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Memory Dysfunction (memory + dysfunction)
Selected AbstractsPerformance deficit of ,7 nicotinic receptor knockout mice in a delayed matching-to-place task suggests a mild impairment of working/episodic-like memoryGENES, BRAIN AND BEHAVIOR, Issue 6 2006C. Fernandes Patients with schizophrenia exhibit deficits in a range of cognitive functions, particularly working and episodic memory, which are thought to be core features of the disorder. Memory dysfunction in schizophrenia is familial and thus a promising endophenotype for genetic studies. Both human and animal studies suggest a role for the neural nicotinic acid receptor family in cognition and specifically the ,7-receptor subunit in schizophrenia and its endophenotypes. Consequently, we tested mice lacking the ,7 subunit of the neural nicotinic receptor (B6.129S7-Chrna7tm1Bay/J) in the delayed matching-to-place (DMP) task of the Morris water maze, a measure of working/episodic memory akin to human episodic memory. We report that a minor impairment in ,7 knockout mice was observed in the DMP task, with knockout mice taking longer to find the hidden platform than their wildtype controls. This suggests a role for the ,7 subunit in working/episodic memory and a potential role for the ,7 neural nicotinic receptor gene (CHRNA7) in schizophrenia and its endophenotypes. [source] Neuropharmacology and therapeutic potential of cannabinoidsADDICTION BIOLOGY, Issue 1 2000Roger G. Pertwee Mammalian tissues contain at least two types of cannabinoid receptor, CB 1, found mainly on neurones and CB 2, found mainly in immune cells. Endogenous ligands for these receptors have also been identified. These endocannabinoids and their receptors constitute the endogenous cannabinoid system. Two cannabinoid receptor agonists, ,9 -tetrahydrocannabinol and nabilone, are used clinically as anti-emetics or to boost appetite. Additional therapeutic uses of cannabinoids may include the suppression of some multiple sclerosis and spinal injury symptoms, the management of pain, bronchial asthma and glaucoma, and the prevention of neurotoxicity. There are also potential clinical applications for CB 1 receptor antagonists, in the management of acute schizophrenia and cognitive/memory dysfunctions and as appetite suppressants. Future research is likely to be directed at characterizing the endogenous cannabinoid system more completely, at obtaining more conclusive clinical data about cannabinoids with regard to both beneficial and adverse effects, at developing improved cannabinoid formulations and modes of administration for use in the clinic and at devising clinical strategies for separating out the sought-after effects of CB 1 receptor agonists from their psychotropic and other unwanted effects. [source] Mechanisms underlying the inability to induce area CA1 LTP in the mouse after traumatic brain injuryHIPPOCAMPUS, Issue 6 2006E. Schwarzbach Abstract Traumatic brain injury (TBI) is a significant health issue that often causes enduring cognitive deficits, in particular memory dysfunction. The hippocampus, a structure crucial in learning and memory, is frequently damaged during TBI. Since long-term potentiation (LTP) is the leading cellular model underlying learning and memory, this study was undertaken to examine how injury affects area CA1 LTP in mice using lateral fluid percussion injury (FPI). Brain slices derived from FPI animals demonstrated an inability to induce LTP in area CA1 7 days postinjury. However, area CA1 long-term depression could be induced in neurons 7 days postinjury, demonstrating that some forms of synaptic plasticity can still be elicited. Using a multidisciplined approach, potential mechanisms underlying the inability to induce and maintain area CA1 LTP were investigated. This study demonstrates that injury leads to significantly smaller N -methyl- D -aspartate potentials and glutamate-induced excitatory currents, increased dendritic spine size, and decreased expression of ,-calcium calmodulin kinase II. These findings may underlie the injury-induced lack of LTP and thus, contribute to cognitive impairments often associated with TBI. Furthermore, these results provide attractive sites for potential therapeutic intervention directed toward alleviating the devastating consequences of human TBI. © 2006 Wiley-Liss, Inc. [source] Self-report of memory and affective dysfunction in association with medication use in a sample of individuals with chronic sleep disturbanceHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 8 2000Mary Pat McAndrews Abstract Benzodiazepines produce memory disturbance after acute administration. It is not clear whether chronic use of benzodiazepines is hazardous to memory processes. Epidemiological data indicate that a large proportion (10,30 per cent) of individuals with sleep dysfunction take hypnotic aids for a year or longer. The purpose of the present study was to evaluate self-reported memory dysfunction in a sample of individuals who considered their sleep disturbance sufficiently severe to seek investigation in sleep clinics. It was hypothesized that individuals taking benzodiazepines for sleep would report greater perceived everyday memory failures than individuals taking other sleep aids or no medication. Questionnaires were given to 368 individuals referred into the study by investigators in six sleep disorders clinics. All respondents completed a lengthy (700-item) questionnaire, which included scales assessing memory difficulties, affective status and sleep disturbance. Respondents also reported any medication use for sleep problems and duration of use of the current drug. Information on medication use was reported by 289 participants. Fifty-six per cent of respondents reported using some form of psychoactive medication (antidepressants, benzodiazepines, Zopiclone). Twenty-two per cent reported using no medication. Analysis of covariance showed that these medications had no detectable effect on subjective memory difficulties during chronic use, F(4,226)=1·34, p=0·25. Copyright © 2000 John Wiley & Sons, Ltd. [source] Neuropsychological components of intellectual disability: the contributions of immediate, working, and associative memoryJOURNAL OF INTELLECTUAL DISABILITY RESEARCH, Issue 5 2010Jamie O. Edgin Abstract Background Efficient memory functions are important to the development of cognitive and functional skills, allowing individuals to manipulate and store information. Theories of memory have suggested the presence of domain-specific (i.e. verbal and spatial) and general processing mechanisms across memory domains, including memory functions dependent on the prefrontal cortex (PFC) and the hippocampus. Comparison of individuals who have syndromes associated with striking contrasts in skills on verbal and spatial tasks [e.g. Down syndrome (DS) and Williams syndrome (WS)] allows us to test whether or not these dissociations may extend across cognitive domains, including PFC and hippocampal memory processes. Methods The profile of memory function, including immediate memory (IM), working memory (WM) and associative memory (AM), was examined in a sample of adolescents and young adults with DS (n = 27) or WS (n = 28), from which closely CA- and IQ-matched samples of individuals with DS (n = 18) or WS (n = 18) were generated. Relations between memory functions and IQ and adaptive behaviour were also assessed in the larger sample. Results Comparisons of the two matched groups indicated significant differences in verbal IM (DS < WS), spatial IM (DS > WS) and spatial and verbal AM (DS > WS), but no between-syndrome differences in WM. For individuals with DS, verbal IM was the most related to variation in IQ, and spatial AM related to adaptive behaviour. The pattern was clearly different for individuals with WS. Verbal and spatial AM were the most related to variation in IQ, and verbal WM related to adaptive behaviour. Conclusions These results suggest that individuals with these two syndromes have very different patterns of relative strengths and weaknesses on memory measures, which do not fully mirror verbal and spatial dissociations. Furthermore, different patterns of memory dysfunction relate to outcome in individuals with each syndrome. [source] Role of interleukin-1, in postoperative cognitive dysfunctionANNALS OF NEUROLOGY, Issue 3 2010Mario Cibelli MD Objective: Although postoperative cognitive dysfunction (POCD) often complicates recovery from major surgery, the pathogenic mechanisms remain unknown. We explored whether systemic inflammation, in response to surgical trauma, triggers hippocampal inflammation and subsequent memory impairment, in a mouse model of orthopedic surgery. Methods: C57BL/6J, knock out (lacking interleukin [IL]-1 receptor, IL-1R,/,) and wild type mice underwent surgery of the tibia under general anesthesia. Separate cohorts of animals were tested for memory function with fear conditioning tests, or euthanized at different times to assess levels of systemic and hippocampal cytokines and microglial activation; the effects of interventions, designed to interrupt inflammation (specifically and nonspecifically), were also assessed. Results: Surgery caused hippocampal-dependent memory impairment that was associated with increased plasma cytokines, as well as reactive microgliosis and IL-1, transcription and expression in the hippocampus. Nonspecific attenuation of innate immunity with minocycline prevented surgery-induced changes. Functional inhibition of IL-1,, both in mice pretreated with IL-1 receptor antagonist and in IL-1R,/, mice, mitigated the neuroinflammatory effects of surgery and memory dysfunction. Interpretation: A peripheral surgery-induced innate immune response triggers an IL-1,-mediated inflammatory process in the hippocampus that underlies memory impairment. This may represent a viable target to interrupt the pathogenesis of postoperative cognitive dysfunction. ANN NEUROL 2010;68:360,368 [source] Differential working memory impairment in bipolar disorder and schizophrenia: effects of lifetime history of psychosisBIPOLAR DISORDERS, Issue 2 2006David C Glahn Background:, Although bipolar disorder and schizophrenia have long been viewed as distinct illnesses, there is growing evidence that these two complex diseases share some common genes, which may manifest as overlapping neuropsychological impairments. Although working memory dysfunction has been proposed to be central to the pathophysiology of schizophrenia, it has received less attention in studies of bipolar disorder. Method:, We applied measures of working memory to patients with schizophrenia (n = 15), patients with schizoaffective disorder (n = 15), patients with psychotic (n = 11) and non-psychotic (n = 15) bipolar disorder, and demographically matched healthy subjects (n = 32), in order to determine the extent to which these groups show common or unique impairments. Results:, While patients with bipolar disorder (with and without psychotic features) and those with schizophrenia/schizoaffective disorder were impaired on backward digit span, only patients with a lifetime history of psychotic features, regardless of diagnosis, were impaired on spatial delayed response task. Conclusions:, Backward digit span performance is comparable in bipolar disorder and schizophrenia, and may be an appropriate endophenotypic marker that cuts across diagnostic categories. In contrast, spatial working memory performance clearly distinguishes non-psychotic bipolar disorder patients from patients with functional psychosis. [source] Genetic reductions of ,-site amyloid precursor protein-cleaving enzyme 1 and amyloid-, ameliorate impairment of conditioned taste aversion memory in 5XFAD Alzheimer's disease model miceEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2010Latha Devi Abstract Although transgenic mouse models of Alzheimer's disease (AD) recapitulate amyloid-, (A,)-related pathologies and cognitive impairments, previous studies have mainly evaluated their hippocampus-dependent memory dysfunctions using behavioral tasks such as the water maze and fear conditioning. However, multiple memory systems become impaired in AD as the disease progresses and it is important to test whether other forms of memory are affected in AD models. This study was designed to use conditioned taste aversion (CTA) and contextual fear conditioning paradigms to compare the phenotypes of hippocampus-independent and -dependent memory functions, respectively, in 5XFAD amyloid precursor protein/presenilin-1 transgenic mice that harbor five familial AD mutations. Although both types of memory were significantly impaired in 5XFAD mice, the onset of CTA memory deficits (,9 months of age) was delayed compared with that of contextual memory deficits (,6 months of age). Furthermore, 5XFAD mice that were genetically engineered to have reduced levels of ,-site amyloid precursor protein-cleaving enzyme 1 (BACE1) (BACE1+/,·5XFAD) exhibited improved CTA memory, which was equivalent to the performance of wild-type controls. Importantly, elevated levels of cerebral ,-secretase-cleaved C-terminal fragment (C99) and A, peptides in 5XFAD mice were significantly reduced in BACE1+/,·5XFAD mice. Furthermore, A, deposition in the insular cortex and basolateral amygdala, two brain regions that are critically involved in CTA performance, was also reduced in BACE1+/,·5XFAD compared with 5XFAD mice. Our findings indicate that the CTA paradigm is useful for evaluating a hippocampus-independent form of memory defect in AD model mice, which is sensitive to rescue by partial reductions of the ,-secretase BACE1 and consequently of cerebral A,. [source] | |||||||||||||