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remote memory [keywords]
- Adverse Consequences of Glucocorticoid Medication: Psychological, Cognitive, and Behavioral Effects. [JOURNAL ARTICLE]
- Am J Psychiatry 2014 Oct 1; 171(10):1045-1051.
Glucocorticoids are the most commonly prescribed anti-inflammatory/immunosuppressant medications worldwide. This article highlights the risk of clinically significant and sometimes severe psychological, cognitive, and behavioral disturbances that may be associated with glucocorticoid use, as well as ways to prevent and treat these disturbances. An illustrative case vignette is presented describing a patient's experience of cycles of manic-like behavior and depression while on high-dosage prednisone, with long-term cognitive disorganization, vulnerability to stress, and personality changes. Severe neuropsychiatric consequences (including suicide, suicide attempt, psychosis, mania, depression, panic disorder, and delirium, confusion, or disorientation) have been reported to occur in 15.7 per 100 person-years at risk for all glucocorticoid courses, and 22.2 per 100 person-years at risk for first courses. The majority of patients experience less severe but distressing and possibly persistent changes in mood, cognition, memory, or behavior during glucocorticoid treatment or withdrawal. Although prediction of such effects is difficult, risks vary with age, gender, dosage, prior psychiatric history, and several biological markers. Key mechanisms thought to underlie these risk factors are briefly described. Recommendations are given for identifying individual risk factors and for monitoring and managing adverse neuropsychiatric effects of glucocorticoids.
- The Telehealth Satisfaction Scale: Reliability, Validity, and Satisfaction with Telehealth in a Rural Memory Clinic Population. [JOURNAL ARTICLE]
- Telemed J E Health 2014 Oct 1.
Abstract Introduction: Patient satisfaction is a key aspect of quality of care and can inform continuous quality improvement. Of the few studies that have reported on patient satisfaction with telehealth in programs aimed at individuals with memory problems, none has reported on the psychometric properties of the user satisfaction scales used. Materials and Methods: We evaluated the construct validity and internal consistency reliability of the Telehealth Satisfaction Scale (TeSS), a 10-item scale adapted for use in a rural and remote memory clinic (RRMC). The RRMC is a one-stop interprofessional clinic for rural and remote seniors with suspected dementia, located in a tertiary-care hospital. Telehealth videoconferencing is used for preclinic assessment and for follow-up. Patients and caregivers completed the TeSS after each telehealth appointment. With data from 223 patients, exploratory factor analysis was conducted using the principal components analysis extraction method. Results: The eigenvalue for the first factor (5.2) was greater than 1 and much larger than the second eigenvalue (0.92), supporting a one-factor solution that was confirmed by the scree plot. The total variance explained by factor 1 was 52.1%. Factor loadings (range, 0.54-0.84) were above recommended cutoffs. The TeSS items demonstrated high internal consistency reliability (Cronbach's alpha=0.90). Satisfaction scores on the TeSS items ranged from 3.43 to 3.72 on a 4-point Likert scale, indicating high satisfaction with telehealth. Conclusions: The study findings demonstrate high user satisfaction with telehealth in a rural memory clinic and the sound psychometric properties of the TeSS in this population.
- Positive feedback of NR2B-containing NMDA receptor activity is the initial step towards visual imprinting, a model for juvenile learning. [JOURNAL ARTICLE]
- J Neurochem 2014 Oct 1.
Imprinting in chicks is a good model for elucidating the processes underlying neural plasticity changes during juvenile learning. We recently reported that neural activation of a telencephalic region, the core region of the hyperpallium densocellulare (HDCo), was critical for success of visual imprinting, and that NMDA receptors containing the NR2B subunit (NR2B/NR1) in this region were essential for imprinting. Using electrophysiological and multiple-site optical imaging techniques with acute brain slices, we found that long-term potentiation (LTP) and enhancement of NR2B/NR1 currents in HDCo neurons were induced in imprinted chicks. Enhancement of NR2B/NR1 currents as well as an increase in surface NR2B expression occurred even following a brief training that was too weak to induce LTP or imprinting behavior. This means that NR2B/NR1 activation is the initial step of learning, well before the activation of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors which induces LTP. We also showed that knockdown of NR2B/NR1 inhibited imprinting, and inversely, increasing the surface NR2B expression by treatment with a casein kinase 2 inhibitor successfully reduced training time required for imprinting. These results suggest that imprinting stimuli activate postsynaptic NR2B/NR1 in HDCo cells, increase NR2B/NR1 signaling through upregulation of its expression, and induce LTP and memory acquisition. This article is protected by copyright. All rights reserved.
- Rapamycin reveals an mTOR-independent Repression of Kv1.1 Expression during Epileptogenesis. [JOURNAL ARTICLE]
- Neurobiol Dis 2014 Sep 27.
Changes in ion channel expression are implicated in the etiology of epilepsy. However, the molecular mechanisms leading to long-term aberrant expression of ion channels are not well understood. The mechanistic/mammalian target of rapamycin (mTOR) is a serine/threonine protein kinase that mediates activity-dependent protein synthesis in neurons. mTOR is overactive in epilepsy, suggesting that excessive protein synthesis may contribute to the neuronal pathology. In contrast, we found that mTOR activity and the microRNA miR-129-5p reduces the expression of the voltage-gated potassium channel Kv1.1 in an animal model of temporal lobe epilepsy (TLE). When mTOR activity is low, Kv1.1 expression is high and the frequency of behavioral seizures is low. However, as behavioral seizure activity rises, mTOR activity increases and Kv1.1 protein levels drop. In CA1 pyramidal neurons, the reduction in Kv1.1 lowers the threshold for action potential firing. Interestingly, blocking mTOR activity with rapamycin reduces behavioral seizures and temporarily keeps Kv1.1 levels elevated. Overtime, seizure activity increases and Kv1.1 protein decreases in all animals, even those treated with rapamycin. Notably, the concentration of miR-129-5p, the negative regulator of Kv1.1 mRNA translation, increases by 21days post-status epilepticus (SE), sustaining Kv1.1 mRNA translational repression. Our results suggest that following kainic-acid induced status epilepticus there are two phases of Kv1.1 repression: (1) an initial mTOR-dependent repression of Kv1.1 that is followed by (2) a miR-129-5p persistent reduction of Kv1.1.
- Prior high corticosterone exposure reduces activation of immature neurons in the ventral hippocampus in response to spatial and non-spatial memory. [JOURNAL ARTICLE]
- Hippocampus 2014 Oct 1.
Chronic stress or chronically high glucocorticoids attenuate adult hippocampal neurogenesis by reducing cell proliferation, survival, and differentiation in male rodents. Neurons are still produced in the dentate gyrus during chronically high glucocorticoids, but it is not known whether these new neurons are appropriately activated in response to spatial memory. Thus, the goal of this study was to determine whether immature granule neurons generated during chronically high glucocorticoids (resulting in a depressive-like phenotype) are differentially activated by spatial memory retrieval. Male Sprague Dawley rats received either 40 mg/kg corticosterone (CORT) or vehicle for 18 d prior to behavioral testing. Rats were tested in the forced swim test (FST) and then tested in a spatial (hippocampus-dependent) or cued (hippocampus-independent) Morris Water Maze (MWM). Tissue was then processed for doublecortin (DCX) to identify immature neurons and zif268, an immediate early gene product. As expected, CORT increased depressive-like behavior (greater immobility in the FST) however, prior CORT modestly enhanced spatial learning and memory compared with oil. Prior CORT reduced the number of DCX-expressing cells and proportion of DCX-expressing cells colabeled for zif268, but only in the ventral hippocampus. Prior CORT shifted the proportion of cells in the ventral hippocampus away from postmitotic cells and toward immature, proliferative cells, likely indicates postmitotic cells were produced and matured under CORT conditions but proliferative cells were produced after high CORT exposure ceased. Compared with cue, spatial training slightly increased DCX-expressing cells and shifted cells toward the postmitotic stage in the ventral hippocampus. These data suggest that the effects of CORT and spatial training on immature neurons are more pronounced in the ventral hippocampus. Further, high CORT reduced activation of immature neurons, suggesting that exposure to high CORT may have long-term effects on cell integration or function. © 2014 Wiley Periodicals, Inc.
- Chronic early-life stress alters developmental and adult neurogenesis and impairs cognitive function in mice. [JOURNAL ARTICLE]
- Hippocampus 2014 Oct 1.
Early-life stress (ES) increases vulnerability to psychopathology and impairs cognition in adulthood. These ES-induced deficits are associated with lasting changes in hippocampal plasticity. Detailed information on the neurobiological basis, the onset and progression of such changes and their sex-specificity is currently lacking but is required to tailor specific intervention strategies. Here we use a chronic ES mouse model based on limited nesting and bedding material from postnatal day (P) 2-9 to investigate; 1) if ES leads to impairments in hippocampus-dependent cognitive function in adulthood, and 2) if these alterations are paralleled by changes in developmental and/or adult hippocampal neurogenesis. ES increased developmental neurogenesis (proliferation and differentiation) in the dentate gyrus (DG) at P9, and the number of immature (NeurD1(+) ) cells migrating postnatally from the secondary dentate matrix, indicating prompt changes in DG structure in both sexes. ES lastingly reduced DG volume and the long-term survival of developmentally born neurons in both sexes at P150. In adult male mice only, ES reduced survival of adult-born neurons (BrdU/NeuN(+) cells), while proliferation (Ki67(+) ) and differentiation (DCX(+) ) were unaffected. These changes correlated with impaired performance in all learning and memory tasks used here. In contrast, in female mice, despite early alterations in developmental neurogenesis, no lasting changes were present in adult neurogenesis after ES and the cognitive impairments were less prominent and only apparent in some cognitive tasks. We further show that, although neurogenesis and cognition correlate positively, only the hippocampus-dependent functions depend on changes in neurogenesis, whereas cognitive functions that are not exclusively hippocampus-dependent do not. This study indicates that chronic ES has lasting consequences on hippocampal structure and function in mice and suggests that male mice are more susceptible to ES than females. Unraveling the mechanisms that underlie the persistent ES-induced effects may have clinical implications for treatments to counteract ES-induced deficits. © 2014 Wiley Periodicals, Inc.
- Measuring the impact of cognitive and psychosocial interventions in persons with mild cognitive impairment with a randomized single-blind controlled trial: rationale and design of the MEMO+ study. [JOURNAL ARTICLE]
- Int Psychogeriatr 2014 Sep 30.:1-15.
ABSTRACT Background: Several studies have suggested that cognitive training is a potentially effective way to improve cognition and postpone cognitive decline in older adults with mild cognitive impairment (MCI). The MEMO+ study is a randomized, controlled, single-blind trial designed to test the efficacy, specificity, and long-term effect of a cognitive training intervention and a psychosocial intervention in persons with MCI. Methods: One hundred and sixty-two participants with MCI will be recruited. They will be randomized into three groups: cognitive training, psychosocial intervention, and no-contact. Each intervention will last for eight weeks (one session per week) and a booster training session will be provided three months after the end of the intervention. Various proximal and distal outcomes will be measured at pre-intervention as well as at one week, three months, and six months post-training. Proximal outcomes include memory and psychological health measures. Distal outcomes focus on self-rated functioning in complex daily activities and strategies used in daily life to enhance function. Socio-demographic factors (age, gender, and education), general cognition, personality traits, engagement in activities, and self-efficacy will be used as moderators. Enrolment began in April 2012 and will be completed by December 2014. Conclusions: This study is likely to have a significant impact on the well-being of persons with MCI by contributing to the development of adapted and scientifically supported cognitive and psychosocial interventions.
- Magnesium Protects Cognitive Functions and Synaptic Plasticity in Streptozotocin-Induced Sporadic Alzheimer's Model. [JOURNAL ARTICLE]
- PLoS One 2014; 9(9):e108645.
Alzheimer's disease (AD) is characterized by profound synapse loss and impairments of learning and memory. Magnesium affects many biochemical mechanisms that are vital for neuronal properties and synaptic plasticity. Recent studies have demonstrated that the serum and brain magnesium levels are decreased in AD patients; however, the exact role of magnesium in AD pathogenesis remains unclear. Here, we found that the intraperitoneal administration of magnesium sulfate increased the brain magnesium levels and protected learning and memory capacities in streptozotocin-induced sporadic AD model rats. We also found that magnesium sulfate reversed impairments in long-term potentiation (LTP), dendritic abnormalities, and the impaired recruitment of synaptic proteins. Magnesium sulfate treatment also decreased tau hyperphosphorylation by increasing the inhibitory phosphorylation of GSK-3β at serine 9, thereby increasing the activity of Akt at Ser473 and PI3K at Tyr458/199, and improving insulin sensitivity. We conclude that magnesium treatment protects cognitive function and synaptic plasticity by inhibiting GSK-3β in sporadic AD model rats, which suggests a potential role for magnesium in AD therapy.
- EphrinA4 mimetic peptide targeted to EphA binding site impairs the formation of long-term fear memory in lateral amygdala. [JOURNAL ARTICLE]
- Transl Psychiatry 2014.:e450.
Fear conditioning leads to long-term fear memory formation and is a model for studying fear-related psychopathologies conditions such as phobias and posttraumatic stress disorder. Long-term fear memory formation is believed to involve alterations of synaptic efficacy mediated by changes in synaptic transmission and morphology in lateral amygdala (LA). EphrinA4 and its cognate Eph receptors are intimately involved in regulating neuronal morphogenesis, synaptic transmission and plasticity. To assess possible roles of ephrinA4 in fear memory formation we designed and used a specific inhibitory ephrinA4 mimetic peptide (pep-ephrinA4) targeted to EphA binding site. We show that this peptide, composed of the ephrinA4 binding domain, interacts with EphA4 and inhibits ephrinA4-induced phosphorylation of EphA4. Microinjection of the pep-ephrinA4 into rat LA 30 min before training impaired long- but not short-term fear conditioning memory. Microinjection of a control peptide derived from a nonbinding E helix site of ephrinA4, that does not interact with EphA, had no effect on fear memory formation. Microinjection of pep-ephrinA4 into areas adjacent to the amygdala had no effect on fear memory. Acute systemic administration of pep-ephrinA4 1 h after training also impaired long-term fear conditioning memory formation. These results demonstrate that ephrinA4 binding sites in LA are essential for long-term fear memory formation. Moreover, our research shows that ephrinA4 binding sites may serve as a target for pharmacological treatment of fear and anxiety disorders.
- A flavonol, epicatechin, reverses the suppressive effects of a stressor on LTM formation. [JOURNAL ARTICLE]
- J Exp Biol 2014 Sep 29.
Learning and subsequent memory formation are influenced by both environmental and lifestyle factors, such as stress and diet. Epicatechin, a plant flavonol found in cocoa, red wine, and green tea enhances long term memory formation (LTM) in Lymnaea; while an ecologically relevant stressor, low calcium pond water, suppress LTM formation. We tested the hypothesis that epicatechin overcomes the suppressive effects of the stressor on LTM formation in the continued presence of the stressor. Snails trained in low calcium pond water exhibit learning but not LTM. Epicatechin (15 mg/L) in control pond water enhances LTM formation. When epicatechin was added to the low calcium pond water an enhanced LTM similar to that seen in control pond water was observed. Thus, a naturally occurring bioactive plant compound was able to overcome the suppressive effects of an ecologically relevant stressor on LTM formation.