scholarly journals Epigenetic regulation of the circadian genePer1in the hippocampus mediates age-related changes in memory and synaptic plasticity

2018 ◽  
Author(s):  
Janine L. Kwapis ◽  
Yasaman Alaghband ◽  
Enikö A. Kramár ◽  
Alberto J. López ◽  
Annie Vogel Ciernia ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Circadian Clock ◽  
Clock Gene ◽  
Memory Performance ◽  
Activity Patterns ◽  
Memory Formation ◽  
Long Term Memory ◽  
Term Memory ◽  
Age Related

AbstractAging is accompanied by impairments in both circadian rhythmicity and long-term memory. Although it is clear that memory performance is affected by circadian cycling, it is unknown whether age-related disruption of the circadian clock causes impaired hippocampal memory. Here, we show that the repressive histone deacetylase HDAC3 restricts long-term memory, synaptic plasticity, and learning-induced expression of the circadian genePer1in the aging hippocampus without affecting rhythmic circadian activity patterns. We also demonstrate that hippocampalPer1is critical for long-term memory formation. Together, our data challenge the traditional idea that alterations in the core circadian clock drive circadian-related changes in memory formation and instead argue for a more autonomous role for circadian clock gene function in hippocampal cells to gate the likelihood of long-term memory formation.

scholarly journals Dissociating refreshing and elaboration and their impacts on memory

2018 ◽  
Author(s):  
Lea M. Bartsch ◽  
Vanessa M. Loaiza ◽  
Lutz Jäncke ◽  
Klaus Oberauer ◽  
Jarrod A. Lewis-Peacock
Keyword(s):  
Older Adults ◽  
Memory Performance ◽  
Ethics Committees ◽  
Fmri Data ◽  
Ethical Review ◽  
Long Term Memory ◽  
List Type ◽  
Term Memory ◽  
Age Related

AbstractMaintenance of information in working memory (WM) is assumed to rely on refreshing and elaboration, but clear mechanistic descriptions of these cognitive processes are lacking, and it is unclear whether they are simply two labels for the same process. This fMRI study investigated the extent to which refreshing, elaboration, and repeating of items in WM are distinct neural processes with dissociable behavioral outcomes in WM and long-term memory (LTM). Multivariate pattern analyses of fMRI data revealed differentiable neural signatures for these processes, which we also replicated in an independent sample of older adults. In some cases, the degree of neural separation within an individual predicted their memory performance. Elaboration improved LTM, but not WM, and this benefit increased as its neural signature became more distinct from repetition. Refreshing had no impact on LTM, but did improve WM, although the neural discrimination of this process was not predictive of the degree of improvement. These results demonstrate that refreshing and elaboration are separate processes that differently contribute to memory performance.HighlightsRepeated reading, refreshing, and elaboration are differentiable in brain activation patterns in both young and older adults.Elaboration selectively improved long-term memory for young adults, and the size of the benefit was related to the neural separability of elaboration from other processes.Older adults implemented a sub-optimal form of elaboration, and this may be a factor contributing to age-related deficits in long-term memory.Ethics statementThe study was approved by the ethical review board of the canton of Zurich (BASEC-No. 2017-00190) and all subjects gave informed written consent in accordance with the Declaration of Helsinki.Data and code availability statementAll behavioral data and analysis scripts can be assessed on the Open Science Framework (osf.io/p2h8b/). The fMRI data that support the findings of this study are available on request from the corresponding author, LMB. The fMRI data are not publicly available due to restrictions of the Swiss Ethics Committees on research involving humans regarding data containing information that could compromise the privacy of research participants.

scholarly journals Reading Memory Formation from the Eyes

2018 ◽  
Author(s):  
Anne Bergt ◽  
Anne E. Urai ◽  
Tobias H. Donner ◽  
Lars Schwabe
Keyword(s):  
Synaptic Plasticity ◽  
Memory Formation ◽  
Pupil Dilation ◽  
Long Term Memory ◽  
Term Memory ◽  
Pupil Response ◽  
Rapid Formation ◽  
The Brain

At any time, we are processing thousands of stimuli, but only few of them will be remembered hours or days later. Is there any way to predict which ones? Here, we show that the pupil response to ongoing stimuli, an indicator of physiological arousal, is a reliable predictor of long-term memory for these stimuli, over at least one day. Pupil dilation was tracked while participants performed visual and auditory encoding tasks. Memory was tested immediately after encoding and 24 hours later. Irrespective of the encoding modality, trial-by-trial variations in pupil dilation predicted which stimuli were recalled in the immediate and 24 hours-delayed tests. These results show that our eyes may provide a window into the formation of long-term memories. Furthermore, our findings underline the important role of central arousal systems in the rapid formation of memories in the brain, possibly by gating synaptic plasticity mechanisms.

scholarly journals Engram reactivation during memory retrieval predicts long-term memory performance in aged mice

2020 ◽  
Author(s):  
Kubra Gulmez Karaca ◽  
David V.C. Brito ◽  
Benjamin Zeuch ◽  
Ana M.M. Oliveira
Keyword(s):  
Cognitive Decline ◽  
Memory Performance ◽  
Underlying Mechanism ◽  
Long Term Memory ◽  
Memory Recall ◽  
Term Memory ◽  
Aged Mice ◽  
Neuronal Ensembles ◽  
Age Related

AbstractAge-related cognitive decline preferentially targets long-lasting episodic memories that require intact hippocampal function. Memory traces (or engrams) are believed to be encoded within the neurons activated during learning (neuronal ensembles), and recalled by reactivation of the same population. However, whether engram reactivation dictates memory performance in late life is not known. Here, we labelled neuronal ensembles formed during object location recognition learning in the dentate gyrus, and analyzed the reactivation of this population by long-term memory recall in young adult, cognitively impaired- and unimpaired-aged mice. We found that reactivation of memory-encoding neuronal ensembles at long-term memory recall was disrupted in impaired- but not unimpaired-aged mice. Furthermore, we showed that the memory performance in the aged population correlated with the degree of engram reactivation at long-term memory recall. Overall, our data implicates recall-induced engram reactivation as a prediction factor of memory performance throughout aging. Moreover, our findings suggest impairments in neuronal ensemble stabilization and/or reactivation as an underlying mechanism in age-dependent cognitive decline.

scholarly journals A clock gene, period, plays a key role in long-term memory formation in Drosophila

2004 ◽  
Vol 101 (45) ◽  
pp. 16058-16063 ◽  
Author(s):  
T. Sakai ◽  
T. Tamura ◽  
T. Kitamoto ◽  
Y. Kidokoro
Keyword(s):  
Clock Gene ◽  
Memory Formation ◽  
Long Term Memory ◽  
Term Memory

scholarly journals lncRNA Neat1 drives neuronal histone methylation and age-related memory impairments

2019 ◽  
Author(s):  
Anderson A. Butler ◽  
Daniel R. Johnston ◽  
Simranjit Kaur ◽  
Farah D. Lubin
Keyword(s):  
Histone Methylation ◽  
Transcriptional Repression ◽  
Rna Binding ◽  
Gene Activation ◽  
Memory Formation ◽  
Long Term Memory ◽  
Mrna Levels ◽  
Term Memory ◽  
Age Related

AbstractHistone methylation is critical for the formation and maintenance of long-term memories. Long noncoding RNAs (lncRNAs) are regulators of histone methyltransferases and other chromatin modifying enzymes (CMEs). We investigated how lncRNA Neat1-mediated histone methylation contributes to hippocampus-dependent long-term memory formation, using a combination of transcriptomics, RNA binding protein immunoprecipitation, CRISPR mediated gene activation, and behavioral approaches. Suppression of the lncRNA Neat1 revealed widespread changes in gene transcription as well as perturbations of histone 3 lysine 9 dimethylation (H3K9me2), a repressive histone modification mark that is dysregulated in the aging hippocampus. We identified a Neat1-dependent mechanism of transcriptional repression via H3K9me2 at the c-Fos promoter corresponding with observed changes in c-Fos mRNA levels. Overexpression of hippocampal Neat1 via CRISPRa is sufficient to impair memory formation in young adults, recapitulating observed memory deficits in old adults, while Neat1 suppression in both young and old adult mice improves memory. These results suggest that lncRNA Neat1 is a potent epigenetic regulator of hippocampus-dependent long-term memory formation.

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