moment correlation coefficient and follows a t distribution using the cor.test function in R package stats. For every gene, a correlation coefficient was calculated (Pearson correlation) together with the respective P-value. A Correlation between gene expression and Alu RNA processing ratio for AD up-regulated genes (Dataset EV3) (upper panel) and a random set of non-differentially expressed genes (Dataset EV5) (lower panel). Overall, our data show that RNAs from SINE elements in the human brain show a similar pattern of deregulation during amyloid beta pathology as in mouse.Īlu RNA destabilization leads to increase in expression of Alu RNA processing correlated genes. In vitro assays show that processing of Alu RNAs is accelerated by HSF1. This increased processing correlates with the activation of genes up-regulated in AD patients, while increased intact Alu RNA levels correlate with down-regulated gene expression in AD. Here, we show that similar to mouse SINE RNAs, human Alu RNAs, are processed, and the processing rate is increased in brains of AD patients.
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They also possess self-cleaving activity that is accelerated through their interaction with certain proteins disabling this suppression. RNAs from SINE B2 repeats in mouse and SINE Alu repeats in humans, long regarded as "junk" DNA, control gene expression by binding RNA polymerase II and suppressing transcription. Here, we focus on the role of non-coding RNAs produced by small interspersed nuclear elements (SINEs). Despite significant steps in our understanding of Alzheimer's disease (AD), many of the molecular processes underlying its pathogenesis remain largely unknown.