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- W2897212512 abstract "Lysine-specific demethylase 1 (LSD1) function as a transcriptional repressor or activator by demethylation of histone H3 on lysine 4 or 9 and regulates different physiological processes including inflammatory responses and learning and memory. In the present study, we investigate chronological hippocampal levels of LSD1 and its correlation with the expression of pro-inflammatory markers, analyzing simultaneously β-amyloid levels and cognitive performance of our transgenic AD-like rats. We used the hemizygous McGill-R-Thy1-APP transgenic rats, which progressively accumulates intraneuronal Aβ peptide and display cognitive deficits (Leon, et al. 2010). Posterior to cognitive status test assessed by Morris water maze, hippocampal β-amyloid accumulation, LSD1 levels and inflammatory protein markers expression were measured by western blot at different ages (3, 6, 12 and 18 months old) of non-transgenic (APP-/-) and hemizygous (APP+/-) transgenic rats. Increased levels of LSD1 at very early stages of the amyloid pathology (6 months old) in hippocampus of APP+/- transgenic rats displayed a positive correlation through age during the progression of Aβ pathology (Pearson r2=0.77 (6 months); 0.87 (12 months) and 0.82 (18 months), respectively p<0.05). Furthermore, we observe a strong positive correlation between LSD1 and the expression of certain inflammatory markers such as IL1- β, nNOS and Cox-2. Surprisingly, we found a negative correlation between hippocampal TNF-α levels and LSD-1 suggesting that increased protein expression of LSD1 may interfere negatively in TNF-α gene expression. Behavioral studies showed deficits in cognitive performance beginning at 18 months old of hemizygous transgenic rats compared to non-transgenic aged matched rats. In our model, hippocampal LSD1 levels begins to increase at very early stages of amyloid pathology, suggesting a possible epigenetic protective mechanism by which, transgenic rats, could trigger to preserve cognitive functions in response to the progressive β-amyloid accumulation. However, starting at 18 months of age, the excessive accumulation of Aβ display a positive correlation with cognitive deficits and also with LSD1 levels, not perceived at previous ages and not observed in non-transgenic age-matched controls. We reasoned that increased LSD1 expression would contribute to pro-inflammatory markers deregulation pointing LSD1 as a candidate target for further clinical manipulation." @default.
- W2897212512 created "2018-10-26" @default.
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- W2897212512 date "2018-07-01" @default.
- W2897212512 modified "2023-10-16" @default.
- W2897212512 title "P2‐189: CHRONOLOGICAL CORRELATION BETWEEN LSD1, β‐AMYLOID AND PRO‐INFLAMMATORY MARKERS WITH COGNITIVE PERFORMANCE IN AN AD‐LIKE TRANSGENIC RAT MODEL" @default.
- W2897212512 doi "https://doi.org/10.1016/j.jalz.2018.06.876" @default.
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