Over the last ten years, scientists have developed a method called targeted memory reactivation (TMR) for selectively strengthening memories during sleep. Prior to this, memory manipulation during sleep was at most a plot device in science fiction movies, but a large corpus of studies now demonstrates that TMR is both reliable and effective. TMR studies hypothesize that this method taps into normal consolidation mechanisms that require the repeated replay of memories during sleep. This idea has recently been supported by several new studies demonstrating that TMR upregulates the reactivation of cued memories, and that such upregulation predicts subsequent memory performance. This new body of work provides a unique window onto many properties of memory reactivation and helps to close the gap between our understanding of replay in rodents, where it has been visualised at the neural level for many years, and humans, where such studies are only just starting to become possible. We will discuss this new literature and highlight the vast potential of these new methods for future research.
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http://dx.doi.org/10.1016/j.cub.2019.08.019 | DOI Listing |
Nat Struct Mol Biol
January 2025
IGMM, University of Montpellier, CNRS, Montpellier, France.
Random X-chromosome inactivation is a hallmark of female mammalian somatic cells. This epigenetic mechanism, mediated by the long noncoding RNA Xist, occurs in the early embryo and is stably maintained throughout life, although inactivation is lost during primordial germ cell (PGC) development. Using a combination of single-cell allele-specific RNA sequencing and low-input chromatin profiling on developing mouse PGCs, we provide a detailed map of X-linked gene reactivation.
View Article and Find Full Text PDFJ Infect Dev Ctries
December 2024
Department of Immunology, School of Medicine and Dr. Jose Eleuterio Gonzalez University Hospital, Universidad Autónoma de Nuevo León, Monterrey, Mexico.
Co-inhibitory molecules, such as cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1), known as immune checkpoints, regulate the activity of T and myeloid cells during chronic viral infections and are well-established for their roles in cancer therapy. However, their involvement in chronic bacterial infections, particularly those caused by pathogens endemic to developing countries, such as Mycobacterium tuberculosis (Mtb), remains incompletely understood. Cytokine microenvironment determines the expression of co-inhibitory molecules in tuberculosis: Results indicate that the cytokine IL-12, in the presence of Mtb antigens, can enhance the expression of co-inhibitory molecules while preserving the effector and memory phenotypes of CD4+ T cells.
View Article and Find Full Text PDFVision Res
January 2025
School of Psychological and Cognitive Sciences, and Beijing Key Laboratory of Behavior and Mental Health, Peking University, Beijing, China. Electronic address:
Visual perceptual learning often requires a substantial number of trials to observe significant learning effects. Previously Amar-Halpert et al. (2017) have shown that brief reactivation (5 trials/day) is sufficient to improve the performance of the texture discrimination task (TDT), yielding comparable improvements to those achieved through full practice (252 trials/day).
View Article and Find Full Text PDFSci Rep
January 2025
INSERM, Bergonié Institute, BPH, U1219, CIC-P 1401, University of Bordeaux, Bordeaux, France.
In vitro and animal studies have suggested that inoculation with herpes simplex virus 1 (HSV-1) can lead to amyloid deposits, hyperphosphorylation of tau, and/or neuronal loss. Here, we studied the association between HSV-1 and Alzheimer's disease biomarkers in humans. Our sample included 182 participants at risk of cognitive decline from the Multidomain Alzheimer Preventive Trial who had HSV-1 plasma serology and an amyloid PET scan.
View Article and Find Full Text PDFCell Mol Biol Lett
January 2025
PhD Program in Medical Neuroscience, Taipei Medical University, Taipei, Taiwan (R.O.C.).
Background: Regulation of messenger RNA (mRNA) transport and translation in neurons is essential for dendritic plasticity and learning/memory development. The trafficking of mRNAs along the hippocampal neuron dendrites remains translationally silent until they are selectively transported into the spines upon glutamate-induced receptor activation. However, the molecular mechanism(s) behind the spine entry of dendritic mRNAs under metabotropic glutamate receptor (mGluR)-mediated neuroactivation and long-term depression (LTD) as well as the fate of these mRNAs inside the spines are still elusive.
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