Short-term and long-term memory deficits in handedness learning in mice with absent corpus callosum and reduced hippocampal commissure

2013 ◽  
Vol 245 ◽  
pp. 145-151 ◽  
Author(s):  
Andre S. Ribeiro ◽  
Brenda A. Eales ◽  
Fred G. Biddle
Keyword(s):  
Corpus Callosum ◽  
Memory Deficits ◽  
Long Term Memory ◽  
Short Term ◽  
Term Memory ◽  
Hippocampal Commissure

Cutting of the rat hippocampal commissure impairs short-term memory but not long-term memory

2020 ◽  
Author(s):  
Yukitoshi Sakaguchi
Keyword(s):  
Short Term Memory ◽  
Memory Formation ◽  
Long Term Memory ◽  
Short Term ◽  
Term Memory ◽  
Dynamic Memory ◽  
Hippocampal Commissure ◽  
Functional Laterality ◽  
Left And Right

Split-brain experiments, which have been actively conducted since the twentieth century, have provided a great deal of insight into inter-hemispheric functional laterality and interactions. However, how communication between the left and right hippocampi directly contributes to memory formation is still poorly understood. To address this issue, we cut the rat hippocampal commissure (HC) connecting the left and right hippocampi prior to behavioral tests, which comprised of four memory tasks. The result showed that cutting the HC impairs short-term memory but not long-term memory. This suggests that the HC contributes mainly to the appropriate formation of short-term memory by mediating communication between the left and right hippocampi. Our findings would help to elucidate dynamic memory formation in the hippocampus and contribute to the development of therapeutics for some neurological diseases which cause a reduction in the inter-hemispheric interaction.

Long-Term Memory Deficits and Early Onset Dementia in Aging Adult Survivors of Childhood Acute Lymphoblastic Leukemia Treated with Cranial Irradiation

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 664-664
Author(s):  
Gregory T. Armstrong ◽  
Petersen C. Ronald ◽  
Nan Zhang ◽  
Aimee Santucci ◽  
Deokumar Srivastava ◽  
...  
Keyword(s):  
Early Onset ◽  
Memory Impairment ◽  
Adult Survivors ◽  
Memory Deficits ◽  
Cognitive Status ◽  
Long Term Memory ◽  
Short Term ◽  
Term Memory ◽  
Early Onset Dementia

Abstract Abstract 664 Background: Survivors of childhood acute lymphoblastic leukemia (ALL) who received prophylactic cranial radiation therapy (CRT) are at increased risk for deficits in neurocognitive skills, including attention, working memory and processing speed. As survivors age, global brain injury from CRT may reduce cognitive reserve, placing them at risk for early onset dementia or long-term memory deficits. The prevalence of dementia and memory abnormalities in adult survivors of childhood ALL has not previously been established. Methods: Analyses were conducted on 265 of 445 (60%) eligible survivors of childhood ALL (median age 36 years, range 26–54 years; 52% female) treated with 18Gy (n=127) or 24Gy (n=138) CRT with a median time from CRT of 30 years (range 15–46 years). Participants completed the Wechsler Memory Scale IV, including the Brief Cognitive Status Exam (BSCE), and the Wechsler Abbreviated Scale of Intelligence (WASI). Age-adjusted standard scores were calculated and the BSCE was also adjusted for education level. Prevalence of memory impairment (<1 SD below age-expected mean), stratified by RT dose exposure, is reported and logistic regression used to identify risk factors for impairment. A subset of survivors (n=85) completed brain magnetic resonance imaging (MRI), including assessment of hippocampal volume, cortical thickness, white matter volume, diffusion tensor imaging, and functional MRI (fMRI) during a cued-recall memory task. Results: Survivors who received 24 Gy CRT had increased impairment on global measures of both short-term recall (33%; p<0.001) and long-term recall (30%; p<0.001), while no increase in impairment was seen after 18Gy. Impaired short-term recall was associated with smaller right (p=0.02) and left (p<0.01) temporal lobe volumes, while impaired long-term recall was associated with thinner parietal and frontal cortices. On subtests evaluating narrative memory (i.e. story recall) and design memory, increasing RT dose (24 vs. 18Gy) was associated with an increased prevalence of long-term memory impairment (narrative: 28% vs. 12%, p=0.001; designs: 13% vs. 3.2%, p=0.003). However, no CRT dose response was identified for short term narrative and design memory. Survivors with impaired long-term memory for designs demonstrated a compensatory increase in left hippocampal fMRI activation (p=0.005), and the effect was greater in the higher dose group (p = 0.04). The mean score for long-term narrative memory among survivors who received 24Gy was equivalent to the mean score of a 70–74 year old adult population. Neither young age (0–4 years) at CRT (Odds Ratio [OR] 1.4, 95% confidence interval [CI] 0.8–2.7), time from CRT (OR 1.0, 95% CI 0.9–1.1) nor intrathecal methotrexate exposure (OR 3.9, 95% CI 0.4–36.1) were significantly associated with long-term memory deficits. Reduced cognitive status (by BSCE) was identified after 18Gy (9%, p=0.11) and 24Gy (18%, p<0.001), suggesting a CRT dose-response effect. On diffusion tensor imaging, increased radial diffusivity in the frontal, parietal and temporal regions, an inverse measure of white matter integrity, was associated with reduced BSCE. Current employment rates were equivalent (63%) in both CRT dose groups, suggesting no difference in functional status. Conclusions: Aging adult survivors of ALL who received 24Gy CRT have reduced cognitive status and significant impairment in short-term and long-term memory. There appears to be a dose response effect selective for long-term narrative and design memory, but not for short term narrative and design memory. These patterns are consistent with early onset of age-related (long-term) memory loss, and early stage dementia, yet at a median age of only 36 years. After 24Gy, survivors have the narrative memory equivalent to a 70 year-old in the general population. Survivors with memory impairment demonstrated reduced integrity on structural and functional neuroimaging in anatomical regions established as essential for memory formation and long-term recall. However, these memory impairments do not seem to affect functional status (employment rates) suggesting that, rather than frank dementia, deficits in middle adulthood are consistent with mild cognitive impairment (MCI). Longitudinal evaluation of this population is needed as MCI often progresses into early onset dementia with age. Disclosures: No relevant conflicts of interest to declare.

scholarly journals BIN1 recovers tauopathy-induced long-term memory deficits in mice and interacts with Tau through Thr348 phosphorylation

2018 ◽  
Author(s):  
Maxime Sartori ◽  
Tiago Mendes ◽  
Shruti Desai ◽  
Alessia Lasorsa ◽  
Adrien Herledan ◽  
...  
Keyword(s):  
Short Term Memory ◽  
Phosphorylation Site ◽  
Memory Deficits ◽  
Long Term Memory ◽  
Compensatory Mechanism ◽  
Cyclin Dependent Kinase ◽  
Short Term ◽  
Term Memory ◽  
Kinase Phosphorylation

AbstractThe bridging integrator 1 gene (BIN1) is a major genetic risk factor for Alzheimer’s disease (AD). In this report, we investigated how BIN1-dependent pathophysiological processes might be associated with Tau. We first generated a cohort of control and transgenic mice either overexpressing human MAPT (TgMAPT) or both human MAPT and BIN1 (TgMAPT;TgBIN1), which we followed-up from 3 to 15 months. In TgMAPT;TgBIN1 mice short-term memory deficits appeared earlier than in TgMAPT mice; however – unlike TgMAPT mice – TgMAPT;TgBIN1 mice did not exhibit any long-term or spatial memory deficits for at least 15 months. After sacrifice of the cohort at 18 months, immunohistochemistry revealed that BIN1 overexpression prevents both Tau mislocalization and somatic inclusion in the hippocampus, where an increase in BIN1-Tau interaction was also observed. We then sought mechanisms controlling the BIN1-Tau interaction. We developed a high-content screening approach to characterize modulators of the BIN1-Tau interaction in an agnostic way (1,126 compounds targeting multiple pathways), and we identified – among others – an inhibitor of Calcineurin, a Ser/Thr phosphatase. We determined that Calcineurin dephosphorylates BIN1 on a Cyclin-dependent kinase phosphorylation site at T348, promoting the open conformation of the neuronal BIN1 isoform. Phosphorylation of this site increases the availability of the BIN1 SH3 domain for Tau interaction, as demonstrated by nuclear magnetic resonance experiments and in primary neurons. Finally, we observed that the levels of the neuronal BIN1 isoform were decreased in AD brains, whereas phospho-BIN1(T348):BIN1 ratio was increased, suggesting a compensatory mechanism. In conclusion, our data support the idea that BIN1 modulates the AD risk through an intricate regulation of its interaction with Tau. Alteration in BIN1 expression or activity may disrupt this regulatory balance with Tau and have direct effects on learning and memory.

Conceptual short-term memory (CSTM) supports core claims of Christiansen and Chater

2016 ◽  
Vol 39 ◽  
Author(s):  
Mary C. Potter
Keyword(s):  
Working Memory ◽  
Rapid Serial Visual Presentation ◽  
Language Comprehension ◽  
Short Term Memory ◽  
Visual Presentation ◽  
Long Term Memory ◽  
Short Term ◽  
Term Memory ◽  
Use Of Knowledge

AbstractRapid serial visual presentation (RSVP) of words or pictured scenes provides evidence for a large-capacity conceptual short-term memory (CSTM) that momentarily provides rich associated material from long-term memory, permitting rapid chunking (Potter 1993; 2009; 2012). In perception of scenes as well as language comprehension, we make use of knowledge that briefly exceeds the supposed limits of working memory.

Comparison of Auditory, Language, Memory, and Attention Abilities in Children With and Without Listening Difficulties

2020 ◽  
Vol 29 (4) ◽  
pp. 710-727
Author(s):  
Beula M. Magimairaj ◽  
Naveen K. Nagaraj ◽  
Alexander V. Sergeev ◽  
Natalie J. Benafield
Keyword(s):  
Auditory Processing ◽  
Short Term Memory ◽  
Group Differences ◽  
Long Term Memory ◽  
Short Term ◽  
Significant Group ◽  
Term Memory ◽  
Memory And Attention ◽  
Speed And Accuracy

Objectives School-age children with and without parent-reported listening difficulties (LiD) were compared on auditory processing, language, memory, and attention abilities. The objective was to extend what is known so far in the literature about children with LiD by using multiple measures and selective novel measures across the above areas. Design Twenty-six children who were reported by their parents as having LiD and 26 age-matched typically developing children completed clinical tests of auditory processing and multiple measures of language, attention, and memory. All children had normal-range pure-tone hearing thresholds bilaterally. Group differences were examined. Results In addition to significantly poorer speech-perception-in-noise scores, children with LiD had reduced speed and accuracy of word retrieval from long-term memory, poorer short-term memory, sentence recall, and inferencing ability. Statistically significant group differences were of moderate effect size; however, standard test scores of children with LiD were not clinically poor. No statistically significant group differences were observed in attention, working memory capacity, vocabulary, and nonverbal IQ. Conclusions Mild signal-to-noise ratio loss, as reflected by the group mean of children with LiD, supported the children's functional listening problems. In addition, children's relative weakness in select areas of language performance, short-term memory, and long-term memory lexical retrieval speed and accuracy added to previous research on evidence-based areas that need to be evaluated in children with LiD who almost always have heterogenous profiles. Importantly, the functional difficulties faced by children with LiD in relation to their test results indicated, to some extent, that commonly used assessments may not be adequately capturing the children's listening challenges. Supplemental Material https://doi.org/10.23641/asha.12808607

scholarly journals The influence of aging on short-term and long-term memory in the continuous recognition paradigm.

2002 ◽  
Vol 72 (6) ◽  
pp. 516-521 ◽  
Author(s):  
Osamu Ishihara ◽  
Yasuyuki Gondo ◽  
W. Poon Leonard
Keyword(s):  
Long Term Memory ◽  
Short Term ◽  
Term Memory

scholarly journals An Approach toward the Development of a Functional Encoding Model of Short Term Memory during Reading

1978 ◽  
Vol 10 (2) ◽  
pp. 141-148
Author(s):  
Mary Anne Herndon
Keyword(s):  
Cluster Analysis ◽  
Storage Capacity ◽  
Short Term Memory ◽  
Long Term Memory ◽  
Short Term ◽  
Processing Efficiency ◽  
Term Memory ◽  
Information Unit ◽  
Subsequent Storage

In a model of the functioning of short term memory, the encoding of information for subsequent storage in long term memory is simulated. In the encoding process, semantically equivalent paragraphs are detected for recombination into a macro information unit. This recombination process can be used to relieve the limited storage capacity constraint of short term memory and subsequently increase processing efficiency. The results of the simulation give a favorable indication of the success for the use of cluster analysis as a tool to simulate the encoding function in the detection of semantically similar paragraphs.

scholarly journals Remember like humans

2017 ◽  
Vol 14 (1) ◽  
pp. 172988141769231 ◽  
Author(s):  
Ning An ◽  
Shi-Ying Sun ◽  
Xiao-Guang Zhao ◽  
Zeng-Guang Hou
Keyword(s):  
Short Term Memory ◽  
Three Dimensional ◽  
Sensory Memory ◽  
Long Term Memory ◽  
Observation Model ◽  
Two Dimensional ◽  
Short Term ◽  
Term Memory ◽  
Memory Register

Visual tracking is a challenging computer vision task due to the significant observation changes of the target. By contrast, the tracking task is relatively easy for humans. In this article, we propose a tracker inspired by the cognitive psychological memory mechanism, which decomposes the tracking task into sensory memory register, short-term memory tracker, and long-term memory tracker like humans. The sensory memory register captures information with three-dimensional perception; the short-term memory tracker builds the highly plastic observation model via memory rehearsal; the long-term memory tracker builds the highly stable observation model via memory encoding and retrieval. With the cooperative models, the tracker can easily handle various tracking scenarios. In addition, an appearance-shape learning method is proposed to update the two-dimensional appearance model and three-dimensional shape model appropriately. Extensive experimental results on a large-scale benchmark data set demonstrate that the proposed method outperforms the state-of-the-art two-dimensional and three-dimensional trackers in terms of efficiency, accuracy, and robustness.

Abstract P783: Alpha 7 -Acetylcholine Receptor Signaling Reduces Neuronal Apoptosis After Subarachnoid Hemorrhage

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Ari Dienel ◽  
Remya A Veettil ◽  
Kanako Matsumura ◽  
Peeyush Kumar T. ◽  
Spiros Blackburn ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Acetylcholine Receptor ◽  
Neuronal Apoptosis ◽  
Neuronal Survival ◽  
Memory Function ◽  
Memory Deficits ◽  
Long Term Memory ◽  
Term Memory ◽  
Receptor Knockout Mouse

Subarachnoid hemorrhage induces neuronal apoptosis which causes acute and long-term memory deficits. Ourhypothesis is that agonism of α7-acetylcholine receptors attenuates neuronal apoptosis and improves memorydeficits in SAH mice. Mice were randomly assigned into the experimental groups. One cohort was euthanizedone day after SAH to assess neuronal apoptosis and signaling pathways. A second cohort survived for 30 dayspost-SAH to test long-term memory function. Inhibitors and an α7-acetylcholine receptor knockout mouse wereused. Neurobehavioral performance was assessed on days 1-3, 5, 7, and 23-28. All outcomes were performedand all data was analyzed by a blinded investigator. The α7-acetylcholine receptor agonist prevented neuronalapoptosis and improved acute memory deficits caused by SAH via activation of the PI3K/Akt pathway in neurons.Agonism of the α7-acetylcholine receptor was beneficial in both male and female mice, although the protectionin females was significantly better than in male mice. α7-acetylcholine receptor agonism did not provide anybenefit in α7-acetylcholine receptor knockout mice subjected to SAH. Treatment with the α7-acetylcholinereceptor agonist for 3 days after SAH led to improved working memory one month after SAH suggesting thatacutely improving neuronal survival can have long-lasting benefits. The α7-acetylcholine receptor may be atherapeutic target for SAH which can promote neuronal survival acutely after SAH, but also confer long-lastingmemory benefits. The findings of this study support the α7-acetylcholine receptor as a treatment target whichmay attenuate the long-term memory deficits which SAH patients suffer from.

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