Short-term Memory Deficits Research Articles

The last decade's experience of management of central neurocytomas: Treatment strategies and new options.

Background: The purpose of the presented work is to evaluate the last decade’s experience in surgical management of central neurocytoma (CN) and elucidate on the treatment strategies and new options.Methods: The current series consists of the remaining 125 patients (70 females and 55 males) operated on during the past decade from 2008 to 2018. Most tumors were resected through transcortical (n = 76, 61%), or transcallosal (n = 40, 32%) approaches. In 5 (4%) patients with predominantly posterior location of the tumor, non-dominant superior parietal lobule approach was utilized. Both approaches (transcortical + transcallosal) were used in 4 (3%) of cases. Seven consecutive patients with large CN underwent prophylactic intraventricular stenting to prevent hydrocephalus.Results: Gross total resection was achieved in 45 patients (36%), subtotal resection (STR) in 40 (32%) cases. After surgery, 63 (50%) patients had neurocognitive problems, including disorientation, attention deficit, global amnesia, short-term memory deficits, and perceptual motor and social cognition problems. A total of 26 patients (21%) had postoperative hemorrhage in the resection bed. Obstructive hydrocephalus was noted in 25 (20%) patients. The entrapment of the occipital and/or temporal horns was observed in seven cases. None of the seven patients with prophylactic intraventricular stents required shunting.Conclusion: Although high rates of gross total or STR can be expected, the mortality and morbidity remain significant even in the modern neurosurgical era. Prophylactic intraventricular stenting in patients with large posteriorly located tumors with hydrocephalus may prevent ventricular entrapment and shunting. The main risk factors for recurrence are presence of residual disease and Ki-67 index over 5%. Recurrent symptomatic tumors should be treated surgically, whereas asymptomatic progression can be managed with stereotactic radiosurgery. Both treatment modalities are associated with low risk of complications and high tumor control rates.

Psychopathology mediates between maltreatment and memory functioning in Burundian refugee youth

BackgroundThe detrimental impact of child maltreatment on children and adolescents' academic achievement and later socioeconomic wellbeing is well known. However, it is still unclear (1) whether maltreatment is actually linked to youth's long- and short-term memory deficits and (2) whether potential impairments are due to maltreatment per se or related psychopathology. ObjectiveBased on the Attentional Control Theory, we investigated a mediational model in which maltreatment would be related to psychopathology (internalizing symptoms, posttraumatic stress symptoms, posttraumatic cognitions), which would in turn be related to impaired memory functioning. Participants and settingWe drew on a sample of 155 Burundian refugee youth (aged 11 to 15) currently living in refugee camps in Tanzania and at high risk of experiencing ongoing maltreatment by parents. MethodsYouth reported on their experiences of maltreatment and psychopathology in structured clinical interviews and completed visuospatial memory tasks involving a short-term and a working memory component (Corsi Block Tapping Test) and delayed recall from long-term memory (Rey-Osterrieth Complex Figure). ResultsStructural equation modeling showed that psychopathology mediated the association between increased maltreatment and reduced working memory capacity (β = −0.07, p = .02), with a trend towards mediation for short-term memory (β = −0.05, p = .06). Higher levels of maltreatment, but not psychopathology, were directly linked to long-term memory deficits (β = −0.20, p = .02). ConclusionsPreventive efforts targeting maltreatment and interventions focusing on related psychopathology are needed to counter memory deficits and their potential negative implications for academic and socioeconomic outcomes.

JM-20 Treatment After Mild Traumatic Brain Injury Reduces Glial Cell Pro-inflammatory Signaling and Behavioral and Cognitive Deficits by Increasing Neurotrophin Expression.

Traumatic brain injury (TBI) is considered a public health problem and is often related to motor and cognitive disabilities, besides behavioral and emotional changes that may remain for the rest of the subject's life. Resident astrocytes and microglia are the first cell types to start the inflammatory cascades following TBI. It is widely known that continuous or excessive neuroinflammation may trigger many neuropathologies. Despite the large numbers of TBI cases, there is no effective pharmacological treatment available. This study aimed to investigate the effects of the new hybrid molecule 3-ethoxycarbonyl-2-methyl-4-(2-nitrophenyl)-4,11-dihydro1H-pyrido[2,3-b][1,5]benzodiazepine (JM-20) on TBI outcomes. Male Wistar rats were submitted to a weight drop model of mild TBI and treated with a single dose of JM-20 (8mg/kg). Twenty-four hours after TBI, JM-20-treated animals showed improvements on locomotor and exploratory activities, and short-term memory deficits induced by TBI improved as well. Brain edema was present in TBI animals and the JM-20 treatment was able to prevent this change. JM-20 was also able to attenuate neuroinflammation cascades by preventing glial cells-microglia and astrocytes-from exacerbated activation, consequently reducing pro-inflammatory cytokine levels (TNF-α and IL-1β). BDNF mRNA level was decreased 24h after TBI because of neuroinflammation cascades; however, JM-20 restored the levels. JM-20 also increased GDNF and NGF levels. These results support the JM-20 neuroprotective role to treat mild TBI by reducing the initial damage and limiting long-term secondary degeneration after TBI.

Rare presentation of autoimmune limbic encephalitis with anti-Yo antibodies: Case report

Introduction: Paraneoplastic limbic encephalitis is a non-metastatic complication of malignant disease characterized by subacute neuropsychiatric symptoms and short-term memory deficits. Case: We present an atypical case of a 38-year-old, previously healthy female with recurrent seizures, severe persistent short-term memory loss, and emotional lability. The patient was diagnosed with autoimmune limbic encephalitis confirmed by magnetic resonance imaging findings and positive anti-Yo antibodies. She screened negative for occult malignancies. The patient responded to daily prednisone and intravenous immunoglobulins and her cognitive deficits were resolved. Conclusion: This is an unusual case of autoimmune encephalitis as anti-Yo antibodies are typically associated with cerebellar dysfunction. Our patient’s case adds to the one other published case showing induction of limbic encephalitis due to anti-Yo antibodies, and prompts consideration of paraneoplastic anti-Yo limbic encephalitis as a rare cause of symptoms in patients with limbic encephalitis-like symptoms and no known etiology.

Phonological Short-Term Memory Impairment in Children with Down Syndrome

Abstract Background: Children with Down Syndrome commonly suffer from phonological and other language disorders which have been partly attributed to underlying deficit in phonological short term memory. Its evaluation was previously confined to non word repetition and/or forward digit span tasks. Aim of Study: To assess phonological short term memory in children with Down Syndrome with mild degree of intel-lectual disability in comparison with non syndromic children with mild degree of intellectual disability to find out any possible correlation between Down Syndrome and phonolog-ical short term memory deficits through comprehensive eval-uation. Subjects and Methods: This case control study has been conducted on 40 children (20 Down Syndrome children with mild degree of intellectual disability, 20 non syndromic children with mild degree of intellectual disability with matched mental age). All of them underwent psychometric evaluation, audiological evaluation, language evaluation using Arabic version of Modified Preschool Language Scale-4th edition (PLS-4), and Arabic version of Phonological Short Term Memory Test (PSTM). Results: Down Syndrome group scored significantly lower than non syndromic children with mild degree of intellectual disability in all items of phonological short term memory test; digit span, syllable repetition, non sense word repetition, dissimilar word set recall, similar word set recall, total score (p-value 0.000, 0.001, 0.004, 0.000, 0.000, 0.000 respectively) and language test; expressive abilities was lower in Down syndrome children (p-value 0.002) but both groups were equal in their receptive abilities (p-value 0.054). Conclusion: Children with Down Syndrome scored below expected for phonological short term memory and their pho-nological store was extensively impaired.

Cocoa supplementation reduces amyloid-beta1–42 (Aβ1–42) induced deficits in a transgenic C. elegans

BACKGROUND: Cocoa, a significant contributor of polyphenols to the western diet has been shown to be effective against Aβ induced toxicity in vitro. However, the effects of long-term cocoa supplementation on Aβ induced behavioural deficits, particularly on the short-term memory loss observed in human AD are not well defined. OBJECTIVE: This study characterized the phenotype of a pan-neuronal Aβ expressing C. elegans strain and investigated the effects of long-term cocoa supplementation on Aβ induced behavioural deficits including short-term memory loss and lifespan. METHODS: Cocoa powder was supplemented to the E. coli OP50 diet of C. elegans starting from L1 stage until they die. Neuronally controlled processes including locomotion, learning and memory were studied at different stages of the lifespan. In addition, lifespan was evaluated with different cocoa doses. Aβ fibril levels were determined with Thioflavin T. RESULTS: Aβ expressing worms showed a reduced growth, a reduced maximum speed at old age, short-term memory deficits at middle age and a reduced lifespan. Cocoa-supplementation reversed the deficits in growth, maximum speed, short-term memory loss and lifespan to reach similar levels to control counterparts while reducing the Aβ fibril levels. CONCLUSIONS: Long-term cocoa supplementation seemed to improve Aβ induced deficits in C. elegans.

Marked Mild Cognitive Deficits in Humanized Mouse Model of Alzheimer's-Type Tau Pathology.

Hyperphosphorylation and the subsequent aggregation of tau protein into neurofibrillary tangles (NFTs) are well-established neuropathological hallmarks of Alzheimer’s disease (AD) and associated tauopathies. To further examine the impact and progression of human tau pathology in neurodegenerative contexts, the humanized tau (htau) mouse model was originally created. Despite AD-like tau pathological features recapitulated in the htau mouse model, robustness of behavioral phenotypes has not been fully established. With the ultimate goal of evaluating the htau mouse model as a candidate for testing AD therapeutics, we set out to verify, in-house, the presence of robust, replicable cognitive deficits in the htau mice. The present study shows behavioral data collected from a carefully curated battery of learning and memory tests. Here we report a significant short-term spatial memory deficit in aged htau mice, representing a novel finding in this model. However, we did not find salient impairments in long-term learning and memory previously reported in this mouse model. Here, we attempted to understand the discrepancies in the literature by highlighting the necessity of scrutinizing key procedural differences across studies. Reported cognitive deficits in the htau model may depend on task difficulty and other procedural details. While the htau mouse remains a unique and valuable animal model for replicating late onset AD-like human tau pathology, its cognitive deficits are modest under standard testing conditions. The overarching message is that before using any AD mouse model to evaluate treatment efficacies, it is imperative to first characterize and verify the presence of behavioral deficits in-house.

Differential effects of alkaloids on memory in rodents

Nicotinic acetylcholine receptors (nAChRs) play a critical role in the neuropharmacology of learning and memory. As such, naturally occurring alkaloids that regulate nAChR activity have gained interest for understanding and potentially improving memory function. In this study, we tested the acute effects of three known nicotinic alkaloids, nicotine, cotinine, and anatabine, in suppressing scopolamine-induced memory deficit in rodents by using two classic memory paradigms, Y-maze and novel object recognition (NOR) in mice and rats, respectively. We found that all compounds were able to suppress scopolamine-induced spatial memory deficit in the Y-maze spontaneous alternation paradigm. However, only nicotine was able to suppress the short-term object memory deficit in NOR, despite the higher doses of cotinine and anatabine used to account for their potential differences in nAChR activity. These results indicate that cotinine and anatabine can uniquely regulate short-term spatial memory, while nicotine seems to have more robust and general role in memory regulation in rodents. Thus, nAChR-activating alkaloids may possess distinct procognitive properties in rodents, depending on the memory types examined.

Ilex kudingcha C.J. Tseng Mitigates Phenotypic Characteristics of Human Autism Spectrum Disorders in a Drosophila Melanogaster Rugose Mutant.

Autism spectrum disorders (ASD) have heterogeneous etiologies involving dysfunction of central nervous systems, for which no effective pan-specific treatments are available. Ilex kudingcha (IK) C.J. Tseng is a nootropic botanical used in Asia for neuroprotection and improvement of cognition. This study establishes that a chemically characterized extract from IK (IKE) mitigates behavioral traits in the Drosophila melanogaster rugose mutant, whose traits resemble human ASD, and examines possible mechanisms. IKE treatment significantly ameliorated deficits in social interaction, short-term memory, and locomotor activity in Drosophila rugose, and significantly increased synaptic bouton number of size more than 2 μm2 in the neuromuscular junctions (NMJs) of Drosophila rugose. To clarify mechanism(s) of IKE action, methylphenidate (MPH), a dopamine transporter inhibitor, was included as a reference drug in the behavioral assays: MPH significantly improved social interaction and short-term memory deficit in Drosophila rugose; administration of the dopamine D1 receptor antagonist SCH23390 and dopamine D2 receptor antagonist sulpiride reversed the ameliorative effects of both MPH and IKE on the social interaction deficits of Drosophila rugose. To extend analysis of IKE treatment to the vertebrate central nervous system, ASD-associated gene expression in mouse hippocampus was studied by RNA-seq: IKE treatment altered the expression of genes coding phosphoinositide 3-kinases/protein kinase B (PI3K-Akt), proteins in glutamatergic, dopaminergic, serotonergic, and GABAergic synapses, cAMP response element-binding protein (CREB), and RNA transporter proteins. These results provide a foundation for further analysis of IKE as a candidate for treatment of some forms of ASD.

Maternal antibodies facilitate Amyloid-\u03b2 clearance by activating Fc-receptor-Syk-mediated phagocytosis

Maternal antibodies (MAbs) protect against infections in immunologically-immature neonates. Maternally transferred immunity may also be harnessed to target diseases associated with endogenous protein misfolding and aggregation, such as Alzheimer’s disease (AD) and AD-pathology in Down syndrome (DS). While familial early-onset AD (fEOAD) is associated with autosomal dominant mutations in the APP, PSEN1,2 genes, promoting cerebral Amyloid-β (Aβ) deposition, DS features a life-long overexpression of the APP and DYRK1A genes, leading to a cognitive decline mediated by Aβ overproduction and tau hyperphosphorylation. Although no prenatal screening for fEOAD-related mutations is in clinical practice, DS can be diagnosed in utero. We hypothesized that anti-Aβ MAbs might promote the removal of early Aβ accumulation in the central nervous system of human APP-expressing mice. To this end, a DNA-vaccine expressing Aβ1-11 was delivered to wild-type female mice, followed by mating with 5xFAD males, which exhibit early Aβ plaque formation. MAbs reduce the offspring’s cortical Aβ levels 4 months after antibodies were undetectable, along with alleviating short-term memory deficits. MAbs elicit a long-term shift in microglial phenotype in a mechanism involving activation of the FcγR1/Syk/Cofilin pathway. These data suggest that maternal immunization can alleviate cognitive decline mediated by early Aβ deposition, as occurs in EOAD and DS.

Hyperactive Behavior and Altered Brain Morphology in Adult Complement C3a Receptor Deficient Mice.

The C3a receptor (C3aR) is a seven trans-membrane domain G-protein coupled receptor with a range of immune modulatory functions. C3aR is activated by the third complement component (C3) activation derived peptide C3a and a neuropeptide TLQP-21. In the central nervous system (CNS), C3aR is expressed by neural progenitors, neurons as well as glial cells. The non-immune functions of C3aR in the adult CNS include regulation of basal neurogenesis, injury-induced neural plasticity, and modulation of glial cell activation. In the developing brain, C3aR and C3 have been shown to play a role in neural progenitor cell proliferation and neuronal migration with potential implications for autism spectrum disorder, and adult C3aR deficient (C3aR−/−) mice were reported to exhibit subtle deficit in recall memory. Here, we subjected 3 months old male C3aR−/− mice to a battery of behavioral tests and examined their brain morphology. We found that the C3aR−/− mice exhibit a short-term memory deficit and increased locomotor activity, but do not show any signs of autistic behavior as assessed by self-grooming behavior. We also found regional differences between the C3aR−/− and wild-type (WT) mice in the morphology of motor and somatosensory cortex, as well as amygdala and hippocampus. In summary, constitutive absence of C3aR signaling in mice leads to neurodevelopmental abnormalities that persist into adulthood and are associated with locomotive hyperactivity and altered cognitive functions.

A Case Series on Neuroborreliosis- An Emerging Infection in India

Lyme disease is a zoonotic disease spread by the bite of Ixodes ticks. These ticks are known to be found in wooded or grassy areas. The disease manifestations can be divided into early Lyme disease and late Lyme disease. The manifestations of late Lyme disease may include arthritis, cranial nerve palsies, short-term memory deficits and Lyme carditis. The disease is diagnosed by a two-step process of Enzyme immunoassay followed by Western blot Test. Disseminated disease is treated with Intravenous (IV) ceftriaxone, cefotaxime or penicillin G, or a combination of oral and IV regimens or in some cases, only oral drugs for up to 28 days. Lyme disease is endemic in temperate regions, especially in America. However, over the years the disease has been reported from various countries of Asia including in India, where there have been sporadic cases. Hereby, the author presents three paediatric cases with varied presentations. The neurological symptoms ranged from Lower Motor Neuron (LMN) facial nerve palsy to acute encephalitis. One patient also had non-erosive arthritis.

Posterior reversible encephalopathy syndrome with reversible cerebral vasoconstriction syndrome in a normal primigravida woman at the 35-week gestational stage: a case report

Background: Herein, we report a case of cerebral hemorrhage in a 21-year-old nulliparous, primi gravida woman caused by posterior reversible encephalopathy syndrome (PRES), which may be associated with reversible cerebral vasoconstriction syndrome (RCVS). Case: The patient’s medical history was unremarkable, apart from the mother having had a cerebral infarction. She had been examined by a local doctor, and showed good progress; however, her blood pressure (BP) was 143/97 mmHg, she had findings of proteinuria (3+) and she had a headache on the 35th week with multiple vomiting episodes. She was admitted to our hospital after poor responsiveness and a consciousness level of GCS14, E4V4M6, a BP of 143/97 mmHg, a pulse rate of 77/min, bilateral abduction of the eyes, and left hemiplegia. Cranial computed tomography (CT) revealed cerebral hemorrhage with ventricular puncture in the right caudate nucleus. Emergency caesarean section was performed on the same day with priority given to maternal lifesaving. Acute cerebral infarction findings and PRES were observed on head magnetic resonance imaging (MRI) on the admission day 1. Head MR angiography on the 4th hospital day showed narrowing of the entire main artery trunk, suspected as RCVS. Short-term memory deficits were diagnosed post-extubation, but gradually improved. Although it became possible and hematoma in the ventricles were absorbed, left paresis and higher dysfunction were observed, and she was discharged on the 21st hospital day. Conclusion: PRES and RCVS occur simultaneously quite frequently, but require opposing treatment approaches. Both cases are reversible, but if they occur simultaneously, RCVS, which progresses slowly, may cause irreversible symptoms, thereby requiring careful treatment.

Developing the Concept of Working Memory: The Role of Neuropsychology1.

The evolution of the concept of a multicomponent working memory is described with particular reference to the contribution from neuropsychology. Early evidence from patients with the classic amnesic syndrome, together with others showing the opposite deficit of impaired short-term but preserved long-term memory argued strongly for a separation between long- and short-term memory systems. Simulation of the short-term deficit in healthy participants using a dual task approach suggested the need to assume a three component system serving as a multi-purpose working memory comprising an overall attentional control system, the Central Executive, aided by separable temporary buffer stores for phonological and visuospatial information. An account is then given of the way in which evidence from patients was combined with the study of healthy participants to test and expand the model over subsequent years. This led to the need to propose a fourth component, the Episodic Buffer, a system that combines information from multiple sources and makes it accessible to conscious awareness. I conclude with a brief account of how the multicomponent approach resembles and differs from that of other current models of working memory.

Memory Deficits in Children with Developmental Dyslexia: A Reading-Level and Chronological-Age Matched Design.

Developmental Dyslexia (DD) is considered a multifactorial deficit. Among the neurocognitive impairments identified in DD, it has been found that memory plays a particularly important role in reading and learning. The present study aims to investigate whether short-term memory (STM) and long-term memory (LTM) deficits could be related to poor reading experience or could be causal factors in DD. To verify that memory deficits in DD did not simply reflect differences in reading experience, 16 children with DD were not only compared to 16 chronological age-matched children (CA) but also to 16 reading level-matched children (RL) in verbal, visual-object, and visual-spatial STM and LTM tasks. Children with DD performed as well as RL, but worse than CA in all STM tasks. Considering LTM, the three groups did not differ in Visual-Object and Visual-Spatial Learning tasks. In the Verbal LTM task, DD recalled significantly fewer words than CA but not RL, while CA and RL showed a similar performance. The present results suggest that when reading experience was equated, children with DD and typical readers did not differ in STM and LTM, especially in the verbal modality, weakening claims that memory has a causal effect in reading impairments.

Bacopa monnieri supplementation increases learning and short-term memory retention of sleep-deprived Drosophila melanogaster

Aversive phototaxic suppression (APS) assay is a behavioral assay in which photopositive fruit flies (Drosophila melanogaster) are trained to avoid light using quinine as an aversive stimulus. This conditioned behavior is found to be impaired by sleep deprivation in D. melanogaster. This study tested whether supplementation with Bacopa monnieri can counter this impairment. Three sublethal and effective concentrations of B. monnieri supplement (4.62 � 10−4 g/ ml, 4.62 � 10−3 g/ml, and 4.62 � 10−2 g/ml) were given to test groups of non-sleep-deprived (slp+) and sleep-deprived (slp−) flies subjected to the APS assay. The extent of learning and short-term memory (STM) retention was based on average pass rates (APRs) defined as the number of trials that each fly exhibited a photonegative response before and after conditioning. B. monnieri supplement improved the APR of both slp+ and slp− flies as compared to the unsupplemented flies. These effects were found to be dose-dependent from the low- to the mid-level (4.62 � 10−4 g/ml to 4.62 � 10−3 g/ml) concentrations of the supplement on D. melanogaster learning and STM retention. Supplementing fly food with B. monnieri improved learning and STM of slp− flies with learning and STM deficits caused by sleep deprivation. The slp− flies given B. monnieri supplementation had higher learning rates and longer STM retention than slp+ flies without B. monnieri supplementation. Unexpectedly, slp− flies given B. monnieri supplementation had the same learning and STM retention levels as slp+ flies also given B. monnieri supplementation. Bacopa monnieri supplementation enhances both the learning capacities and the STM retention of both non-sleep-deprived and sleep-deprived fruit flies. Advantageous effects were dose-dependent for both learning and STM retention.

The role of cap-dependent translation in aged-related changes in neuroimmunity and affective behaviors

Translation regulation in the context of aged-associated inflammation and behavioral impairments is not well characterized. Aged individuals experience lower life quality due to behavioral impairments. In this study, we used young and aged transgenic mice that are unable to activate the cap-binding protein, eukaryotic translation initiation factor 4E (eIF4E) to examine the role of protein translation control in aging, memory, depression, and anxiety. To determine how products of cap-dependent translation play a permissive role in aged-associated inflammation, we assessed levels of pro-inflammatory cytokines in various brain regions involved in the above-mentioned behaviors. We found that functional eIF4E is not necessary for age-related deficits in spatial and short-term memory but is important for depressive and anxiety-like behavior and this is correlated with pro-inflammatory cytokines in discrete brain regions. Thus, we have begun to elucidate a role for eIF4E phosphorylation in the context of aged-related behavioral impairments and chronic low-grade inflammation that may help identify novel immune modulators for therapeutic targets and decrease the burden of self-care among the geriatric population.

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.

Effects of vapourized THC and voluntary alcohol drinking during adolescence on cognition, reward, and anxiety-like behaviours in rats

Cannabis and alcohol co-use is prevalent in adolescence, but the long-term behavioural effects of this co-use remain largely unexplored. The aim of this study is to investigate the effects of adolescent alcohol and Δ9-tetrahydracannabinol (THC) vapour co-exposure on cognitive- and reward-related behaviours. Male Sprague-Dawley rats received vapourized THC (10 mg vapourized THC/four adolescent rats) or vehicle every other day (from post-natal day (PND) 28–42) and had continuous voluntary access to ethanol (10% volume/volume) in adolescence. Alcohol intake was measured during the exposure period to assess the acute effects of THC on alcohol consumption. In adulthood (PND 56+), rats underwent behavioural testing. Adolescent rats showed higher alcohol preference, assessed using the two-bottle choice test, on days on which they were not exposed to THC vapour. In adulthood, rats that drank alcohol as adolescents exhibited short-term memory deficits and showed decreased alcohol preference; on the other hand, rats exposed to THC vapour showed learning impairments in the delay-discounting task. Vapourized THC, alcohol or their combination had no effect on anxiety-like behaviours in adulthood. Our results show that although adolescent THC exposure acutely affects alcohol drinking, adolescent alcohol and cannabis co-use may not produce long-term additive effects.

Effect of short-term memory and working memory in diabetes with comorbidities condition

Cognitive function refers to the ability of humans to function normally which includes physical as well as mental interpretation like ability to focus, concentrate, learn, plan, determine, execute, manipulate and problem solving. Etiologic of cognitive dysfunction includes AD, depression, anxiety and vascular dementia, hippocampal sclerosis etc., Diabetes associated with cognitive decline are related to short fall of learning and memory. Cognitive impairment/dysfunction in diabetic patients has been divided into three stages, stage one, stage two and stage three. Stage one, occur in all groups of different ages and it is characterized by mild and subtle changes in cognition. Deficit in short-term memory and working memory leads to major problems like Alzheimer disease and dementia. The pathophysiology of cognitive decline associated involves microvascular injury, hyperglycaemia, insulin resistance and oxidative stress. Diabetes associated with comorbidities condition leads to decrease in short-term memory and working memory. From this review we observed short term memory retains small amount of data in cognizance which are readily available state for short period of time whereas working memory manipulates the information through visual and auditory storage and it is important in understanding and improving the memory. Conclusion of this review is that, there is a decrease in short-term memory and working memory in type 2 diabetes patient condition. But there is no evidence of which type comorbidity condition affects more in short-term memory and working memory. So, further research study to be carried out.