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At least 667 records · Page 37Linked to original sources
PubMed2004

DHEAS improves learning and memory in aged SAMP8 mice but not in diabetic mice.

Dehydroepiandrosterone sulfate (DHEAS) has been reported to improve memory in aged animals and suggested as a treatment for age-related dementias. The SAMP8 mouse, a model of Alzheimer's disease, has an age-related impairment in learning and memory and an increase in brain levels of amyloid precursor protein (APP) and amyloid beta protein (Abeta). Male SAMP8 mice also have a decrease in testosterone, to which DHEA is a precursor. Diabetes has been suggested as a model of aging and to be linked to Alzheimer's disease. Diabetics can have memory deficits and lower DHEAS levels. Here, we examined the effects of chronic oral DHEAS on acquisition and retention for T-maze footshock avoidance in 12 mo male SAMP8 mice and in CD-1 mice with streptozocin-induced diabetes. Learning and memory were improved in aged SAMP8 mice, but not in CD-1 mice with streptozocin-induced diabetes. These findings suggest that DHEAS is more effective in reversing the cognitive impairments associated with overexpression of Abeta than with diabetes.

Alzheimer Disease↗
PubMedDate not supplied

Neuropeptide modulation of learning and memory processes.

The ubiquitous nature of neuropeptides and their respective receptors in the central and peripheral nervous systems suggests that peptides play a key role in controlling physiological processes. Investigations on a cellular level have demonstrated that neuropeptides exert powerful modulatory effects on neurons and neuronal circuits; however, despite these compelling considerations, investigators have rarely been able to assign discrete functional roles to individual neuropeptides. Numerous studies have addressed the influence of neuropeptides on learning and memory processes. Workers have primarily utilized peripheral or central injection of neuropeptides to suggest a facilitatory, or less commonly inhibitory, role in acquisition, retention, or retrieval of memories. Although highly suggestive, critical concerns regarding the specificity of the observed effects have often remained. Recently, the neurogenetic approach has demonstrated the role of a novel neuropeptide in a specific memory phase, high affinity antagonists have confirmed the importance of some endogenous neuropeptides, and evidence of neuropeptide dysfunction in disease states, particularly Alzheimer's disease, has emerged. Continued refinement of traditional techniques, combined with information from alternative approaches, promises to consolidate the role of neuropeptides in learning and memory.

Animals↗
PubMed2006

Protective effect of N-acetyl-L-cysteine on amyloid beta-peptide-induced learning and memory deficits in mice.

This study aimed to examine the effects of N-acetyl-L-cysteine (NAC) on protecting neurons function and improving learning and memory deficits in mice. Mice were intracerebroventricularly (icv) injected with the aggregated amyloid beta-peptide (Abeta) to produce Alzheimer's disease (AD). Learning and memory functions in mice were examined by the step through test and the water maze performance. The results showed that the mice pretreated with NAC had significantly greater retention in the step through test and shorter latencies in the water maze performance. Biochemical studies showed the potential role of free radical toxicity and the damage of cholinergic neurons in the Abeta-treated mice. There was an increased lipid peroxidation as indicated by elevated malondehyde (MDA) and decrease of glutathione (GSH) levels. There was also an increase in acetylcholinesterase (AChE) activity and a reduction in the choline acetyltransferase (ChAT) activity and acetylcholine (ACh) levels. NAC pretreatment significantly reversed the elevated MDA, AChE and the reduced GSH, ChAT and ACh in the Abeta-model mice. The results of the present study suggest the potential usage of the neuroprotective action of NAC on AD.

Acetylcholine↗
PubMed1997

Intact spatial learning and memory in transgenic mice with reduced BDNF.

Long-term potentiation (LTP) in hippocampal CA1 pyramidal cells is considered to be a cellular analogue of learning and may be useful in studying the molecular foundations of learning and memory. Because brain-derived neurotrophic factor (BDNF) had been shown to have a role in activity-dependent neuroplasticity in the hippocampus we studied spatial learning in mice with BDNF deficiency produced by gene-targeted mutation. Heterozygous BDNF knockout mice reportedly underexpress BDNF and have reduced LTP, but their spatial memory and search strategy assessed with Morris water maze (distally cued version) as well as their performance on the elevated plus maze were indistinguishable from that of controls. This indicates that extrapolation from LTP in a single brain structure to complex behaviours such as learning and memory may not be justified.

Analysis of Variance↗
PubMed1972

A molecular basis for learning and memory.

Three stages in memory (electrical, short-term and long-term) are reviewed. The short computing time of organized neural systems favors synapses as loci for storage of memory. Transfer of neuronal excitation depends upon transfer of transmitter, involving the steps: vesicle attachment to presynaptic vesicle-release sites, contraction at dithiolate structures of these sites, exocytosis of transmitter, movement of transmitter across synaptic cleft, and reception at postsynaptic sites. Disulfide formation from dithiolates (calcium dithiolate salt) occurs during excitation and can represent a short-term alteration in properties of vesicle-release sites and, thus, short-term memory. Repair by one mechanism of the altered vesicle-release sites through reduction of the disulfide bond returns the system to its original state or, by a second mechanism, enlarges the presynaptic area covered by these sites. Such enlargement is a stable, permanent mode: long-term memory. Suitable concentrations of transmitter at postsynaptic receptor sites lead to mobilization of additional receptor sites through polymerization of monomeric receptor units. Postsynaptic expansion constitutes a metastable long-term storage, readily reconstituted under appropriate stimuli. Reverberations at the electrical stage of memory are suggested as a necessary link to the chemical stage of memory. These ideas constitute the elements of a molecular theory of learning and memory.

Acetylcholine↗
PubMed2005

Impairing forgetting by preventing new learning and memory.

Two causes of forgetting have been promulgated: memory trace decay and retroactive interference. The authors show that forgetting is an active process requiring both new learning and memory. In the present (1)Lymnaea model system, prevention of new learning of a conflicting association, inhibition of memory consolidation, or Right Pedal Dorsal 1 soma ablation, which blocks LTM formation, are all potent means to prevent forgetting. Thus procedures that alter the ability to learn or form memory of a new conflicting aerial respiratory association prevent forgetting of a learned associative behavior. These results are the 1st demonstration in any model system that forgetting requires the soma of a single neuron.

Analysis of Variance↗
PubMed2004

Modulation of learning and memory in Dahl rats by dietary salt restriction.

The Dahl rat represents a robust animal model of salt-sensitive hypertension, with Dahl S rats being salt sensitive and Dahl R rats (the Dahl S counterparts) being salt resistant for the development of hypertension. Here we evaluate the effect of reduced dietary salt intake on learning and memory in the Dahl rat model. Salt restriction produced a significant impairment in social transmission of food preference and social recognition memory in Dahl S rats without affecting spatial learning. In contrast, social transmission of food preference and social recognition memory remained unaffected in Dahl R rats, whereas navigation performance was significantly improved. This effect on learning and memory was not generalized because sodium restriction did not influence object recognition memory in either Dahl S or Dahl R rats. The significant decrement in select cognitive functions in Dahl S rats produced by salt restriction are in sharp contrast to the well known positive effect of dietary salt restriction in alleviating high blood pressure and associated target organ complications, suggesting that caution must be exercised when weighing the benefits of salt restriction in improving cardiovascular health in salt-sensitive hypertension against the potential undesirable effects of reduced cognitive function.

Animals↗
PubMed2004

The effect of chronic restraint stress on spatial learning and memory: relation to oxidant stress.

The aim of this study was to investigate the effect of chronic restraint stress (RS) on spatial learning and memory. Fifty healthy male Wistar rats, aged three months were used. They were equally divided into five groups--C: Control, W: Water Maze, CS-1: Restrained for 21 days (1 h/day) + water maze protocol following stress period, CS-2: Restrained for 28 days (1 h/day) + water maze protocol during last 7 days of stress period, CS-3: Restrained for 21 days and allowed to recovery for 7 days (1 h/day). Corticosterone levels were higher in all stress groups than in C and W groups. Nitrite levels of frontal cortex and hippocampus were found to be elevated in chronic stress groups with respect to C and W groups. Thiobarbituric acid reactive substances (TBARS) of both tissues were increased significantly in CS1 and CS2 groups compared with C, W, and CS3 groups. Escape latencies of CS1 and CS2 groups were longer than those of the W group on each day of acquisition. In transfer test, CS1 and CS2 groups stayed significantly shorter in target quadrant according to the W group. Significant correlations between corticosterone and either nitrite or TBARS of hippocampus and frontal cortex were found. Both acquisition and memory performances were negatively correlated with plasma corticosterone level, nitrite, and TBARS levels of hippocampus and frontal cortex. The results of this study suggest that stress-induced lipid peroxidation may affect the acquisition and memory performances.

Analysis of Variance↗
PubMed1992

Delayed effects of acute oral and chronic inhalational exposure to methylparathion on learning and memory in rats.

Impairment of acquisition phase of the learning process was observed in rats even at 3 weeks after single oral exposure to the near-lethal dose of commercial grade methylparathion (MP) followed by atropine resuscitation. Though there was a trend towards memory impairment in this group of animals, memory retention was not significantly affected. Chronic inhalational exposure to MP (one exposure/day for 3 weeks) did not significantly alter learning or memory. No significant alteration in red blood cell or brain acetylcholinesterase levels were observed in either of the two groups. It appears that behavioural effects can persist even 3 weeks after exposure to acute near-lethal doses of the pesticide, as occurs in the clinical situation of suicidal attempts; while repeated exposure to no-observed-effect-level doses as occurs in farm and factory workers, may not be associated with behavioural changes.

Acetylcholinesterase↗
PubMedDate not supplied

Deterioration in learning and memory of fear conditioning in response to context in aged SAMP8 mice.

This study examined age-dependent deficits in the learning and memory of fear conditioning, using a newly developed senescence-accelerated mouse (SAMP8) model of age-related brain dysfunction and its genetically related inbred strain (SAMR1). The mice were classically conditioned to tone by giving aversive foot shocks in a distinct experimental box (context). After conditioning, fear in response to the original context without the tone and to the tone in a different context were tested with no shocks. Freezing behavior was used as a reliable index of fear. At 4 and 8 months, contextual fear was weaker in the accelerated senescence-prone SAMP8 mice than in the accelerated senescence-resistant SAMR1 mice. However, at 1 and 2 months, both SAMP8 and SAMR1 mice showed significant contextual fear to equivalent levels. Aging did not affect the fear response to tone. These results indicate that SAMP8 mice have age-related learning and memory deficits in their fear response evoked by contextual but not explicit tone stimuli. Age-related hippocampal dysfunction is suggested to be the cause of these age-related deficits in contextual fear conditioning in SAMP8 mice.

Aging↗
PubMed2005

Impairment of hippocampal long-term depression and defective spatial learning and memory in p35 mice.

Cdk5 (cyclin-dependent kinase 5) activity is dependent upon association with one of two neuron-specific activators, p35 or p39. Genetic deletion of Cdk5 causes perinatal lethality with severe defects in corticogenesis and neuronal positioning. p35(-/-) mice are viable with milder histological abnormalities. Although substantial evidence implicates Cdk5 in synaptic plasticity, its role in learning and memory has not been evaluated using mutant mouse models. We report here that p35(-/-) mice have deficiencies in spatial learning and memory. Close examination of hippocampal circuitry revealed subtle histological defects in CA1 pyramidal cells. Furthermore, p35(-/-) mice exhibit impaired long-term depression and depotentiation of long-term potentiation in the Schaeffer collateral CA1 pathway. Moreover, the Cdk5-dependent phosphorylation state of protein phosphatase inhibitor-1 was increased in 4-week-old mice due to increased levels of p39, which co-localized with inhibitor-1 and Cdk5 in the cytoplasm. These results demonstrate that p35-dependent Cdk5 activity is important to learning and synaptic plasticity. Deletion of p35 may shift the substrate specificity of Cdk5 due to compensatory expression of p39.

Amino Acid Sequence↗
PubMed1999

Cognitive and behavioral changes after unilateral posteroventral pallidotomy: relationship with lesional data from MRI.

We investigated cognitive and behavioral changes after unilateral posteroventral pallidotomy, and their relationship with lesion size and location as identified in magnetic resonance image quantitative analysis. Fifteen consecutive patients with Parkinson's disease were assessed neuropsychologically before and after unilateral posteroventral pallidotomy (five right and 10 left). Immediate postsurgery evaluation (1 week) demonstrated significant worsening of memory, motor learning, motor speed, and verbal fluency. In the 3-month follow up, learning, memory, and speed returned to the presurgical level, but verbal fluency remained below the baseline. Significant improvements were observed in visuospatial functions and obsessive-compulsive behavior. Lesional volume did not correlate with neuropsychologic changes. Left lesions produced more impairment in verbal fluency than right-sided lesions. Regression analysis identified two lesional areas in the pallidum mediale internum. These regions accounted for 68% of the variance in the visuospatial changes.

Aged↗
PubMed2004

Effects of a combined extract of Ginkgo biloba and Bacopa monniera on cognitive function in healthy humans.

Extracts of Ginkgo biloba and Bacopa monniera have been shown to produce positive effects on cognitive function in healthy subjects. While the exact mechanisms are not known, it has been suggested that antioxidant properties and cholinergic modulation may play a role. In the current study the sub-chronic (2 weeks) and chronic (4 weeks) effects of an extract containing Ginkgo biloba (120 mg) and Bacopa monniera (300 mg) (Blackmores Ginkgo Brahmi) on cognitive function were examined. The study was a randomized, double-blind, placebo-controlled, independent group design in which 85 healthy subjects were allocated to one of two treatment conditions (placebo or combined Ginkgo biloba and Bacopa monniera extract). Testing was conducted at baseline and 2 and 4 weeks post treatment. The results showed that the combined extract relative to placebo did not demonstrate any significant effects on tests investigating a range of cognitive processes including attention, short-term and working memory, verbal learning, memory consolidation, executive processes, planning and problem solving, information processing speed, motor responsiveness and decision making. These findings suggest that at least within the current treatment duration and doses, an extract containing Ginkgo biloba and Bacopa monniera had no cognitive enhancing effects in healthy subjects.

Adult↗
PubMed2001

No evidence for cognitive side effects after 6 months of vagus nerve stimulation in epilepsy patients.

Vagus nerve stimulation (VNS) can reduce seizure frequency in epilepsy patients and may affect central mechanisms of brain functioning. Experimental studies have provided evidence of cognitive alterations during VNS on phases. This single-arm follow-up study evaluates the potential of VNS to affect cognitive performance following long-term treatment. Thirty-six adult patients with medication-resistant epilepsies enrolled. Cognition was assessed before and at least 6 months after implantation of the stimulation device by a comprehensive neuropsychological assessment battery comprising tests on attention, motor functioning, short-term memory, learning and memory, and executive functions. Neither multiple testing of single score changes nor multivariate testing of cognitive domains revealed significant pre-post changes. Improvements in attentional performance were completely explained by practice effects as is usually expected. In particular, no negative side effects were revealed. These findings are in line with the clinical impression that VNS does not affect cognitive performance.

Journal Article↗
PubMed2003

Effects on postural oscillation and memory functions of a single dose of zolpidem 5 mg, zopiclone 3.75 mg and lormetazepam 1 mg in elderly healthy subjects. A randomized, cross-over, double-blind study versus placebo.

OBJECTIVE: In elderly patients, both falls and impaired memory are considerable medical problems. Hypnotics, which are frequently administered to this patient group for the treatment of insomnia, should ideally not impair equilibrium or memory functions. This double-blind, randomised, four-way, cross-over study investigated the effects of frequently prescribed hypnotics from different classes on postural oscillation and memory under real life conditions. Zolpidem 5 mg, zopiclone 3.75 mg, lormetazepam 1 mg (i.e. usual starting doses in elderly) or placebo were administered at night to 48 healthy elderly volunteers aged 65 years or more. The study included four treatment periods separated by wash-out periods of at least 1 week. METHODS: Psychomotor tests up to 9 h or 10 h after drug intake included, for attention and body sway, clinical stabilometric platform (CSP) tests, simple reaction time (SRT), and the critical tracking test (CTT); for memory, the learning memory tasks (LMT) and the Sternberg memory scanning test (mean reaction time [MRT] and percentage of correct answers) were used. For subjective sleep evaluation the Leeds sleep evaluation questionnaire (LSEQ) and for sedation a visual analogue scale (VAS) were used. For safety evaluations, adverse events (AEs) were recorded. RESULTS: The results demonstrate that compared with placebo, the active drugs increased body sway (area eyes open and closed in the CSP); however, this effect disappeared after 5 h with zolpidem, while it disappeared only after 8 h with lormetazepam and zopiclone. All three drugs did not affect attention assessed by the SRT and CTT. Concerning memory, Sternberg MRT at 9 h was not significantly different up to 5 digits for all groups in comparison with placebo, while for 6 digits it was significantly increased with lormetazepam and zopiclone. In the LMT, an impairment of performance was observed with lormetazepam relative to both zolpidem and placebo. CONCLUSION: The safest compared drug with regard to body sway was zolpidem, because of its short-lasting effect. In addition, zolpidem did not show any significant effect on memory functions, in the present dose comparison.

Aged↗
PubMed2005

Treatment of cognitive dysfunction in schizophrenia.

BACKGROUND: Cognitive impairment has always been regarded as an important characteristic of schizophrenia. Many domains of cognition are disrupted with varying degrees of deficit: attention, executive functions, verbal and visuospatial working memory, learning, and memory. However, it is only recently that cognitive dysfunction has been recognized as a primary and enduring core deficit in schizophrenia (rather than the previous focus on positive and negative symptoms). OBJECTIVE: This article discusses cognitive impairment and the therapeutic effects of newer antipsychotic agents on cognitive functioning in patients with schizophrenia. CONCLUSIONS: Cognitive dysfunction occurs before the first psychotic episode and persists throughout the course of the illness. It involves every aspect of cognitive functioning and has an important impact on long-term social and occupational outcomes. Improvement of cognitive functioning by antipsychotic treatment can be due indirectly to the improvement of therapeutic profiles of the newer antipsychotic agents (eg, higher efficacy on positive and negative symptoms, fewer side effects, less anticholinergic effects) or directly to effects on cerebral functioning (eg, by restoring dopamine prefrontal activity). However, further research is needed regarding the therapeutic effects of the newer antipsychotic drugs on cognitive functioning and their impact on psychosocial outcome. Although newer medications may improve cognitive functioning, they do not normalize neurocognitive deficits in schizophrenia. In addition, various nonpharmacologic, psychological interventions have been used in the rehabilitation of patients with cognitive deficits.

Antipsychotic Agents↗