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PubMed1988

The effect of scopolamine and physostigmine on working and reference memory in pigeons.

A comparison of the effects of scopolamine and physostigmine on working memory and reference memory in White Carneaux pigeons was undertaken. In Experiment 1, the pigeons received injections of scopolamine hydrobromide (0.03 mg/kg), or saline. Scopolamine hydrobromide had greater disruptive effects on working memory trials than on reference memory trials, and the centrally active form of scopolamine disrupted working memory trial accuracy more than the peripherally active form. The differential sensitivity of accuracy on working memory trials to disruption by central cholinergic blockade was obtained even though the discrimination required on reference memory trials was more difficult. In Experiment 2, the pigeons received injections of scopolamine hydrobromide (0.015 mg/kg), physostigmine (0.075 mg/kg) both scopolamine and physostigmine, or saline. Physostigmine given with scopolamine was able to reverse the scopolamine-induced reduction of accuracy on working memory trials. In neither study did scopolamine promote accelerated forgetting as the delay interval was increased. These results indicate that manipulation of central cholinergic neurotransmitter systems influences working memory processes in the pigeon, but these effects occur without alterations in the ability of the birds to actively maintain information during the retention interval.

Animals↗
PubMed1994

Costimulation by purified intercellular adhesion molecule 1 and lymphocyte function-associated antigen 3 induces distinct proliferation, cytokine and cell surface antigen profiles in human "naive" and "memory" CD4+ T cells.

Activation of resting human CD4+ "naive" (CD45RA+CD45RO-) and "memory" (CD45RA-CD45RO+) T cells requires costimulatory signals in addition to engagement of the T cell receptor/CD3 complex (TCR/CD3). The adhesion pathways mediated by lymphocyte function-associated antigen 1/intercellular adhesion molecule 1 (LFA-1/ICAM-1) and CD2/LFA-3 are capable of providing such costimulatory signals. Our work shows that these costimulatory adhesion pathways are critically involved in regulation of T cell differentiation/maturation. Evidence for subset-specific costimulatory requirements is demonstrated by the finding that only memory CD4+ T cells were costimulated by LFA-3, whereas both naive and memory CD4+ T cells were costimulated by ICAM-1. In addition, these costimulatory adhesion pathways regulated reciprocal cytokine secretion patterns for interleukin 5 (IL-5) and granulocyte/macrophage colony-stimulating factor (GM-CSF). Repeated costimulation of CD4+ memory T cells with LFA-3 led to secretion of high levels of IL-5, while repeated costimulation with ICAM-1 induced high levels of secreted GM-CSF. Significant interferon gamma (IFN-gamma) production was observed with either of the costimulatory ligands. Extensive cell surface analysis of these in vitro cultures of peripheral blood derived memory CD4+ T cells, with monoclonal antibodies obtained from the 5th Leucocyte Typing Workshop, revealed differential expression of a singular antigen, CD60. This antigen was preferentially expressed on LFA-3-costimulated cells suggesting a positive correlation between CD60 expression and a T helper type 2-like cytokine profile. In conclusion, this report demonstrates a new functional role for costimulatory adhesion molecules in regulating differential cytokine secretion in human memory CD4+ T cells.

Antibodies, Monoclonal↗
PubMed1999

Differentiation of human CD8 T cells: implications for in vivo persistence of CD8+ CD28- cytotoxic effector clones.

CD8 T cells contain a distinct subset of CD8+ CD28- cells. These cells are not present at birth and their frequency increases with age. They frequently contain expanded clones using various TCRalphabeta receptors and these clones can represent >50% of all CD8 cells, specially in old subjects or patients with chronic viral infections such as HIV-1. Herein, it is shown that a large fraction of CD8+ CD28- cells expresses intracellular perforin by three-color flow cytometry, in particular when this subset is expanded. Together with their known ability to exert potent re-directed cytotoxicity, this indicates that CD8+ CD28- T cells comprise cytotoxic effector cells. With BrdU labeling, we show that CD8+ CD28- cells derive from CD8+ CD28+ precursors in vitro. In addition, sorted CD8+ CD28+ cells gave rise to a population of CD8+ CD28- cells after allo-stimulation. Moreover, ex vivo CD8+ CD28+ cells contain the majority of CD8 blasts, supporting the notion that they contain the proliferative precursors of CD8+ CD28- cells. CD95 (Fas) expression was lower in CD8+ CD28- cells, and this subset was less prone to spontaneous apoptosis in ex vivo samples and more resistant to activation-induced cell death induced by a superantigen in vitro. Thus, the persistence of expanded clones in vivo in the CD8+ CD28- subset may be explained by antigen-driven differentiation from CD8+ CD28+ memory precursors, with relative resistance to apoptosis as the clones become perforin(+) effector cells.

Adult↗
PubMed1995

A neural model of memory impairment in diffuse cerebral atrophy.

BACKGROUND: Computer-supported neural network models have been subjected to diffuse, progressive deletion of synapses/neurons, to show that modelling cerebral neuropathological changes can predict the pattern of memory degradation in diffuse degenerative processes such as Alzheimer's disease. However, it has been suggested that neural models cannot account for more detailed aspects of memory impairment, such as the relative sparing of remote versus recent memories. METHOD: The latter claim is examined from a computational perspective, using a neural associative memory model. RESULTS: The neural network model not only demonstrates progressive memory deterioration as diffuse network damage occurs, but also exhibits differential sparing of remote versus recent memories. CONCLUSIONS: Our results show that neural models can account for a large variety of experimental phenomena characterising memory degradation in Alzheimer's patients. Specific testable predictions are generated concerning the relation between the neuraonatomical findings and the clinical manifestations of Alzheimer's disease.

Aged↗
PubMed2006

Identification of memory B cells using a novel transgenic mouse model.

Memory B cells help to protect the host from invading pathogens by maintaining persistent levels of Ag-specific serum Ab and generating rapid Ab responses upon re-exposure to Ag. Unambiguous identification of memory B cells has been a major obstacle to furthering our knowledge concerning both the development of B cell memory and secondary Ab responses due to an absence of specific cell surface markers. Germinal centers (GCs) are thought to be the major site of Ig hypermutation and Ag-driven selection of memory B cells. To develop a model that would identify GC-derived memory B cells, we generated transgenic mice that expressed cre recombinase in a GC-specific fashion. Interbreeding these mice with the cre-reporter strain, ROSA26R, produced progeny in which beta-galactosidase (beta-gal) was permanently expressed in B cells of the GC-memory pathway. Analysis following immunization with (4-hydroxy-3-nitrophenyl)acetyl coupled to chicken gamma globulin showed that long-lived beta-gal+ B cells exclusively contained somatically mutated lambda1 V regions and were capable of producing Ag-specific Ab-forming cell (AFC) responses that were >100-fold higher than those afforded by beta-gal- B cells following adoptive transfer to naive hosts. Secondary challenge of immune mice showed that only approximately 20% of secondary AFCs expressed beta-gal. Interestingly, we found that somatic hypermutation of rearranged lambda1 V regions within secondary AFCs showed a strong correlation with beta-gal expression, suggesting that nonmutated B cells contribute significantly to secondary Ab responses. This model should provide useful insights into memory B cell development, maintenance, and differentiation following immunization or pathogenic infection.

Animals↗
PubMed1997

[Magnetic resonance imaging of intracerebral hemorrhage].

Computerized tomography (CT) followed with magnetic resonance imaging (MRI) several years later enabled first the direct visualization of extravascular blood and products of it's degradation. Protein component of hemoglobin is from over 90% responsible for the hyperdensity of CT image in case of a hemorrhage, whereas paramagnetic properties of hemoglobin derivates are responsible for signal changes in MRI. CT is capable to diagnose accurately just an acute hemorrhage. It changes towards hypodensity in 3 weeks with posthemorrhagic pseudocyst as a final result that has rather low specificity. Differentiation from contusion, ischemic lesion or even astrocytoma may be difficult. CT has thus "short memory" for hemorrhage. MRI can differentiate 5 stages of hemorrhage according to the time schedule: hyperacute, acute, subacute stage I, subacute stage II and chronic. Sequel of a hemorrhage is detectable even years after the hemorrhagic event. The development of intracranial hemorrhage in daily routine MR imaging is described and documented to serve as a guide of model situation for the use of physician.

Brain↗
PubMed2002

Dissecting the effect of aging on the neural substrates of memory: deterioration, preservation or functional reorganization?

One of the most common deficits observed during late adulthood is a loss in the ability to learn and remember new information. This cognitive ability depends mainly on the integrity of the hippocampal formation and the prefrontal cortex, which are especially susceptible to the effects of age. Here we provide a selective review of the literature gathered from studies carried out in humans and animals, examining the effect of aging on the functional anatomy of memory. We discuss some of the methodological and theoretical difficulties associated with the current approach to the study of aging and, in turn, a series of strategies that may be implemented to ensure the most accurate interpretation of the data. Altogether, the evidence discussed in this review supports the idea that there is no general age-related deterioration of the neural substrates of memory, but rather a differential effect in which some brain areas may be adversely affected while others may compensate for the neurobiological deterioration associated with age.

Aging↗
PubMed2003

The voltage-gated Kv1.3 K(+) channel in effector memory T cells as new target for MS.

Through a combination of fluorescence microscopy and patch-clamp analysis we have identified a striking alteration in K(+) channel expression in terminally differentiated human CCR7(-)CD45RA(-) effector memory T lymphocytes (T(EM)). Following activation, T(EM) cells expressed significantly higher levels of the voltage-gated K(+) channel Kv1.3 and lower levels of the calcium-activated K(+) channel IKCa1 than naive and central memory T cells (T(CM)). Upon repeated in vitro antigenic stimulation, naive cells differentiated into Kv1.3(high)IKCa1(low) T(EM) cells, and the potent Kv1.3-blocking sea anemone Stichodactyla helianthus peptide (ShK) suppressed proliferation of T(EM) cells without affecting naive or T(CM) lymphocytes. Thus, the Kv1.3(high)IKCa1(low) phenotype is a functional marker of activated T(EM) lymphocytes. Activated myelin-reactive T cells from patients with MS exhibited the Kv1.3(high)IKCa1(low) T(EM) phenotype, suggesting that they have undergone repeated stimulation during the course of disease; these cells may contribute to disease pathogenesis due to their ability to home to inflamed tissues and exhibit immediate effector function. The Kv1.3(high)IKCa1(low) phenotype was not seen in glutamic acid decarboxylase, insulin-peptide or ovalbumin-specific and mitogen-activated T cells from MS patients, or in myelin-specific T cells from healthy controls. Selective targeting of Kv1.3 in T(EM) cells may therefore hold therapeutic promise for MS and other T cell-mediated autoimmune diseases.

Adult↗
PubMed2001

Motive-related memories: content, structure, and affect.

Two studies tested hypotheses on the content and structure of autobiographical memories and the affect linked to them. In Study 1, agentic- and communal-motivated individuals recorded their most memorable experiences and completed the PANAS each day for 6 weeks. Memories were coded for content and structure. Agentics and communals reported more motive congruent memories, and their congruent memories were structured using more differentiation and integration, respectively. In addition, agentics had slightly higher PA and lower NA scores. In Study 2, agentics and communals recalled an event pertaining to either social separation or connection and then completed an affect measure of agentic and communal items. Agentics recalled more agentic memories in the separation condition and communals recalled more communal memories in the connection condition. Complexity analyses showed that agentics and communals used differentiation and integration respectively to recall their motive-congruent memories. The affect data showed a modestpredicted pattern. Results suggest that implicit motives have an impact on autobiographical memory but are not as clearly related to self-report affect measures, possibly due to method variance.

Affect↗
PubMed1975

[Amnestic episodes. (Isolated episodes of confusion with amnesia, amnesic ictus, transient global amnesia)].

The author, by giving an outline of one particular case as well as a survey of the relevant literature on transient global amnesia, describes the characteristic clinical picture that is characterized by a sudden loss of what is known as the short-time memory, which usually lasts for several hours, as well as by retrograde amnesia which sometimes dates back to many years. The condition gradually fades away within a few hours or during a night's sleep, and what remains is lack or loss of memory for the episodic period or sometimes retrograde amnesia. Relapses were not observed in the majority of patients. The disease usually develops in people in their sixth to eighth decades of life. The cause of the disease is not yet fully understood. Accordingly, it is justified to use such terms as autochthonous or cryptogenic amnestic episodes. The disease is also discussed from a differential diagnosis point of view.

Age Factors↗
PubMed2004

Differential gene expression by integrin beta 7+ and beta 7- memory T helper cells.

BACKGROUND: The cell adhesion molecule integrin alpha 4 beta 7 helps direct the migration of blood lymphocytes to the intestine and associated lymphoid tissues. We hypothesized that beta 7+ and beta 7- blood memory T helper cells differ in their expression of genes that play a role in the adhesion or migration of T cells. RESULTS: RNA was prepared from beta 7+ and beta 7- CD4+ CD45RA- blood T cells from nine normal human subjects and analyzed using oligonucleotide microarrays. Of 21357 genes represented on the arrays, 16 were more highly expressed in beta 7+ cells and 18 were more highly expressed in beta 7- cells (>/=1.5 fold difference and adjusted P < 0.05). Several of the differentially expressed transcripts encode proteins with established or putative roles in lymphocyte adhesion and chemotaxis, including the chemokine receptors CCR9 and CCR10, the integrin alpha 4 subunit, L-selectin, KLRB1 (CD161), NT5E (CD73), LGALS1 and LGALS2 (galectin-1 and -2), and RGS1. Flow cytometry was used to determine whether differences in levels of transcripts encoding cell surface proteins were associated with differential expression of those proteins. Using this approach, we found that surface expression of KLRB1, LAIR1, and NT5E proteins was higher on beta 7+ memory/effector T cells than on beta 7- cells. CONCLUSIONS: Memory/effector T cells that express integrin beta 7 have a distinct pattern of expression of a set of gene transcripts. Several of these molecules can affect cell adhesion or chemotaxis and are therefore likely to modulate the complex multistep process that regulates trafficking of CD4+ memory T cell subsets with different homing behaviors.

Adult↗
PubMed2006

Expression and regulation of the orphan receptor RDC1 and its putative ligand in human dendritic and B cells.

Based on phylogenetic analysis and chromosomal mapping, the orphan receptor RDC1 was proposed to be a chemokine receptor. In this study we examined the expression of RDC1 on leukocytes by measuring mRNA levels and receptor expression using a new specific mAb. Both mRNA and protein levels were high in monocytes and B cells, relatively low on immature dendritic cells (DC), and up-regulated during final stages of maturation. Strikingly, in mature plasmacytoid DC the mRNA was up-regulated, but did not correlate with protein surface expression. We indeed report that CpG-activated plasmacytoid DC produce a putative ligand for RDC1, which selectively down-regulates RDC1, but not CXCR4 on primary human B cells. RDC1 expression was found to be tightly regulated during B cell development and differentiation. In blood-derived switch memory B cells, the expression of RDC1 appeared to correlate with the ability to differentiate into plasma cells upon activation, suggesting that RDC1 is a marker for memory B cells, which are competent to become Ab-secreting cells.

B-Lymphocytes↗
PubMed1986

Memory assessment using the Strub-Black Mental Status Examination and the Wechsler Memory Scale.

A systematic mental status exam often can differentiate accurately patients with organic brain disease from normal persons and those with functional disorders. The present study attempts to validate the memory portion of the Strub-Black Mental Status Exam by comparing it to the Wechsler Memory Scale. Twenty-five brain-damaged and 25 routine medical patients were given Form I of the Wechsler Memory Scale and the memory portion of the Strub-Black Mental Status Exam at their hospital bedside. Results indicate significant differences in almost all scores between the brain-damaged and normal groups on both the Wechsler Memory Scale and Mental Status exam; the Mental Status Exam differentiated between groups at a higher level of significance of ANOVA and ANCOVA comparisons of total memory scores, as well as several subtests. In these samples, age, more than education, was an important factor that affected memory test performance. The Mental Status Examination appears valid for the differentiation of clinical samples and for the documentation of specific aspects of memory dysfunction in individual brain-damaged patients. This study represents a beginning step in providing normative data on components of the Strub-Black mental status examination.

Adult↗
PubMed2006

T-lymphocyte subset distribution in human spleen.

BACKGROUND: When analyzing human cellular immune responses, most focus is placed on the peripheral blood (PB) and, to a lesser extent, the lymph nodes. To date the spleen has not been analyzed with regard to its role in adaptive cellular immunity and more notably not with respect to T-cell immune responses. MATERIALS AND METHODS: We analyzed the splenic lymphocyte compartment in comparison with the PB lymphocyte compartment regarding the number of NK cells, B cells, CD4(+), CD8(+) T cells and CMV-specific CD8(+) T cells. Furthermore, we analyzed the distribution of naive, memory and effector subsets of CD4(+) and CD8(+) T cells in these compartments. RESULTS: The spleen contains proportionally more B cells and less CD4(+) and CD8(+) T cells than PB. The percentage of CD8(+) T cells is greater in the spleen, leading to an inverse CD4/CD8 ratio. Both splenic CD4(+) and CD8(+) T-cell populations show a greater number of activated cells, and splenic CD8(+) T cells show a more differentiated cytotoxic CD27(-)CD45RA(+) memory phenotype. CONCLUSIONS: Our findings show that the distribution of the different lymphocyte subsets is markedly different between the spleen and the PB, thus inferring an important and distinct role for the spleen in CD4(+) and CD8(+) T-cell activation.

Adult↗
PubMed1989

Issues in memory assessment of the elderly.

The pattern of memory test performance by elderly individuals demonstrates significant overlap between populations. Consequently, the memory tests themselves poorly differentiate normal aging, dementia, and depression. The additional problem of relatively little adequate normative information for elderly individuals compounds this problem. Thus, inferences regarding the nature of assessed deficits should be based in part on information that extends beyond the traditional quantitative numerical analyses of test performances. For example, depressed individuals tend to make fewer false-positive responses and frequently will respond stating "I don't know." Similarly, if there is evidence for risk of memory impairment, the threshold for inferring assessed memory deficit may be altered. Finally, when independent information is present to confirm the presence of structural change in the brain, the inference of specific memory impairments can be strengthened. One not only needs to look at the entire pattern of neuropsychological deficits, but also use the neuropsychological findings in the context of other clinical findings. Perhaps the greatest utility of neuropsychological memory assessment of the elderly is providing standardized assessments for repeat evaluations. By repeating the assessment, deterioration as a function of a progressive dementia can be assessed. Alternatively, the effect of treatment for depression can be monitored and an improvement in memory test scores would be expected. Throughout, however, the careful clinician will remember that the inferences regarding an individual's level of function are not stronger than the reliability, representativeness, and validity of the instruments employed.

Aged↗
PubMed1983

[Study of memory function in depressions in advanced age (problem of transient dementia)].

Mnestic function was examined in 50 patients suffering from late-age endogenous depressions, as well as in 10 patients with pronounced vascular dementia. A deterioration of the memory for recent events was discovered in the patients with the late-age depression, this deterioration correlating with the degree of the depressive mood, the anxiety, and psychomotor inhibition. Dynamic (affective) components were revealed in the psychoorganic syndrome structure in patients with the initial vascular dementia. Patients with a pronounced vascular dementia showed gross and persistent intellectual and mnestic impairments. Administration of single doses of melipramine and diazepam seems to be justified and desirable for differential diagnosis of late-age depressions and dementias, as well as for discovering the dynamic components in the structure of a psychoorganic syndrome.

Aged↗
PubMed1994

Psychological aspects of aging: when does memory loss signal dementia?

With aging comes a normal decline in intelligence and specific cognitive functions such as memory. Distinguishing age-related memory loss from that due to a disease process such as dementia, especially in its early stages, can be difficult. Neuropsychological assessment is probably the most sensitive method of making this determination. A diagnosis of dementia requires impairment in memory plus impairment in at least one more area of cognitive function, such as language or conceptualization. Once the diagnosis of dementia is established, your role is to carefully explain it to the patient and family and answer their questions about causes and possible interventions.

Aging↗
PubMed2004

Transition of late-stage effector T cells to CD27+ CD28+ tumor-reactive effector memory T cells in humans after adoptive cell transfer therapy.

In humans, the pathways of memory T-cell differentiation remain poorly defined. Recently, adoptive cell transfer (ACT) of tumor-reactive T lymphocytes to metastatic melanoma patients after nonmyeloablative chemotherapy has resulted in persistence of functional, tumor-reactive lymphocytes, regression of disease, and induction of melanocyte-directed autoimmunity in some responding patients. In the current study, longitudinal phenotypic analysis was performed on melanoma antigen-specific CD8+ T cells during their transition from in vitro cultured effector cells to long-term persistent memory cells following ACT to 6 responding patients. Tumor-reactive T cells used for therapy were generally late-stage effector cells with a CD27Lo CD28Lo CD45RA- CD62 ligand- (CD62L-) CC chemokine receptor 7- (CCR7-) interleukin-7 receptor alphaLo (IL-7RalphaLo) phenotype. After transfer, rapid up-regulation and continued expression of IL-7Ralpha in vivo suggested an important role for IL-7R in immediate and long-term T-cell survival. Although the tumor antigen-specific T-cell population contracted between 1 and 4 weeks after transfer, stable numbers of CD27+)CD28+ tumor-reactive T cells were maintained, demonstrating their contribution to the development of long-term, melanoma-reactive memory CD8+ T cells in vivo. At 2 months after transfer, melanoma-reactive T cells persisted at high levels and displayed an effector memory phenotype, including a CD27+ CD28+ CD62L- CCR7- profile, which may explain in part their ability to mediate tumor destruction.

Adoptive Transfer↗