Deficits In Memory Function Research Articles

Verbal Learning and Memory Deficits across Neurological and Neuropsychiatric Disorders: Insights from an ENIGMA Mega Analysis.

Deficits in memory performance have been linked to a wide range of neurological and neuropsychiatric conditions. While many studies have assessed the memory impacts of individual conditions, this study considers a broader perspective by evaluating how memory recall is differentially associated with nine common neuropsychiatric conditions using data drawn from 55 international studies, aggregating 15,883 unique participants aged 15-90. The effects of dementia, mild cognitive impairment, Parkinson's disease, traumatic brain injury, stroke, depression, attention-deficit/hyperactivity disorder (ADHD), schizophrenia, and bipolar disorder on immediate, short-, and long-delay verbal learning and memory (VLM) scores were estimated relative to matched healthy individuals. Random forest models identified age, years of education, and site as important VLM covariates. A Bayesian harmonization approach was used to isolate and remove site effects. Regression estimated the adjusted association of each clinical group with VLM scores. Memory deficits were strongly associated with dementia and schizophrenia (p < 0.001), while neither depression nor ADHD showed consistent associations with VLM scores (p > 0.05). Differences associated with clinical conditions were larger for longer delayed recall duration items. By comparing VLM across clinical conditions, this study provides a foundation for enhanced diagnostic precision and offers new insights into disease management of comorbid disorders.

High-fat diet and aging-associated memory impairments persist in the absence of microglia in female rats

Aging is associated with a priming of microglia such that they are hypersensitive to further immune challenges. As such high-fat diet during aging can have detrimental effects on cognition that is not seen in the young. However, conflicting findings also suggest that obesity may protect against cognitive decline during aging. Given this uncertainty we aimed here to examine the role of microglia in high-fat, high-sucrose diet (HFSD)-induced changes in cognitive performance in the aging brain. We hypothesised that 8 weeks of HFSD-feeding would alter microglia and the inflammatory milieu in aging and worsen aging-related cognitive deficits in a microglia-dependent manner. We found that both aging and HFSD reduced hippocampal neuron numbers and open field exploration; they also impaired recognition memory. However, the aging-related deficits occurred in the absence of a pro-inflammatory response and the deficits in memory performance persisted after depletion of microglia in the Cx3cr1-Dtr knock-in rat. Our data suggest that mechanisms additional to the acute microglial contribution play a role in aging- and HFSD-associated memory dysfunction.

Early postnatal moderate catch‑up growth in rats with nutritional intrauterine growth restriction preserves pulmonary vascular and cognitive function in adulthood.

Intrauterine growth restriction (IUGR) with rapid postnatal catch-up growth is strongly associated with pulmonary vascular dysfunction in adulthood, whereas IUGR with delayed growth in early postnatal life results in long-term brain deficits. In the present study, it was hypothesized that IUGR with early moderate catch-up growth may alleviate pulmonary vascular remodeling in adulthood without affecting memory function. An IUGR model was established by restricting maternal nutrition during pregnancy. Different growth patterns were achieved by adjusting the litter size in each group during lactation. Rats meeting the weight requirement at weaning were selected for subsequent studies at three time points (3, 9 and 13 weeks). Cognitive function was evaluated using a Y-maze. Invasive hemodynamic measurements were conducted to measure the mean pulmonary arterial pressure (mPAP). In addition, primary pulmonary artery smooth muscle cells (PASMCs) and pulmonary vascular endothelial cells (PVECs) were cultured to investigate their role in the increase in mPAP following rapid catch-up growth. The results showed that memory function deficits in the rats in the delayed growth group were associated with reduced proliferation of neural stem cells in the subgranular zone of the hippocampus. Furthermore, moderate catch-up growth at the three time points improved memory function while maintaining a normal mPAP. In adult IUGR rats experiencing rapid catch-up growth, although memory function improved, elevated mPAP and medial thickening of pulmonary arterioles were observed. Additionally, PASMCs exhibited excessive proliferation, migration and anti-apoptotic activity in the rapid catch-up group, and PVECs also displayed excessive proliferation. These results suggested that moderate catch-up growth after IUGR is a better strategy for optimal cognition and cardiovascular health in adulthood compared with rapid catch-up growth or delayed growth.

Resveratrol Preconditioning Mitigates Ischemia-Induced Septal Cholinergic Cell Loss and Memory Impairments.

Cholinergic cells originating from the nuclei of the basal forebrain (BF) are critical for supporting various memory processes, yet BF cholinergic cell viability has not been explored in the context of focal cerebral ischemia. In the present study, we examined cell survival within several BF nuclei in rodents following transient middle cerebral artery occlusion. We tested the hypothesis that a previously established neuroprotective therapy-resveratrol preconditioning-would rescue BF cell loss, deficits in cholinergic-related memory performance, and hippocampal synaptic dysfunction after focal cerebral ischemia. Adult (2-3-month old) male Sprague-Dawley rats or wild-type C57Bl/6J mice were injected intraperitoneally with a single dose of resveratrol or vehicle and subjected to transient middle cerebral artery occlusion using the intraluminal suture method 2 days later. Histopathological, behavioral, and electrophysiological outcomes were measured 1-week post-reperfusion. Animals with reduction in cerebral blood flow <30% of baseline were excluded. Cholinergic cell loss was observed in the medial septal nucleus and diagonal band of Broca following transient middle cerebral artery occlusion. This effect was prevented by resveratrol preconditioning, which also ameliorated transient middle cerebral artery occlusion-induced deficits in cognitive performance and hippocampal long-term potentiation. We demonstrate for the first time that focal cerebral ischemia induces cholinergic cell death within memory-relevant nuclei of the BF. The preservation of cholinergic cell viability may provide a mechanism by which resveratrol preconditioning improves memory performance and preserves functionality of memory-processing brain structures after focal cerebral ischemia.

Activation of the PACAP/PAC1 Signaling Pathway Accelerates the Repair of Impaired Spatial Memory Caused by an Ultradian Light Cycle.

The mechanism of light-induced spatial memory deficits, as well as whether rhythmic expression of the pituitary adenylyl cyclase-activating polypeptides (PACAP)-PAC1 pathway influenced by light is related to this process, remains unclear. Here, we aimed to investigate the role of the PACAP-PAC1 pathway in light-mediated spatial memory deficits. Animals were first housed under a T24 cycle (12 h light:12 h dark), and then light conditions were transformed to a T7 cycle (3.5 h light:3.5 h dark) for at least 4 weeks. The spatial memory function was assessed using the Morris water maze (MWM). In line with behavioral studies, rhythmic expression of the PAC1 receptor and glutamate receptors in the hippocampal CA1 region was assessed by western blotting, and electrophysiology experiments were performed to determine the influence of the PACAP-PAC1 pathway on neuronal excitability and synaptic signaling transmission. Spatial memory was deficient after mice were exposed to the T7 light cycle. Rhythmic expression of the PAC1 receptor was dramatically decreased, and the excitability of CA1 pyramidal cells was decreased in T7 cycle-housed mice. Compensation with PACAP1-38, a PAC1 receptor agonist, helped T7 cycle-housed mouse CA1 pyramidal cells recover neuronal excitability to normal levels, and cannulas injected with PACAP1-38 shortened the time to find the platform in MWM. Importantly, the T7 cycle decreased the frequency of AMPA receptor-mediated excitatory postsynaptic currents. In conclusion, the PACAP-PAC1 pathway is an important protective factor modulating light-induced spatial memory function deficits, affecting CA1 pyramidal cell excitability and excitatory synaptic signaling transmission.

P01.02.B Case Report: Disruption of Resting-State Networks and Cognitive Deficits After Whole Brain Irradiation for Singular Brain Metastasis

Abstract Background Long-term survivors of whole brain radiation (WBRT) are at significant risk for developing cognitive deficits, but knowledge about the underlying pathophysiological mechanisms is limited. Therefore, we here report a rare case with a singular brain metastasis treated by resection and WBRT that survived for more than 10 years where we investigated the integrity of brain networks using resting-state functional MRI. Material and Methods A female patient with a left frontal non-small cell lung cancer (NSCLC) brain metastasis had resection and postoperative WBRT (30.0 in 3.0Gy fractions) and stayed free from brain metastasis recurrence for a follow-up period of 11 years. Structural magnetic resonance imaging (MRI) and amino acid [O-(2-[18F]fluoroethyl)-L-tyrosine] positron emission tomography (FET PET) were repeatedly acquired. At the last follow up, neurocognitive functions and resting-state functional connectivity (RSFC) using resting-state fMRI were assessed. Within-network and inter-network connectivity of seven resting-state networks were computed from a connectivity matrix. All measures were compared to a matched group of 10 female healthy subjects. Results At the 11-year follow-up, T2/FLAIR MR images of the patient showed extended regions of hyper-intensities covering mainly the white matter of the bilateral dorsal frontal and parietal lobes while sparing most of the temporal lobes. Compared to the healthy subjects, the patient performed significantly worse in all cognitive domains that included executive functions, attention and processing speed, while verbal working memory, verbal episodic memory, and visual working memory were left mostly unaffected. The connectivity matrix showed a heavily disturbed pattern with a widely distributed, scattered loss of RSFC. The within-network RSFC revealed a significant loss of connectivity within all seven networks where the dorsal attention and fronto-parietal control networks were affected most severely. The inter-network RSFC was significantly reduced for the visual, somato-motor, and dorsal and ventral attention networks. Conclusion As demonstrated here in a patient with a metastatic NSCLC and long-term survival, WBRT may lead to extended white matter damage and cause severe disruption of the RSFC in multiple resting state networks. In consequence, executive functioning which is assumed to depend on the interaction of several networks may be severely impaired following WBRT apart from the well-recognized deficits in memory function.

Neural mechanisms that are related with falls in experimental animal models

In the elderly, falls can result in serious injuries, such as bone fracture, and also in loss of mobility and independence. Thus, with the aging of society, falls incur increasing costs impose a great cost burden on the public health system. In this short review, we introduce two related cases in experimental studies that are strongly correlated with falls: the first is the poorness of anticipatory postural adjustments (APAs) and the other is deficits of working memory in gait. There are two major aspects to postural control: compensatory postural reaction via sensory feedback mechanisms, and APAs via feed-forward mechanisms. The cerebellum has been suggested as being the brain region principally responsible for these postural control mechanisms. The first part of this review focuses on the deficiencies of APAs in a mouse model of spinocerebellar ataxia type 3 (SCA3), also known as Machado-Joseph disease (MJD). Memory function deficits, often encountered in patients with Alzheimer's disease (AD), are believed as being among the important causes of increased tripping in elderly patients. The second part of this review focuses on the impairments of memory-guided limb movements while stepping over an obstacle in triple-transgenic (3 xTg) mice generated as a model of AD.

The effects of divided attention at encoding and at retrieval on multidimensional source memory.

Dividing attention (DA) between a memory task and a secondary task results in deficits in memory performance across a wide array of memory tasks, but these effects are larger when DA occurs at encoding than at retrieval. Although some research suggests the effects of DA are equal for item and associative memory, thereby suggesting that DA disrupts all components of an episode to the same extent, there have been relatively few studies directly examining the effects of DA on multiple features of the same episode. In addition, no studies have examined how DA may affect the stochastic dependency between multiple source dimensions of a given episode, which is central to theories of source memory, and episodic memory in general. Thus, in two experiments, we used a multidimensional source memory task-examining memory for items and multiple source features-and separately investigated how DA at encoding or at retrieval affects item memory, source memory, and joint source retrieval. DA was manipulated at encoding in Experiment 1 and at retrieval in Experiment 2. Whereas DA at encoding disrupted item memory, as well as source memory and source-source binding, though to a lesser extent, DA at retrieval did not affect any of these outcomes. Results are discussed in terms of levels of binding and the role of attention in encoding and retrieval of bounded episodic representations. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Disruption of Tip60 HAT mediated neural histone acetylation homeostasis is an early common event in neurodegenerative diseases

Epigenetic dysregulation is a common mechanism shared by molecularly and clinically heterogenous neurodegenerative diseases (NDs). Histone acetylation homeostasis, maintained by the antagonistic activity of histone acetyltransferases (HATs) and histone deacetylases (HDACs), is necessary for appropriate gene expression and neuronal function. Disruption of neural acetylation homeostasis has been implicated in multiple types of NDs including Alzheimer’s disease (AD), yet mechanisms underlying alterations remain unclear. We show that like AD, disruption of Tip60 HAT/HDAC2 balance with concomitant epigenetic repression of common Tip60 target neuroplasticity genes occurs early in multiple types of Drosophila ND models such as Parkinson’s Disease (PD), Huntington’s Disease (HD) and Amyotrophic Lateral Sclerosis (ALS). Repressed neuroplasticity genes show reduced enrichment of Tip60 and epigentic acetylation signatures at all gene loci examined with certain genes showing inappropriate HDAC2 repressor enrichment. Functional neuronal consequences for these disease conditions are reminiscent of human pathology and include locomotion, synapse morphology, and short-term memory deficits. Increasing Tip60 HAT levels specifically in the mushroom body learning and memory center in the Drosophila brain protects against locomotion and short-term memory function deficits in multiple NDs. Together, our results support a model by which Tip60 protects against neurological impairments in different NDs via similar modes of action.

Prenatal stress impairs memory function in the early development of male-offspring associated with the gaba function

Prenatal stress (PS) induces cognitive deficits, abnormal behavior patterns and physical impairments in offspring, which disturbs the developmental process. GABA systems play a key role in the brain development. The developmental trajectories are less understood although PS increases the expression of GABAAR in young offspring. In the present study, we aimed to examine if the long-lasting effects on memory function and hippocampal synaptic plasticity induced by PS were associated with the GABA function throughout developmental process. Thus, a PS rat model was established by using restraint stress three 45-min periods per day from gestational day 15 until delivery. PS-exposed offspring exhibited the memory function deficits, LTP and depotentiation inhibitions in young and puberty offspring, but the disorder resolved at adult offspring. Meanwhile, the hippocampal spine density was decreased by PS in offspring. Additionally, we found that the balance of excitatory and inhibitory receptors was significantly disturbed after PS. The immunostaining of parvalbumin level was increased in the PS group. Overall, these all results suggest that the PS induces negative effects in memory and hippocampal synaptic plasticity in the early developmental stage, which could be an underlying mechanism of the disturbed GABA function.

T51. VERBAL MEMORY TRAJECTORIES IN CHRONIC INDIVIDUALS WITH SCHIZOPHRENIA ALONG 6 YEARS

BackgroundIndividuals with schizophrenia (SZ) present different positive, negative and cognitive symptoms that impact psychosocial functioning. Cognitive impairments are shown to be present even in premorbid stages of psychosis, which is related to the neurodevelopmental model of SZ. However, although well described in the literature, the trajectories and mechanisms of cognitive symptoms are still unclear. Some evidence suggest that the deficits may remain stable after the first episode and follow the normal course of aging. Conversely, other studies show a decline in cognitive performance related to the chronicity of the disorder. A central domain widely studied in SZ because of its relationship to functional outcomes is verbal memory (VM), which is particularly vulnerable to aging. Therefore, our aim was to investigate the trajectory of memory performance after 6 years in a sample of chronic individuals with SZ to bring further evidence for the two possible hypotheses (stability vs. progression).MethodsWe recruited 28 individuals with SZ (18 male, 10 female) from an outpatient clinic from a tertiary hospital in Porto Alegre, Brazil. These participants were part of a previous study, resulting in two point assessments of 6 years difference. Patients were stable and receiving pharmacological treatment. We conducted clinical interviews to collect sociodemographic and clinical data. Memory was assessed through the Hopkins Verbal Learning Test Revised (HVLT-R) on the two time points. Scores were transformed to z based on a healthy control sample. Analysis were conducted in the SPSS 18 and included general linear models and other exploratory analysis. The local ethics committee approved this study.ResultsOn the first assessment, patients had 37.32(±11.28) years old, 10.54(±3.68) years of education, and 13.96 (±10.52) years since disease onset. Patients showed deficits in memory performance in both time points (T1: Z = -1.56(±1.19), T2: Z = -1.72(±1.19). However, there was no difference between baseline and follow-up after 5.78 (±0.9) years for the total immediate recall (p=.516). Additionally, we did not find significant effects of age and years of education to memory performance. Interestingly, duration of illness had a main effect predicting memory performance, however this was independent of time points (p=.003). Interestingly, 53.6% of patients decreased its performance on the follow-up, while 46.4% increased it. When we considered these two groups, we found an interaction of the time of assessment by increased/decreased trajectory in the prediction of memory performance (p = .001).DiscussionAlthough we did not find differences between baseline and follow-up assessments, we found two different groups with diverse trajectories. The most recent studies in SZ have discussed the existence of these subgroups in the disorder. Our results didn’t showed evidence of impacts of both neurodevelopment or neuroprogression theories, the limited sample size may have influenced this. However, the two moment of assessment were with more than 10 years after the disease onset, adding to the compelling evidence that most of the cognitive deficits occur during early stages of the disorder.

Aging Alters Olfactory Bulb Network Oscillations and Connectivity: Relevance for Aging-Related Neurodegeneration Studies.

The aging process eventually cause a breakdown in critical synaptic plasticity and connectivity leading to deficits in memory function. The olfactory bulb (OB) and the hippocampus, both regions of the brain considered critical for the processing of odors and spatial memory, are commonly affected by aging. Using an aged wild-type C57B/6 mouse model, we sought to define the effects of aging on hippocampal plasticity and the integrity of cortical circuits. Specifically, we measured the long-term potentiation of high-frequency stimulation (HFS-LTP) at the Shaffer-Collateral CA1 pyramidal synapses. Next, local field potential (LFP) spectra, phase-amplitude theta-gamma coupling (PAC), and connectivity through coherence were assessed in the olfactory bulb, frontal and entorhinal cortices, CA1, and amygdala circuits. The OB of aged mice showed a significant increase in the number of histone H2AX-positive neurons, a marker of DNA damage. While the input-output relationship measure of basal synaptic activity was found not to differ between young and aged mice, a pronounced decline in the slope of field excitatory postsynaptic potential (fEPSP) and the population spike amplitude (PSA) were found in aged mice. Furthermore, aging was accompanied by deficits in gamma network oscillations, a shift to slow oscillations, reduced coherence and theta-gamma PAC in the OB circuit. Thus, while the basal synaptic activity was unaltered in older mice, impairment in hippocampal synaptic transmission was observed only in response to HFS. However, age-dependent alterations in neural network appeared spontaneously in the OB circuit, suggesting the neurophysiological basis of synaptic deficits underlying olfactory processing. Taken together, the results highlight the sensitivity and therefore potential use of LFP quantitative network oscillations and connectivity at the OB level as objective electrophysiological markers that will help reveal specific dysfunctional circuits in aging-related neurodegeneration studies.

Hippocampal cognitive impairment in juvenile rats after repeated mild traumatic brain injury

There is growing awareness that repeated mild traumatic brain injury (r-mTBI) can cause deficits in learning and memory performance, however there is still a paucity of preclinical data identifying the extent of these deficits. Epidemiological data shows that juveniles are at high risk to sustain r-mTBI, and these injuries may cause significant changes in cognitive abilities, as they occur during a period where the brain is still maturing. This is particularly true for the hippocampus, a brain region important for learning and memory processes. R-mTBI during the juvenile period may disrupt functional capacity of the hippocampus, and thus the normal development of cognitive processes associated with this structure. To examine this issue we used a model of awake closed head injury (ACHI) and administered 8 impacts over a 4 day period to juvenile male and female rats (P25-28). A neurological assessment was preformed after each impact, and anxiety and learning related behaviours were examined 1 and 7 days after the last impact. Our results indicate that r-mTBI was associated with sensorimotor deficits in the acute phase immediately after each procedure. R-mTBI also reduced the capacity for hippocampal-dependent learning for at least 7 days post-injury, but did not result in any long-lasting changes in anxiety-related behaviours.

A Systematic Review of Human Neuroimaging Evidence of Memory-Related Functional Alterations Associated with Cannabis Use Complemented with Preclinical and Human Evidence of Memory Performance Alterations.

Cannabis has been associated with deficits in memory performance. However, the neural correlates that may underpin impairments remain unclear. We carried out a systematic review of functional magnetic resonance imaging (fMRI) studies investigating brain functional alterations in cannabis users (CU) compared to nonusing controls while performing memory tasks, complemented with focused narrative reviews of relevant preclinical and human studies. Twelve studies employing fMRI were identified finding functional brain activation during memory tasks altered in CU. Memory performance studies showed CU performed worse particularly during verbal memory tasks. Longitudinal studies suggest that cannabis use may have a causal role in memory deficits. Preclinical studies have not provided conclusive evidence of memory deficits following cannabinoid exposure, although they have shown evidence of cannabinoid-induced structural and histological alteration. Memory performance deficits may be related to cannabis use, with lower performance possibly underpinned by altered functional activation. Memory impairments may be associated with the level of cannabis exposure and use of cannabis during developmentally sensitive periods, with possible improvement following cessation of cannabis use.

Cannabis involvement and neuropsychological performance: findings from the Human Connectome Project

There is evidence that heavy cannabis use is associated with decrements in cognitive performance, but findings are mixed and studies are often limited by small sample sizes and narrow adjustment for potential confounding variables. In a comparatively large sample, the current study examined associations between multiple indicators of cannabis use in relation to performance on a variety of neuropsychological tasks. Participants were 1121 adults (54% female) enrolled in the Human Connectome Project. Cannabis involvement comprised recent cannabis use (positive tetrahydrocannabinol screen), total number of lifetime uses, cannabis use disorder and age at first use. The neuropsychological battery comprised performance in episodic memory, fluid intelligence, attention, working memory, executive function, impulsive decision-making, processing speed and psychomotor dexterity. Covariates were age, sex, income, family structure and alcohol and tobacco use. Positive urinary tetrahydrocannabinol status was associated with worse performance in episodic memory and processing speed, and positive cannabis use disorder status was associated with lower fluid intelligence (all p < 0.005). No other significant associations were present. The sample was limited to young adults aged 22–36 years. The measures of cannabis involvement were relatively coarse. Beyond an array of potential confounders, recent cannabis use was associated with deficits in memory and psychomotor performance, and cannabis use disorder was associated with lower overall cognitive functioning in a large normative sample of adults. The findings pertaining to recent use have particular relevance for occupational settings.

Impaired working memory performance in opioid-dependent patients is related to reduced insula gray matter volume: a voxel-based morphometric study.

Opioid-dependent patients frequently show deficits in multiple cognitive domains that might impact on their everyday life performance and interfere with therapeutic efforts. To date, the neurobiological underpinnings of those deficits remain to be determined. We investigated working memory performance and gray matter volume (GMV) differences in 17 patients on opioid maintenance treatment (OMT) and 17 healthy individuals using magnetic resonance imaging and voxel-based morphometry. In addition, we explored associations between substance intake, gray matter volume, and working memory task performance. Patients on OMT committed more errors during the working memory task than healthy individuals and showed smaller insula and putamen GMV. The duration of heroin use prior to OMT was associated with working memory performance and insula GMV in patients. Neither the substitution agent (methadone and buprenorphine) nor concurrent abuse of illegal substances during the 3months prior to the experiment was significantly associated with GMV. Results indicate that impaired working memory performance and structural deficits in the insula of opioid-dependent patients are related to the duration of heroin use. This suggests that early inclusion into OMT or abstinence-oriented therapies that shorten the period of heroin abuse may limit the impairments to GMV and cognitive performance of opioid-dependent individuals.

Autobiographical memory in epileptic patients after temporal lobe resection or bitemporal hippocampal sclerosis.

The human hippocampus is believed to be a crucial node in the neural network supporting autobiographical memory retrieval. Structural mesial temporal damage associated with temporal lobe epilepsy (TLE) provides an opportunity to systematically investigate and better understand the local and distal functional consequences of mesial temporal damage in the engagement of the autobiographical memory network. We examined 19 TLE patients (49.21 ± 11.55years; 12 females) with unilateral mesial TLE (MTLE; 12 with anterior temporal lobe resection: 6 right MTLE, 6 left MTLE) or bilateral mesial TLE (7 BMTLE) and 18 matched healthy subjects. We used functional MRI (fMRI) with an adapted autobiographical memory paradigm and a specific neuropsychological test (Autobiographical Memory Interview, AMI). While engaged in the fMRI autobiographical memory paradigm, all groups activated a large fronto-temporo-parietal network. However, while this network was left lateralized for healthy participants and right MTLE patients, left MTLE and patients with BMTLE also showed strong activation in right temporal and frontal regions. Moreover, BMTLE and left MTLE patients also showed significant mild deficits in episodic autobiographical memory performance measured with the AMI test. The right temporal and extra-temporal fMRI activation, along with the impairment in autobiographical memory retrieval found in left MTLE and BMTLE patients suggest that alternate brain areas-other than the hippocampus-may also support this process, possibly due to neuroplastic effects.

Prospective memory (partially) mediates the link between ADHD symptoms and procrastination

Individuals with attention deficit hyperactivity disorder (ADHD) often show poor planning and poor organization of tasks and activities which has been related to reduced memory for delayed intentions (prospective memory) and procrastination—in addition to other cognitive or motivational factors. This study set out to bring the fields of prospective memory and procrastination research together and to explore possible relations between the two constructs in ADHD. Twenty-nine adults with ADHD and 24 healthy controls performed several laboratory-based and real-life prospective memory tasks and filled in questionnaires measuring their symptom severity and procrastination behaviour. Overall, individuals’ with ADHD showed clear deficits in everyday prospective memory performance. Individuals with ADHD recalled and executed less of their own real-life intentions. Moreover, there were clear links between everyday prospective memory performance and reported procrastination behaviour, and everyday prospective memory performance mediated the link between ADHD symptoms and procrastination behaviour.

Brain transcriptome changes in the aging Drosophila melanogaster accompany olfactory memory performance deficits.

Cognitive decline is a common occurrence of the natural aging process in animals and studying age-related changes in gene expression in the brain might shed light on disrupted molecular pathways that play a role in this decline. The fruit fly is a useful neurobiological model for studying aging due to its short generational time and relatively small brain size. We investigated age-dependent changes in the Drosophila melanogaster whole-brain transcriptome by comparing 5-, 20-, 30- and 40-day-old flies of both sexes. We used RNA-Sequencing of dissected brain samples followed by differential expression, temporal clustering, co-expression network and gene ontology enrichment analyses. We found an overall decline in expression of genes from the mitochondrial oxidative phosphorylation pathway that occurred as part of aging. We also detected, in females, a pattern of continuously declining expression for many neuronal function genes, which was unexpectedly reversed later in life. This group of genes was highly enriched in memory-impairing genes previously identified through an RNAi screen. We also identified deficits in short-term olfactory memory performance in older flies of both sexes, some of which matched the timing of certain changes in the brain transcriptome. Our study provides the first transcriptome profile of aging brains from fruit flies of both sexes, and it will serve as an important resource for those who study aging and cognitive decline in this model.

Radiation- induced cognitive impairments

Introduction: Ionizing radiation is non-surgical treatment of brain tumors and metastases. Preclinical studies have showed main insights into harmful effects of radiation on the nervous system in vivo and in vitro. Cognitive impairment such as progressive memory, executive and attention performance deficits indicates a significant risk for patients experiencing conventional radiotherapy. Changes in hippocampus-dependent cognition often state radiation-induced cognitive destruction. Radiation-induced brain injury can impair neuronal, glial and vascular parts of the brain and may cause to molecular, cellular and functional alterations. Materials and Method: In order to investigate this topic, the articles were searched for in the following bibliographic database: PubMed, Scopus, Science Direct and Google scholar and among the words used when searching were: cranial irradiation, cognitive impairment. Results and Conclusion: To avoid of the hippocampus impairment in cranial irradiating, whereas allowing for same dose sending to the remainder of the brain, poses severe challenges given the central position and unique anatomic shape of the hippocampus. Recently, previous studies showed that the ability of modern intensity-modulated radiotherapy methods, like LINAC-based intensity-modulated radiotherapy and helical tomotherapy, to permit for the delivery of extremely conformal dose distributions.