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PubMed2004

Neuropsychological markers of dementia in patients with memory complaints.

OBJECTIVES: To identify neuropsychological markers able to predict evolution towards dementia, through the detection of differential neuropsychological characteristics in a group of subjects complaining of memory loss, in a longitudinal, two-year follow-up study. METHODS: Longitudinal and retrospective comparisons of neuropsychological performance in: (a) subjects complaining of memory loss who, after a two-year period, met neurological and clinical diagnostic criteria for probable AD, and (b) subjects from the same group who did not progress towards dementia. A sample of 43 subjects were administered a comprehensive neuropsychological battery evaluating orientation, logical-verbal and visuoperceptive reasoning, immediate and delayed verbal and visual memory, attention, learning, executive functions and semantic and phonemic verbal fluency. RESULTS: Of the 43 subjects evaluated and then re-evaluated two years later, ten (23%) progressed to dementia according to the NINCS-ADRDA criteria for probable Alzheimer's disease. The neuropsychological performance of the rest of the subjects (n=33) over the two examinations was stable. In the retrospective analysis the principal differences between the two groups were found in the intensity of the initial memory deficits (WMS-R) and in the impairment of other cognitive areas in the dementia group: formation of concepts, vocabulary and similarities (WAIS), learning (WMS-R) and several executive functions. CONCLUSIONS: The deficits in cognitive areas other than memory are significant in subjects with memory complaints who progress towards dementia within two years. Memory complaints represent a risk factor that is at least as important as actual memory loss. Recent proposals for adding descriptive labels to the diagnosis of Mild Cognitive Impairment (MCI) in order to reflect the neuropsychological functions impaired in addition to memory (Petersen, 2001a), may be decisive from the prognostic viewpoint.

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PubMed2006

Response inhibition and everyday memory complaints in older adult women.

OBJECTIVE: To explore the association of executive functions to the everyday memory complaints of healthy older adults. METHODS: Ninety-nine community-dwelling women aged 60 and above were administered a battery that included neuropsychological tests of executive functions and memory, along with self-report measures of everyday memory complaints, depression, and anxiety. RESULTS: Multivariate regression analyses revealed that a measure of response inhibition (Stroop Color-Word) accounted for unique variance in predicting memory complaints above and beyond measures of episodic memory, depression, and anxiety. Depression, however, accounted for the largest variance in memory complaints. CONCLUSIONS: Higher frequency of everyday memory complaints among older adults was associated with decreased response inhibition independent of episodic memory and affective state. Further research is needed to understand the interrelationships among these and other predictors of everyday memory complaints.

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PubMed2006

Do symptoms of memory impairment correspond to cognitive impairment: a cross sectional study of a clinical cohort.

BACKGROUND: Symptoms of memory loss are a common complaint within the general population and a frequent reason for seeking medical advice. However, the clinical relevance of these symptoms to future development of neurodegenerative disease is uncertain. The aim of this study is to characterise a cohort of individuals with symptoms of memory loss and varying memory impairment, who will be followed longitudinally with serial neuropsychology and neuroimaging to evaluate the clinical relevance of symptoms of memory loss. METHOD: Fifty-eight subjects with symptoms of memory loss were recruited from the National Hospital for Neurology and Neurosurgery. All subjects underwent clinical assessment, APOE4 genotyping, neuroimaging and neuropsychological tests. RESULTS: Those with mild cognitive impairment (MCI) had an increased prevalence of the APOE4 allele, impaired performance on tests of memory, measures of IQ and naming compared to controls. Baseline brain volumes were decreased and ventricular size increased. Those with symptoms of memory loss but no cognitive impairment (SNCI) performed significantly worse on tests of memory than the control group. CONCLUSIONS: The MCI represent a group with multiple risk factors for progression to AD. The SNCI group may represent a heterogeneous group with some individuals in the early stages of AD whilst others' memory complaints are more likely linked to anxiety or personality traits.

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PubMed2002

Synaptic reentry reinforcement based network model for long-term memory consolidation.

The conversion of newly formed declarative memories into long-term memories is known to be dependent on the hippocampus. Recent experiments suggest that memory consolidation requires reactivation of the NMDA receptor in CA1 during the initial week(s) after training. This led to the hypothesis that the repeated post-learning reinforcement of synaptic modifications, termed synaptic reentry reinforcement (SRR), is essential for long-term memory consolidation and storage. Based on experimental observations, we have built a computational model to further illustrate and explore the effect of the SRR process on the formation of long-term memory. We show that SRR is capable of strengthening and maintaining memory traces despite inherent variability in the system due to such processes as the turnover of synaptic receptors and their associated signaling and structural proteins. Furthermore, we demonstrate that new rounds of synaptic modification triggered by memory reactivation, either during conscious recall or sleep, could lead to the selective consolidation of a subset of memory traces. Finally, we show why the SRR process in the hippocampus is required during the initial post-training weeks for synaptic reinforcement based memory consolidation in the cortex.

Animals↗

PubMed2001

GABAergic septohippocampal neurons are not necessary for spatial memory.

The medial septum/vertical limb of the diagonal band of Broca (MSDB) provides a major input to the hippocampus and is important for spatial memory. Both cholinergic and GABAergic MSDB neurons project to the hippocampus, and nonselective lesions of the MSDB or transections of the septohippocampal pathway impair spatial memory. However, selective lesions of cholinergic MSDB neurons using 192-IgG saporin (SAP) do not impair or only mildly impair spatial memory. Previously, intraseptal kainic acid was found to reduce levels of glutamic acid decarboxylase, a marker of GABAergic neurons, but not to alter the levels of choline acetyltransferase, a marker of cholinergic neurons. The present study further characterized the effects of kainic acid on GABAergic MSDB neurons and examined the effects of intraseptal kainic acid on spatial memory. Saline, kainic acid, SAP, or the combination of kainic acid and SAP was administered into the MSDB of rats. Spatial memory was assessed in an eight-arm radial maze and a water maze. Kainic acid destroyed GABAergic septohippocampal neurons, but spared cholinergic neurons. SAP eliminated MSDB cholinergic neurons, sparing noncholinergic neurons. Coadministration of kainic acid and SAP destroyed GABAergic and cholinergic MSDB neurons. Acquisition of the radial maze task and performance on this task with 4-h delays were unimpaired by intraseptal kainic acid or SAP, but were impaired by coadministration of kainic acid and SAP. Acquisition of the water maze task was unaffected by intraseptal kainic acid, delayed slightly by SAP, and impaired severely by coadministration of kainic acid and SAP. These results provide evidence that kainic acid at appropriate concentrations effectively destroys GABAergic septohippocampal neurons, while sparing cholinergic MSDB neurons. Furthermore, lesions of the GABAergic septohippocampal neurons do not impair spatial memory. While lesions of cholinergic MSDB neurons may mildly impair spatial memory, the combined lesion of GABAergic and cholinergic septohippocampal neurons resulted in a memory impairment that was greater than that observed after a selective lesion to either population. Thus, damage of GABAergic or cholinergic MSDB neurons, which together comprise the majority of the septohippocampal pathway, cannot totally account for the spatial memory impairment that is observed after nonselective lesions of the MSDB.

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PubMed1992

Intact verbal and nonverbal short-term memory following damage to the human hippocampus.

Short-term memory was assessed in two groups of amnesic patients. Six patients had confirmed or suspected damage to the hippocampal formation, and six patients had diencephalic damage as a result of alcoholic Korsakoff's syndrome. Verbal short-term memory was evaluated with seven separate administrations of the standard digit span test in order to obtain a precise measure of short-term memory. Nonverbal short-term memory was evaluated with four tests that assessed apprehension, retention, and the ability to manipulate nonverbal material--all within the span of immediate memory. One of these four tests assessed short-term memory for spatial location. Patients with damage to the hippocampal formation had a digit span equivalent to that of control subjects and also performed normally on the four tests of nonverbal short-term memory. The patients with Korsakoff's syndrome had a marginally low digit span and performed poorly on three of the four nonverbal tasks, a finding consistent with the deficits in attention and visuospatial processing previously described for this patient group. These deficits are likely due to the frontal lobe atrophy typically associated with Korsakoff's syndrome, rather than to diencephalic damage. The results support the view that short-term (immediate) memory, including short-term spatial memory, is independent of the hippocampus.

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PubMed2003

Interactions among memory-related centers in the brain.

The structures associated with learning and memory have been widely studied for over 100 years. The idea of the famous neuropsychologist K.S. Lashley, that learning and memory are stored diffusely in the brain, dominated neuroscience in the early half of Twentieth Century. Since Scoville reported in 1957 a persistent impairment of recent memory caused by bilateral medial temporal lobe resection in a patient, the concept that different brain structures play different roles in learning and memory has been established, but the structures were thought to work separately. The connections and functional influences between hippocampus and prefrontal cortex, thalamus and hippocampus, prefrontal cortex and thalamus, amygdala and hippocampus, basal nucleus of Meynert and medial temporal lobe system, and amygdala and thalamus were successively reported. The marginal division (MrD) is a pan-shaped structure consisting of spindle-shaped neurons at the caudal margin of the neostriatum in the mammalian brain. The MrD has been shown to contribute to associative learning and declarative memory by behavioral study in rats and by functional magnetic resonance image study in humans. Lesions in the MrD influenced the learning and memory function of the basal nucleus of Meynert and attenuated hippocampal long-term potentiation. The MrD is likely, based on its position, advanced development in higher mammalian brains, abundant and swift blood supply, and complex connections, to be an important subcortical memory center in the brain. The above-mentioned studies demonstrated that memory-related centers could influence each other and play different roles. Therefore, we propose that there are very possibly hierachical memory centers in the brain.

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PubMed2005

Dominance-related changes in spatial memory are associated with changes in hippocampal cell proliferation rates in mountain chickadees.

It is well established that spatial memory is dependent on the hippocampus in both mammals and birds. As memory capacity can fluctuate on a temporal basis, it is important to understand the mechanisms mediating such changes. It is known that early memory-dependent experiences in young animals result in hippocampal enlargement and in increased neurogenesis, including cell proliferation and neuron survival. It is less clear, however, whether temporal changes in spatial memory are also associated with changes in hippocampal anatomy and cell proliferation in fully grown and experienced adult animals. In a previous study, we experimentally demonstrated that socially subordinate mountain chickadees (Poecile gambeli) showed inferior spatial memory performance compared to their dominant group mates, in the absence of significant differences in baseline corticosterone levels. Here we investigated whether these differences in memory between dominant and subordinate birds were associated with changes in the hippocampus. Following memory tests, chickadees were injected with 5-bromo-2'-deoxyuridine to label dividing cells and sacrificed 2 days after the injections. We found no significant differences in volume or the total number of neurons in the hippocampal formation between dominant and subordinate chickadees, but subordinate birds had significantly lower cell proliferation rates in the ventricular zone adjacent to both the hippocampus and mesopallium compared to the dominants. Individuals, which performed better on spatial memory tests tended to have higher levels of cell proliferation. These results suggest that social status can affect cell proliferation rates in the ventricular zone and support the hypothesis that neurogenesis might be involved in memory function in adult animals.

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PubMed1997

Differential involvement of left temporolateral and temporomesial structures in verbal declarative learning and memory: evidence from temporal lobe epilepsy.

A wealth of animal and human research has pointed to a significant involvement of the temporal lobes in memory processing, and yet the different functional roles of temporal cortical vs. mesial structures remain unclear. We studied verbal declarative memory, by using a word list paradigm that differentiates among learning (immediate recall), memory (delayed recall), and recognition, in epilepsy patients being considered for surgical resection of the left temporal lobe. Verbal memory was evaluated preoperatively and during the recording of intracranial event related potentials and postoperatively after selective hippocampectomy, temporal cortical lesionectomy, or anterior two-thirds en bloc temporal lobe resection procedures. Preoperative differences in verbal memory performance as a function of differences in underlying neuropathology, concurrent event-related potentials, and specific patterns of postoperative memory impairments lead to converging evidence that verbal declarative memory relies on a synergistic interaction of at least two functionally distinct brain systems. Material-specific data acquisition, or working memory, is mediated by neocortical temporal structures, whereas long-term consolidation/retrieval is particularly mediated by temporomesial structures. In contrast to the left temporal neocortex, the function of the temporomesial system appears to be material nonspecific. Apparently, its preferential involvement in verbal memory is due to its close interaction with overlying neocortical structures that are specialized for language processing.

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PubMed1999

Hippocampal involvement in spatial and working memory: a structural MRI analysis of patients with unilateral mesial temporal lobe sclerosis.

Forty-seven patients with unilateral temporal lobe epilepsy (TLE) were investigated on the Nine-Box Maze. The task was designed to compare working memory and spatial mapping theories of the functions of the hippocampus and provide measures of spatial, object, working, and reference memory. The results extended our previous findings in a larger group of patients. Spatial memory deficits across both working and reference memory conditions were found in patients with a right epileptogenic focus. There was no evidence of an object working memory deficit, but a nonlateralized impairment in object reference memory was revealed, which is consistent with our previous findings. The pattern of results was confirmed in a subgroup of 33 patients with unilateral atrophy localized to the hippocampus and parahippocampal gyrus, as verified by volumetric analysis of magnetic resonance images. In addition spatial memory errors significantly correlated with volumetric measures of mesial temporal lobe structures and not with measures of the remaining temporal cortex. In contrast, object reference memory errors correlated with volumetric measures of the temporal cortex and not with mesial temporal lobe structures. These findings support a specialized role for the right hippocampal region in spatial memory.

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PubMed1996

Regulatory interactions between virgin and memory CD4 T lymphocytes.

Naive and memory CD4 T cells from mouse spleen, alone or in a 1:1 mixture, were tested for Con A-induced proliferation in limiting dilution cultures. Dose-response curves for naive cells were linear, but curves for memory cells were hyperbolic, suggesting that positive responses required the activation of several cells of the memory type. Mixtures (1:1) gave zig-zag curves, consistent with a previously described quantitative model in which memory cells block naive cell proliferation at low multiplicities and generate their own positive responses at higher multiplicities. Inhibition of naive cell proliferation by memory cells could be mimicked by IL-10 and blocked by anti-IL-10 antibody. IL-2 addition converted the multihit dose curves of memory T cells to single-hit curves, suggesting that poor IL-2 production limits growth in memory cell cultures. Surprisingly, IL-2 addition to cultures of naive cells led to a decrease in proliferation at high cell input doses. This inhibitory effect of IL-2 could be blocked by antibody to IL-10, and may reflect the presence of contaminating memory cells in the naive cell preparations. These models for analysis of interaction between naive and memory T cells in limiting dilution conditions point to a series of reciprocal interactions between IL-10 and IL-2 producing cells.

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PubMed1997

Memory T cell tolerance to superantigens is not due to increased susceptibility to apoptosis.

Naive (virgin) and memory T lymphocytes differ markedly in their response to superantigens (SAg). When cultured with the SAg staphylococcal enterotoxin B (SEB), virgin but not memory CD4(+) T cells proliferate and secrete lymphokines. Memory cells do express increased levels of activation markers after interaction with SEB, which suggests that the cells are not ignorant of the SAg. In this report, we have considered whether SEB, rather than activating memory cells, promotes their death by apoptosis. Our results indicate that while in vivo exposure to SEB induces apoptosis, there is no greater level of cell death in the memory cell population relative to virgin cells. Further, elimination of the Fas-mediated cell death pathway does not permit memory cells to be stimulated by SEB. Memory T cells from either Fas-expressing or Fas-deficient (MRL-lpr/lpr) mice are hyporesponsive to SEB. Blockade of Fas/Fas-ligand interactions by a Fas-Fc chimeric protein does not permit BALB/c memory cells to proliferate upon culture with SEB. These results provide evidence that the failure of memory T cells to respond to SEB is not due to cell death and that inactivation (anergy) is the likely fate of these cells when they encounter SEB.

Animals↗

PubMed1998

Childhood anxiety and memory functioning: a comparison of systemic and processing accounts.

Information-processing models of childhood anxiety highlight the centrality of memory processes in the maintenance and intensification of anxiety. Recent advances in memory research allow for an increasingly fine-grained analysis of the relation between anxiety and memory. The relation between childhood anxiety and memory was examined in a sample of 160 high- and low-trait-anxious sixth through eighth grade children. Results indicated that anxiety predicted a memory bias toward negative relative to neutral information during conceptual but not perceptual tasks. Further, anxiety predicted a memory bias toward positive relative to neutral information on procedural tasks and a memory bias away from positive relative to neutral information on declarative tasks. These findings accent the complexity and multidimensionality of relations among childhood anxiety, the emotional valence of stimuli, types of cognitive processing, and memory systems in contributing to biases in children's memory functioning.

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PubMed2004

Memory, reconsolidation and extinction in Lymnaea require the soma of RPeD1.

The central pattern generator (CPG) that drives aerial respiratory behaviour in Lymnaea consists of 3 neurons. One of these, RPeD1--the cell that initiates activity in the circuit, plays an absolutely necessary role as a site for memory formation, memory reconsolidation, and extinction. Using an operant conditioning training procedure that results in a long-term non-declarative memory (LTM), we decrease the occurrence of aerial respiratory behaviour. Since snails can still breathe cutaneously learning this procedure is not harmful. Concomitant with behavioural memory are changes in the spiking activity of RPeD1. Going beyond neural correlates of memory we directly show that RPeD1 is a necessary site for LTM formation. Expanding on this finding we show that this neuron is also a necessary site for memory reconsolidation and 'Pavlovian' extinction. As far as we can determine, this is the first time a single neuron has been shown to be a necessary site for these different aspects memory. RPeD1 is thus a key neuron mediating different hierarchical aspects of memory. We are now in a position to determine the necessary neuronal, molecular and proteomic events in this neuron that are causal to memory formation, reconsolidation and extinction.

Animals↗

PubMed1988

Sleep and memory.

Generally sleep is considered a time of amnesia. It is not uncommon for an individual to experience 8 h of sleep and have no memory for events during that time. Similarly, a substantial proportion of the population has no memory for dreams that occurred during the night, despite the fact that the literature on awakening during rapid eye movement (REM) sleep clearly shows that individuals normally have four to six "dream experiences" a night. Research on this issue seems to indicate that the lack of memory cannot be explained by the organisms' inability to perceive stimuli. The data indicate that although perceptual thresholds are elevated, organisms can clearly perceive stimuli, and, in fact, can discriminate between them during sleep. The amnesia also cannot be explained by a defect in long-term memory, as studies have indicated that stimuli put into the memory during wakefulness are more efficiently retrieved after a sleep period than after a comparable period of wakefulness. The most likely explanation for the amnestic property of sleep seems to be the inability of organisms to transfer information from short-term memory to long-term memory during sleep. There are several sources of evidence to support this hypothesis. First, the probability of remembering a stimulus given during wakefulness is related to the proximity of sleep onset to the stimulus. Generally, information put into the system within 5 min of sleep onset is lost from memory. Secondly, disorders of excessive daytime somnolence which cause individuals to have frequent microsleeps are often associated with complains of memory problems.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1988

Measures of memory and information processing in elderly volunteers.

A screening study was carried out in normal elderly volunteers to determine 1. their scores in measures of memory and information processing 2. how the measures correlate with sample characteristics 3. how the measures correlate with each other and with the EEG. We report here on 111 subjects, 56 women and 55 men aged 53-77 years (63.9 +/- 6.8) with average intelligence (Coloured Progressive Matrices CPM 26.7 +/- 5.1). In the C-normed measures of the word list from the Nuremberg Geriatric Inventory (NGI) our sample scored better than average (immediate recall of words C = 7.5, delayed recall of words C = 8.2; mean C = 5). The sample even attained ceiling scores in the test of recognition. The sample likewise had a better than average speed in a color-word test (CWT) of focused attention similar to the Stroop test (e.g., reading C = 7.5, color-naming C = 6.7, interference task C = 6.3) and in the ZVT trail-making test (C = 7.0). In contrast, speed-free focused attention was only average (C = 5.2 and C = 5.5). The following sample characteristics correlated with test measures of memory and information processing (p less than 0.01): age negatively with immediate recall, trail making, incidental episodic memory, focused attention, speed in the CWT; intelligence correlated positively with 10-min adding which relies on working memory (Pauli test) and immediate recall; education correlated positively with delayed recall, visual memory performance in a figures test, immediate recall, and reading speed in the CWT; occupation correlated positively with figures test performance; exercise of profession correlated positively with incidental episodic memory and immediate recall. Age and occupation correlated more with motor measures than with cognitive measures (pegboard, 1 min tapping at maximal speed). Sex had no bearing on memory characteristics, but did on tracking (men better) and color-naming performance in the CWT (women better). Of the semiluxuries, only regular alcohol consumption showed a relationship with the test measures (negatively with color-naming speed, immediate recall, and pegboard performance). Analysis of memory and information processing measures revealed no correlations (r greater than or equal to 0.40) between memory measures from the word list, Pauli test, figures test, and learning. Measures of the CWT correlated with Pauli test and pegboard. ZVT score was the variable with the most correlations (CWT, Pauli test, pegboard). A factor analysis with a reduced set of variables should further clarify the inner structure of our subject's performance.(ABSTRACT TRUNCATED AT 400 WORDS)

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PubMed1988

Modulation of memory by post-training epinephrine: involvement of cholinergic mechanisms.

Extensive evidence indicates that memory storage can be modulated by peripheral epinephrine as well as by drugs affecting the muscarinic cholinergic system. Low doses of epinephrine (Epi) facilitate memory while high doses induce amnesia. Retention is enhanced by post-training administration of cholinergic muscarinic agonists and impaired by antagonists. The present experiments examined the interaction of peripheral Epi and cholinergic drugs in memory modulation. Male CFW mice (60 days old) were trained on an inhibitory avoidance response (IA) or a Y-maze discrimination response (YMD), injected (IP) immediately post-training and tested 24 h later. In the Y-maze task, retention was assessed by discrimination reversal training. Findings obtained in the two tasks were comparable. Epi (IA: 3.0 micrograms/kg; YMD: 30.0 micrograms/kg) potentiated the memory-enhancing effect of low doses of oxotremorine (Otm) (IA: 16; YMD: 5.0 micrograms/kg) and physostigmine (Phy) (6.8 and 22.0 micrograms/kg for both IA and YMD). The memory-facilitating effect of Otm (50.0 micrograms/kg) was not blocked by an amnestic dose of Epi (IAT: 0.3 mg/kg; YMD: 1.0 mg/kg). Retention was not affected when these amnestic doses of Epi were administered together with a memory-facilitating dose of Phy (68.0 micrograms/kg). In contrast, atropine (IA: 10.0 mg/kg; YMD: 3.0 mg/kg) completely blocked the facilitatory effect of Epi (IA: 10.0 micrograms/kg; YMD: 300 micrograms/kg). These findings indicate that, when administered in low doses, Epi interacts with Otm and Phy. However, cholinergic drugs can block both the memory-enhancing and the memory-impairing effects of Epi. The findings suggest that Epi may modulate memory through cholinergic systems.

Animals↗

PubMed1987

Naloxone and beta-endorphin alter the effects of post-training epinephrine on memory.

These experiments examined the involvement of opioid peptides in the memory-modulating effects of post-training epinephrine (Epi). Mice were trained on inhibitory avoidance (IA) and Y-maze discrimination (YMD) tasks and given post-training injections followed by retention tests 24 h later. In the IA task retention was enhanced by low doses of Epi and impaired by high doses. In both tasks, naloxone facilitated retention and blocked the memory-impairing effects of Epi. These findings are consistent with other evidence suggesting that the memory-impairing effects of beta-endorphin are mediated by the release of opioid peptides. Previous studies have shown that a novel exploratory experience given 1 h prior to training blocks the release of brain beta-endorphin and blocks the memory-enhancing effects of post-training naloxone. In the present study we found that a novel experience given 1 h prior to training blocked the memory-impairing effect of post-training Epi otherwise obtained in both tasks. The effects of a low, memory-enhancing dose of Epi appear not to involve the release of opioid peptides: a low dose of Epi blocked the memory-impairing effect of beta-endorphin. Further, low doses of Epi and naloxone, which were ineffective when administered alone, significantly enhanced retention when administered together. We interpret these findings as indicating that the memory-enhancing and memory-impairing effects of Epi are mediated by different mechanisms.

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