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Charis Eng - One of the best experts on this subject based on the ideXlab platform.
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verbal Memory Dysfunction is associated with alterations in brain transcriptome in dominant temporal lobe epilepsy
Epilepsia, 2020Co-Authors: Robyn M Busch, Lamis Yehia, Peter Bazeley, Marilyn Seyfi, Ingmar Blumcke, Bruce P Hermann, Imad Najm, Charis EngAbstract:Objective Memory Dysfunction is prevalent in many neurological disorders and can have a significant negative impact on quality of life. The genetic contributions to Memory impairment in epilepsy, particularly temporal lobe epilepsy (TLE), remain poorly understood. Here, we compare the brain transcriptome between TLE patients with and without verbal Memory impairments to identify genes and signaling networks important for episodic Memory. Methods Brain tissues were resected from 23 adults who underwent dominant temporal lobectomy for treatment of pharmacoresistant epilepsy. To control for potential effects of APOE on Memory, only those homozygous for the APOE e3 allele were included. A battery of Memory tests was performed, and patients were stratified into two groups based on preoperative Memory performance. The groups were well matched on demographic and disease-related variables. Total RNA-Seq and small RNA-Seq were performed on RNA extracted from the brain tissues. Pathway and integrative analyses were subsequently performed. Results We identified 1092 differentially expressed transcripts (DETs), with the majority (71%) being underexpressed in brain tissues from patients with impaired Memory compared to those from patients with intact Memory. Enrichment analysis revealed overrepresentation of genes in pathways pertaining to brain-related neurological Dysfunction, including a subset associated with neurodegenerative diseases, Memory, and cognition (APP, MAPT, PINK1). Despite including patients with identical APOE genotypes, we identify APOE as a differentially expressed gene associated with Memory status. Small RNA-Seq identified four differentially expressed microRNAs (miRNAs) that were predicted to target a subset (22%) of all DETs. Integrative analysis showed that these miRNA-predicted DET targets impact brain-related pathways and biological processes also pertinent to Memory and cognition. Significance TLE-associated Memory status may be influenced by differences in gene expression profiles within the temporal lobe. Upstream processes influencing differential expression signatures, such as miRNAs, could serve as biomarkers and potential treatment targets for Memory impairment in TLE.
Heii Arai - One of the best experts on this subject based on the ideXlab platform.
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Time course for Memory Dysfunction in early-life and late-life major depression: A longitudinal study from the Juntendo university mood disorder project
Journal of affective disorders, 2013Co-Authors: Hitoshi Maeshima, Hajime Baba, Yoshiyuki Nakano, Emi Satomura, Yuki Namekawa, Naoko Takebayashi, Toshihito Suzuki, Masaru Mimura, Hiroshi Nomoto, Heii AraiAbstract:Abstract Background Previous studies have demonstrated that patients with depression also have Memory Dysfunctions during depressive episodes. These Dysfunctions partially remain immediately after remission from a depressive state; however, it is unclear whether these residual Memory Dysfunctions may disappear through long-term remission from depression. The present study compared patients during early-life (age Methods Logical Memory from the Wechsler Memory Scale-Revised was administered to 67 patients with major depressive disorder (MDD) (47 patients with early-life depression and residual 20 patients with late-life depression) and 50 healthy controls. MDD patients received Memory assessments at the time of their initial remission and at a follow-up three years after remission. Results At the time of initial remission, scores for logical Memory were significantly lower in both patient groups compared to matched controls. At follow-up, Memory Dysfunction for early-life MDD patients disappeared, whereas scores in the late-life MDD group remained significantly lower than those of matched controls. Limitations All patients in the present study were on antidepressant medications. Conclusions Our findings suggested that the progress of Memory performance in late-life MDD patients may be different from early-life MDD patients.
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Residual Memory Dysfunction in recurrent major depressive disorder--a longitudinal study from Juntendo University Mood Disorder Project.
Journal of Affective Disorders, 2012Co-Authors: Hitoshi Maeshima, Hajime Baba, Yoshiyuki Nakano, Emi Satomura, Yuki Namekawa, Naoko Takebayashi, Toshihito Suzuki, Masaru Mimura, Heii AraiAbstract:Abstract Background Depression may increase the risk of developing Alzheimer's disease. Large cohort studies have shown that recurrent depression is associated with a risk of developing dementia. Other studies have documented smaller hippocampal volume in patients with recurrent depression. It is speculative that a greater risk of developing dementia may result from a higher number of previous depressive episodes. This study compared patients with recurrent and single-episode depression in the remitted stage, and healthy controls to elucidate the impact of the number of depressive episodes on Memory. Methods Logical Memory and visual reproduction subtests of the Wechsler Memory Scale-Revised were given to 68 patients with major depressive disorder (MDD) (30 patients with a single episode and residual 38 patients with recurrent multiple episodes) and 57 healthy controls. The patients with MDD received Memory assessment at the time of initial remission and at the follow-up period 3 years after remission. Results At the time of initial remission, scores of both logical Memory and visual reproduction subtests were significantly lower in both patient groups compared with healthy controls. At follow-up, Memory Dysfunction of the single-episode group disappeared, whereas scores in the recurrent group remained significantly lower than those of the single-episode group and controls. Limitations All patients in the present study were on antidepressant medications. Conclusions Patients with recurrent MDD with multiple depressive episodes showed residual Memory Dysfunction even after 3 years of remission. Persistence of Memory deficits in the recurrent depression may be a risk factor for developing dementia.
Pramod K. Dash - One of the best experts on this subject based on the ideXlab platform.
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Persistent working Memory Dysfunction following traumatic brain injury: evidence for a time-dependent mechanism.
Neuroscience, 2009Co-Authors: Meg M. Hoskison, Anthony N. Moore, Sara A. Orsi, Nobuhide Kobori, Pramod K. DashAbstract:The prefrontal cortex is highly vulnerable to traumatic brain injury (TBI) resulting in the Dysfunction of many high-level cognitive and executive functions such as planning, information processing speed, language, Memory, attention, and perception. All of these processes require some degree of working Memory. Interestingly, in many cases, post-injury working Memory deficits can arise in the absence of overt damage to the prefrontal cortex. Recently, excess GABA-mediated inhibition of prefrontal neuronal activity has been identified as a contributor to working Memory Dysfunction within the first month following cortical impact injury of rats. However, it has not been examined if these working Memory deficits persist, and if so, whether they remain amenable to treatment by GABA antagonism. Our findings show that working Memory Dysfunction, assessed using both the delay match-to-place and delayed alternation T-maze tasks, following lateral cortical impact injury persists for at least 16 weeks post-injury. These deficits were found to be no longer the direct result of excess GABA-mediated inhibition of medial prefrontal cortex neuronal activity. Golgi staining of prelimbic pyramidal neurons revealed that TBI causes a significant shortening of layers V/VI basal dendrite arbors by 4 months post-injury, as well as an increase in the density of both basal and apical spines in these neurons. These changes were not observed in animals 14 days post-injury, a time point at which administration of GABA receptor antagonists improves working Memory function. Taken together, the present findings, along with previously published reports, suggest that temporal considerations must be taken into account when designing mechanism-based therapies to improve working Memory function in TBI patients.
Raj C. Shah - One of the best experts on this subject based on the ideXlab platform.
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hippocampal disconnection contributes to Memory Dysfunction in individuals at risk for alzheimer s disease
Proceedings of the National Academy of Sciences of the United States of America, 2006Co-Authors: Travis R. Stoub, Glenn T. Stebbins, Sue Leurgans, David A. Bennett, Leyla Detoledomorrell, Raj C. ShahAbstract:The concept of amnestic mild cognitive impairment (MCI) describes older people who show a decline predominantly in Memory function, but who do not meet criteria for dementia. Because such individuals are at high risk for developing Alzheimer’s disease, they are of great interest for understanding the prodromal stages of the disease process. The mechanism underlying Memory Dysfunction in people with MCI is not fully understood. The present study uses quantitative, high-resolution structural MRI techniques to investigate, in vivo, the anatomical substrate of Memory Dysfunction associated with MCI. Changes in brain structures were assessed with two imaging techniques: (i) whole-brain, voxel-based morphometry to determine regions of reduced white matter volume and (ii) sensitive volumetric segmentation of the entorhinal cortex and hippocampus, gray matter regions that are critically important for Memory function. In participants with amnestic MCI, compared with age-matched controls, results showed a significant decrease in white matter volume in the region of the parahippocampal gyrus that includes the perforant path. There was also significant atrophy in both the entorhinal cortex and the hippocampus. Regression models demonstrated that both hippocampal volume and parahippocampal white matter volume were significant predictors of declarative Memory performance. These results suggest that, in addition to hippocampal atrophy, disruption of parahippocampal white matter fibers contributes to Memory decline in elderly individuals with MCI by partially disconnecting the hippocampus from incoming sensory information.
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Hippocampal disconnection contributes to Memory Dysfunction in individuals at risk for Alzheimer’s disease
Proceedings of the National Academy of Sciences of the United States of America, 2006Co-Authors: Travis R. Stoub, Leyla Detoledo-morrell, Glenn T. Stebbins, Sue Leurgans, David A. Bennett, Raj C. ShahAbstract:The concept of amnestic mild cognitive impairment (MCI) describes older people who show a decline predominantly in Memory function, but who do not meet criteria for dementia. Because such individuals are at high risk for developing Alzheimer’s disease, they are of great interest for understanding the prodromal stages of the disease process. The mechanism underlying Memory Dysfunction in people with MCI is not fully understood. The present study uses quantitative, high-resolution structural MRI techniques to investigate, in vivo, the anatomical substrate of Memory Dysfunction associated with MCI. Changes in brain structures were assessed with two imaging techniques: (i) whole-brain, voxel-based morphometry to determine regions of reduced white matter volume and (ii) sensitive volumetric segmentation of the entorhinal cortex and hippocampus, gray matter regions that are critically important for Memory function. In participants with amnestic MCI, compared with age-matched controls, results showed a significant decrease in white matter volume in the region of the parahippocampal gyrus that includes the perforant path. There was also significant atrophy in both the entorhinal cortex and the hippocampus. Regression models demonstrated that both hippocampal volume and parahippocampal white matter volume were significant predictors of declarative Memory performance. These results suggest that, in addition to hippocampal atrophy, disruption of parahippocampal white matter fibers contributes to Memory decline in elderly individuals with MCI by partially disconnecting the hippocampus from incoming sensory information.
Takanari Kitazono - One of the best experts on this subject based on the ideXlab platform.
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cerebral oxidative stress induces spatial working Memory Dysfunction in uremic mice neuroprotective effect of tempol
Nephrology Dialysis Transplantation, 2014Co-Authors: Kiichiro Fujisaki, Kazuhiko Tsuruya, Mayumi Yamato, Jiro Toyonaga, Hideko Noguchi, Toshiaki Nakano, Masatomo Taniguchi, Masanori Tokumoto, Hideki Hirakata, Takanari KitazonoAbstract:Background. Chronic kidney disease (CKD) is frequently associated with uremic encephalopathy and cognitive impairment. Recent studies have demonstrated that cerebral oxidative stress contributes to cognitive Dysfunction. Although oxidative stress has been reported to increase in the uremic rat brain, the relationship between increased oxidative stress and cognitive impairment in uremia is unclear. In the present study, the effects of tempol (TMP), an antioxidant drug, were investigated in uremic mice. Methods. CKD was induced in male C57BL/6 mice (n=8) by left nephrectomy and 2/3 electrocoagulation of the right renal cortex. Working Memory performance was tested by the radial arm water maze test. We have prepared two protocols (‘time course study’ and ‘treatment study’). First, we examined the working Memory test and histological examination of mouse brains after 4 and 8 weeks. Next, we investigated the effect of TMP (3 mM) against uremia-induced neurodegeneration and oxidative stress in the mouse brain. Results. Eight weeks after CKD induction, vehicle-treated mice made significantly more errors than sham-operated control mice, while TMP improved working Memory performance in CKD mice. CKD was associated with accumulation of 8hydroxy-2 0 -deoxyguanosine in the hippocampal neuronal cells, but not in TMP-treated CKD mice. Increased numbers of pyknotic neuronal cells were observed in the hippocampus of CKD mice at 8 weeks, but pyknotic neuronal cell numbers were decreased under the influence of TMP in uremic mice. Conclusions. The present study provided evidence that uremia is associated with spatial working Memory Dysfunction in mice and that treatment with TMP protects against cerebral oxidative stress and improves cognitive Dysfunction in uremic mice, suggesting their potential usefulness for the treatment of cognitive Dysfunction in uremia.