Neuroscience
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The perirhinal cortex (PRH) is considered a crucial cortical area for familiarity memory and electrophysiological studies have reported the presence of visual familiarity encoding neurons in PRH. However, recent evidence has questioned the existence of these neurons. ⋯ However, the PRH showed no response modulation with respect to familiarity under a variety of different conditions or retention delays. These results indicate that the PRH does not contribute to familiarity/novelty encoding using passively exposed visual stimuli.
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Alzheimer's disease (AD) is the most common cause of dementia in the elderly, characterized by progressive cognitive dysfunction. Aquaporin 9 (AQP9) is an aquaglyceroporin membrane channel shown biophysically to conduct water, glycerol, and other small solutes. In our study, we reported for the first time an age-associated decrease in AQP9 mRNA and protein expressions in both hippocampus and cerebral cortex of APPswe/PS1dE9 (Tg) AD mice at 3, 6 and 10 months of age. ⋯ Pre-treatment with AQP9 small interfering RNA led to a more severe neurotoxicity in PC12 cells in response to Aβ1-40. Furthermore, we corroborated that the active participation of AQP9 in AD progression is associated with Aβ-induced apoptosis both in vitro and in vivo. Taken together, our results reveal an important role of AQP9 in Aβ-induced pathogenesis of AD which deserves further investigation.
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Audiovisual cuts involve spatial, temporal, and action narrative leaps. They can even change the meaning of the narrative through film editing. Many cuts are not consciously perceived, others are, just as we perceive or not the changes in real events. ⋯ This was reflected by differences in the theta rhythm between 200 and 400 ms, in visual and frontal zones, and can be connected to the different demands that each style of edition makes on working memory and conscious processing after cutting. Also, at the time of cuts, the causality between visual, somatosensory, and frontal networks is altered in any editing style. Our findings suggest that cuts affect media perception and chaotic and fast audiovisuals increase attentional scope but decrease conscious processing.
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Apolipoprotein E4 (apoE4), one of the three apoE isoforms, is the strongest factor for raising the risk for late-onset Alzheimer's disease (AD) and has been proposed to play a major role in AD pathogenesis. Amyloid-peptide β 42 (Aβ42) has also been proposed to affect neuronal degeneration and AD pathogenesis, possibly by interacting with apoE. Previous studies have shown that the functions of apoE forms can be dictated by their structural and biophysical properties. ⋯ Structural and thermodynamic analyses showed that all three apoE4 mutants have significantly increased α-helical and decreased β-sheet content, have reduced portion of hydrophobic surfaces exposed to the solvent and have a reduced conformational stability during chemical denaturation. Overall, our data highlight a pathogenic role of apoE4 that could be linked to the capacity of the protein to form oligomeric species especially in the presence of Aβ42 and to induce cytotoxicity. Carboxyl-terminal residues L279, K282 or Q284 appear to be involved in the conformation of apoE4 that may underlie the protein's functional properties related to neurotoxicity.
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Neuropathic pain is associated with gene expression changes within the dorsal root ganglion (DRG) after peripheral nerve injury, which involves epigenetic mechanisms. Coactivator-associated arginine methyltransferase 1 (CARM1), an epigenetic activator, regulates gene transcriptional activity by protein posttranslational modifications. ⋯ Furthermore, pharmacological inhibition of CARM1 mitigated peripheral nerve injury-induced mechanical allodynia and thermal hyperalgesia. Given that CARM1 inhibition or knockdown attenuated the induction and maintenance of neuropathic pain after peripheral nerve injury, our findings suggest that CARM1 may serve as a promising therapeutic target for neuropathic pain treatment in clinical applications.