Roberto Carlos Agis-Balboa

TL;DR: It is shown that memory disturbances in the aging brain of the mouse are associated with altered hippocampal chromatin plasticity, and data suggest that deregulated H4K12 acetylation may represent an early biomarker of an impaired genome-environment interaction in the Aging mouse brain.

TL;DR: It is demonstrated that 5α-R type I and 3α-HSD colocalize in cortical, hippocampal, and olfactory bulb glutamatergic principal neurons and in some output neurons of the amygdala and thalamus, and data suggest that ALLO and THDOC modulate GABA action at GABAA receptors, either with an autocrine or a paracrine mechanism or by reaching GabAA receptor intracellular sites through lateral membrane diffusion.

TL;DR: The data suggest that miR‐34c could be a marker for the onset of cognitive disturbances linked to AD and indicate that targeting miR-34ccould be a suitable therapy.

TL;DR: It is shown that severe amyloid pathology correlates with a pronounced dysregulation of histone acetylation in the forebrain of APPPS1-21 mice, and prolonged treatment with the pan-HDAC inhibitor sodium butyrate improved associative memory in APPPS 1- 21 mice even when administered at a very advanced stage of pathology.

TL;DR: In these mice the histone deacetylase inhibitor valproate, which increases acetylated histone content in cortical GABAergic interneurons, also prevents MET-induced RELN promoter hypermethylation and reduces the methyl-CpG binding domain protein binding to RELN and GAD67 promoters.