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PubMed1997

Early cognitive markers of the incidence of dementia and mortality: a longitudinal population-based study of the oldest old.

This study examines whether cognitive markers at prior examinations are indicative of subsequent dementia and mortality. The sample was composed of subjects aged 84-90 at baseline who were reexamined three times over a 6-year period on a comprehensive biobehavioral battery. Dementia was evaluated at each examination using DSM-III-R criteria. Results indicated that incident cases of dementia had lower cognitive scores both 2 and 4 years prior to diagnosis, compared to non-demented survivors. Evidence for terminal decline was also found, as people who subsequently died also had lower cognitive performance at prior examinations, compared to non-demented survivors. The findings suggest that mild cognitive dysfunction is an important clinical finding among the oldest old and may herald either the onset of dementia or mortality.

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PubMed1993

Cognitive impairment following traumatic brain injury: the effect of pre- and post-injury administration of scopolamine and MK-801.

In order to examine the effectiveness of pre- and post-injury administration of muscarinic cholinergic and NMDA antagonists in reducing cognitive deficits following traumatic brain injury (TBI), rats were injected with either scopolamine (1 mg/kg) or MK-801 (0.3 mg/kg) 15 min prior to or 15 min after fluid percussion TBI. Cognitive performance was assessed with the Morris water maze procedure on days 11-15 after TBI or sham injury. When scopolamine and MK-801 were injected 15 min before injury, Morris water maze deficits were significantly reduced (P < 0.01 and P < 0.05, respectively). When scopolamine and MK-801 were injected 15 min after TBI, neither drug was effective in attenuating Morris water maze deficits. Consistent with other research, these results suggest that the cognitive deficits produced by TBI are the consequence of a brief period of excessive excitation of cholinergic and NMDA receptor systems. The results of this experiment also suggest that the temporal therapeutic window for the treatment of cognitive dysfunction with receptor antagonist intervention appears to be quite brief (< 15 min) in the rat.

Animals↗

PubMed2003

Event-related potentials P300 in type 2 diabetes mellitus.

OBJECTIVE: To investigate event-related potentials (ERP) P(300) in patients with type 2 diabetes mellitus (DM) for early detection of the abnormalities in cognitive function and studying the related factors. METHODS: With the assistance of Nicolet Vinking IV equipment, ERP (P(300)) were tested in 30 type 2 diabetic patients and 30 healthy subjects matched for age, gender, and education background, and the the results were analyzed statistically. The relationships of each ERP parameter with glucose hemoglobin (GHb) and blood lipid levels and renal function were analyzed. RESULTS: No significant difference was found in P(300) latencies in the control group irrespective of the gender and education (P > 0.05), while the latencies were significantly prolonged (P < 0.01) and the amplitudes decreased (P < 0.05) in diabetic patients. It was found that P(300) correlated with glucose hemoglobin (GHb) and blood lipid levels (P < 0.05). CONCLUSION: ERP test is useful for early detection of cognition dysfunction in DM cases, helping to timely identify diabetic patients with potential dementia.

Adult↗

PubMed2005

[Use of cognitive evoked potentials P300 in diagnosis of affection of the higher mental functions after surgery on the heart in conditions of cardiopulmonary bypass].

Parameters of cognitive evoked potentials P300 were studied in 40 patients with ischemic heart disease subjected to coronary artery bypass graft surgery in conditions of cardiopulmonary bypass before and 7-9 days after operation. Patients underwent also neurological and neuropsychological examination. The most significant P300 parameters proved to be P3 and N2 latency, an increase of which correlated with the level of developing cognitive deficiency. A neuroprotective effect of Tracilol during the surgery was confirmed. In patients receiving this drug, cognitive deficiency and changes of P300 parameters were less pronounced. A study of cognitive evoked potentials P300 may be recommended for detecting early cognitive dysfunction and estimation of neuroprotective therapy in patients operated on in conditions of cardiopulmonary bypass.

Aprotinin↗

PubMed2002

Measuring cognition in advanced Alzheimer's disease for clinical trials.

Measurement of cognitive dysfunction and treatment response in the early stages of Alzheimer's disease (AD) has used such scales as the Mini-Mental State Examination (MMSE) and the AD Assessment Scale (ADAS). With the exception of clinical rating scales, however, there are only a few objective measures of cognition for tracking progression in advanced AD. Given renewed interest in potential therapies for advanced AD, objective measures of cognition are important for the adequate evaluation of change due to AD progression or therapy. Several cognitive measures for advanced AD are reviewed. One measure, the Severe Impairment Battery (SIB) is reviewed in detail. Preliminary analyses from a trial of memantine show significant change on the SIB in memory (p < 0.001) and visuospatial functions (p < 0.02) over six-months with a trend for language and praxis. Data from a donepezil trial also highlight the importance of accurate assessment in advanced AD.

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PubMed1993

A prospective study of delirium in elderly patients admitted to a psychiatric hospital.

Seventy consecutive elderly patients meeting the DSM-III criteria for non-alcohol delirium were examined during the acute stage and followed to four years later. The mean age of the patients at the beginning of the index admission was 74.8 +/- 6.4 years. The most common aetiologies for delirium were stroke, infections and metabolic disorders. Coexistent structural brain disease predisposing to delirium was found in 57 cases (81%). During the index admission, the cognitive dysfunction associated with delirium ameliorated significantly (mean +/- S.D. Mini Mental State Examination score 9.7 +/- 6.6 at admission and 13.9 +/- 7.2 at discharge, P < 0.001), but during the follow-up period of four years progression of the basic central nervous system disease was observed together with declining cognition and deteriorating functions of daily living. Four patients died during the index admission and 42 patients during the follow-up period. In decreased patients there was a statistically significant connection between the levels of cognitive functioning and functions of daily living at the end of the index admission and the life span after delirium.

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PubMed2004

Anaemia and the brain.

PURPOSE OF REVIEW: This article reviews the physiological and pathophysiological effects of anaemia on the brain, focusing on the hypothesis that anaemia-induced cerebral hypoxia contributes to anaemic cerebral dysfunction and injury. It also reviews evidence that the regulated increase in cerebral blood flow observed during anaemia represents a compensatory neuroprotective mechanism invoked to optimize cerebral oxygen delivery, thereby protecting the brain from hypoxic injury. RECENT FINDINGS: Severe anaemia, or low haematocrit, has been associated with cognitive dysfunction, impaired cerebral vascular regulation, neurological injury, and increased mortality, which suggests that the brain is vulnerable to anaemia-induced injury. Reduced cerebral tissue oxygen tension has been measured directly at haemoglobin concentrations near 35 g/l, suggesting that hypoxia may contribute to anaemic cerebral injury. A demonstration of increased hypoxic cerebral gene expression, including neuronal nitric oxide synthase, may provide a more sensitive means of determining the minimum haemoglobin concentration at which anaemia-induced cerebral hypoxia can be detected. The measurement of increased cerebral cortical neuronal nitric oxide synthase messenger RNA and protein levels in rats, at haemoglobin concentrations between 50 and 60 g/l, suggests that cerebral hypoxia occurred at these higher haemoglobin concentrations. Mechanisms regulating anaemic cerebral vasodilation and increased cerebral oxygen delivery, including nitric oxide, require further elucidation to establish their role in protecting the brain during anaemia. SUMMARY: Characterization of mechanisms of anaemia-induced cerebral injury will contribute to the development of optimal therapeutic strategies for anaemic patients. Such strategies would include a clearer definition of transfusion triggers based on physiological endpoints. The overall goal of these efforts would be to minimize morbidity and mortality associated with anaemia.

Journal Article↗

PubMed1989

Thought disorder or allusive thinking in the relatives of schizophrenics? A response to Callahan, Madsen, Saccuzzo, and Romney.

Romney and Saccuzzo et al. (J Nerv Ment Dis 176:364-367; 368-371, 1988) disagreed concerning the need for further studies investigating the presence of thought disorder and associative cognitive dysfunction in relatives of schizophrenics. Saccuzzo et al. were concerned at the variations in the results of previous studies. Methodological issues relevant to such variation are discussed. It is pointed out that the study (McConaghy J Neurol Neurosurg Psychiatry 22:243-246, 1959) initiating psychometric investigation of cognitive processes of relatives of schizophrenics was based on the belief that what was familially transmitted was not thought disorder, but a nonpathological looseness of associations, shown also by a percentage of normal subjects. This looseness was later termed allusive thinking. It was considered that allusive thinking acted as an inherited predisposition to schizophrenia. It required the addition of impairment of abstract thinking to constitute the characteristic thought disorder originally described by Bleuler. To account for the significant degree of thought disorder found in 6% to 12% of normal subjects, some researchers now accept that thought disorder exists in normal subjects on a continuum with schizophrenic thought disorder. It is suggested that replication of a later study demonstrating familial transmission of allusive thinking in university students and their parents could aid in clarifying the significance of the findings of increased incidence of looseness of associations in the families of schizophrenics.

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PubMed1997

Muscarinic agonists for the treatment of Alzheimer's disease: progress and perspectives.

Much interest has focused on the development of selective muscarinic agonists for the treatment of Alzheimer's disease (AD). Cholinergic replacement therapy is thought to be beneficial in alleviating some of the cognitive dysfunctions in this disorder. The cholinergic neuronal tracts are involved in memory and learning processes, and the extent of the degeneration of the cortical projections correlates with the severity of the dementia. An M1 selective muscarinic agonist may be effective in treating at least some of the cognitive symptoms in AD. Highly selective M1 agonists, producing cellular excitation, should be beneficial in AD, regardless of the extent of degeneration of presynaptic cholinergic projections to the frontal cortex or hippocampus. Functional abnormalities in AD may also occur along various signal transduction pathways mediated, in part, at least, by muscarinic receptors. In general, activities associated with mAChR subtypes and m1 receptors, in particular, indicate that M1 agonists may also be useful for this aspect of AD. Mismetabolism of amyloid precursor proteins (APPs) may induce AD. Recent studies indicate that the formation of the b-amyloid peptide (Abeta) and amyloid plaques is linked to the loss of cholinergic function in AD. New data on the activation of m1 mAChRs in conjunction with recent findings that the induction of such receptors stimulates neurotrophic-like activities, decreases tau phosphorylation and inhibits apoptosis indicate that restoring the cholinergic tone in AD may be useful both in improving memory function and in altering the onset and progression of AD dementia. This article focuses on the recent, promising developments in this field and assesses the value of muscarinic agonists currently under development for the treatment of AD.

Journal Article↗

PubMed1982

Negative v positive schizophrenia. Definition and validation.

We developed criteria for dividing the schizophrenic syndrome into three subtypes: positive, negative, and mixed schizophrenia. Positive schizophrenia is characterized by prominent delusions, hallucinations, positive formal thought disorder, and persistently bizarre behavior; negative schizophrenia, by affective flattening, alogia, avolition, anhedonia, and attentional impairment. In mixed schizophrenia either both negative and positive symptoms are prominent, or neither is prominent. We explored the validity of these criteria in a variety of ways. Significant differences between the three types were noted using external validators such as premorbid adjustment, indices of cognitive dysfunction, ventricular brain ratio, and course in hospital. The correlational structure of the symptom complexes also provided further support for our approach to subtyping.

Adult↗

PubMed2001

Pregnenolone sulfate and aging of cognitive functions: behavioral, neurochemical, and morphological investigations.

Neurosteroids are a subclass of steroids that can be synthesized in the central nervous system independently of peripheral sources. Several neurosteroids influence cognitive functions. Indeed, in senescent animals we have previously demonstrated a significant correlation between the cerebral concentration of pregnenolone sulfate (PREG-S) and cognitive performance. Indeed, rats with memory impairments exhibited low PREG-S concentrations compared to animals with correct memory performance. Furthermore, these memory deficits can be reversed by intracerebral infusions of PREG-S. Neurotransmitter systems modulated by this neurosteroid were unknown until our recent report of an enhancement of acetylcholine (ACh) release in basolateral amygdala, cortex, and hippocampus induced by central administrations of PREG-S. Central ACh neurotransmission is involved in the regulation of memory processes and is affected in normal aging and in human neurodegenerative pathologies like Alzheimer's disease. ACh neurotransmission is also involved in the modulation of sleep-wakefulness cycle and relationships between paradoxical sleep and memory are well documented in the literature. PREG-S infused at the level of ACh cell bodies induces a dramatic increase of paradoxical sleep in young animals. Cognitive dysfunctions, particularly those observed in Alzheimer's disease, have also been related to alterations of cerebral plasticity. Among these mechanisms, neurogenesis has been recently studied. Preliminary data suggest that PREG-S central infusions dramatically increase neurogenesis. Taken together these data suggest that PREG-S can influence cognitive processes, particularly in senescent subjects, through a modulation of ACh neurotransmission associated with paradoxical sleep modifications; furthermore our recent data suggest a role for neurosteroids in the modulation of hippocampal neurogenesis.

Aging↗

PubMed2002

Is mild cognitive impairment bridging the gap between normal aging and Alzheimer's disease?

Mild cognitive impairment (MCI) is one label applied to cognitive dysfunction that is beyond normal aging but of insufficient magnitude to qualify for the diagnosis dementia. Various opinions exist about the proportion of people who fall in this boundary condition, the rate at which they will progress to a full dementia syndrome, and the nature and extent of cognitive impairment at the time of MCI diagnosis. There are at least four important dimensions along which studies of boundary conditions must be compared in order to understand the discrepant findings. The first is the population frame sampled to establish MCI cohorts. The second is the nature of memory complaints. The third and fourth respectively, are the type of memory assessment and number and type of other cognitive domains assessed to identify and follow these groups. The contributions of each of these dimensions to the diagnosis of MCI and it's outcome are discussed.

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PubMed2006

Use of p300 cognitive evoked potentials in the diagnosis of impairments of higher mental functions after cardiac surgery in conditions of cardiopulmonary bypass.

A total of 40 patients with ischemic heart disease undergoing aortocoronary shunting surgery in conditions of cardiopulmonary bypass were studied. Parameters of the P300 cognitive evoked potentials were studied before surgery and 7-9 days after surgery. Neurological and neuropsychological assessments were also performed. The most significant parameters of the P300 potential were found to be the latencies of the P3 and N2 components, increases in which showed positive correlations with the extent of the developing cognitive deficit. Evidence supporting the neuroprotective effects of Trasylol given during surgery was obtained. Patients given Trasylol showed less marked cognitive deficit and smaller changes in P300 parameters. Analysis of the P300 cognitive evoked potential can be recommended for detecting early cognitive dysfunction and assessing the efficacy of neuroprotective therapy in patients undergoing surgery with cardiopulmonary bypass.

Aprotinin↗

PubMed2006

Continuous ASL perfusion fMRI investigation of higher cognition: quantification of tonic CBF changes during sustained attention and working memory tasks.

Arterial spin labeling (ASL) perfusion fMRI is an emerging method in clinical neuroimaging. Its non-invasiveness, absence of low frequency noise, and ability to quantify the absolute level of cerebral blood flow (CBF) make the method ideal for longitudinal designs or low frequency paradigms. Despite the usefulness in the study of cognitive dysfunctions in clinical populations, perfusion activation studies to date have been conducted for simple sensorimotor paradigms or with single-slice acquisition, mainly due to technical challenges. Using our recently developed amplitude-modulated continuous ASL (CASL) perfusion fMRI protocol, we assessed the feasibility of a higher level cognitive activation study in twelve healthy subjects. Taking advantage of the ASL noise properties, we were able to study tonic CBF changes during uninterrupted 6-min continuous performance of working memory and sustained attention tasks. For the visual sustained attention task, regional CBF increases (6-12 ml/100 g/min) were detected in the right middle frontal gyrus, the bilateral occipital gyri, and the anterior cingulate/medial frontal gyri. During the 2-back working memory task, significantly increased activations (7-11 ml/100 g/min) were found in the left inferior frontal/precentral gyri, the left inferior parietal lobule, the anterior cingulate/medial frontal gyri, and the left occipital gyrus. Locations of activated and deactivated areas largely concur with previous PET and BOLD fMRI studies utilizing similar paradigms. These results demonstrate that CASL perfusion fMRI can be successfully utilized for the investigation of the tonic CBF changes associated with high level cognitive operations. Increased applications of the method to the investigation of cognitively impaired populations are expected to follow.

Adult↗

PubMed2004

Chronic cognitive effects of bilateral subdural haematomas in the rat.

Humans suffering from subdural haematomas often show long-term cognitive dysfunctions. For identifying putative, recovery-enhancing therapeutics, animal models need to be developed in which recovery of function can be measured. For investigating whether and which type of recovery, i.e. spontaneous or training-induced recovery, or continuous partial retardation, is present in the rat model for bilateral subdural haematomas, spatial navigation abilities were assessed in the Morris water escape task in independent groups of rats at 1, 2, 4, 8, or 18 weeks after surgery. Complete spontaneous recovery seemed to occur at 8 weeks after injury. However, at 18 weeks after injury, the subdural haematoma caused a renewed deterioration of water maze performance, which was of a lesser degree than the impairments observed immediately after injury. This second phase performance deterioration was accompanied by an increase in generalised astrocyte reactivity. The rat subdural haematoma model provides an interesting tool for investigating spontaneous recovery processes of spatial navigation (8 weeks after injury), but also for progressive brain dysfunctions, considering the second phase of behavioural impairments seen at 18 weeks after injury.

Animals↗

PubMed2000

Selective regional loss of exocytotic presynaptic vesicle proteins in Alzheimer's disease brains.

We tested whether regional or selective alterations in presynaptic proteins occur in Alzheimer's disease (AD) and correlate with tests of cognitive function. We measured the levels of seven presynaptic proteins (synaptobrevin, synaptotagmin, SNAP-25, syntaxin, SV2, Rab3a, and synapsin I) by immunoblotting in postmortem tissue from four brain regions (hippocampus, entorhinal cortex, caudate nucleus, and occipital cortex). Three subject groups were studied: AD, possible/early AD (p-AD), and age-matched controls. Synaptobrevin and synaptotagmin were significantly reduced (29%, P<0.08; 38%, P<0. 07) in hippocampus in p-AD compared to controls. In definite AD compared to controls, selective regional reductions in vesicle proteins were found: synaptobrevin (46%, P<0.05), synaptotagmin (52%, P<0.01), and Rab3a (30%, P<0.05) in hippocampus; synaptobrevin (31%, P<0.01), synaptotagmin (15%, P<0.05), and Rab3a (44%, P<0.05) in entorhinal cortex. In contrast, the levels of two vesicle proteins (synapsin I and SV2) and two presynaptic membrane proteins (syntaxin and SNAP-25) were similar to controls. Synaptobrevin was the only vesicle protein reduced in AD in all four brain regions (occipital cortex 37%, P<0.05; caudate nucleus 31%, P<0.05). By univariate analysis of all cases, Mini-Mental State Examination, Blessed (BIMC) and Free Recall scores were strongly correlated with reduced levels of synaptic vesicle proteins synaptobrevin, synaptotagmin, and Rab3a in hippocampus and entorhinal cortex. These results suggest that there are selective and early defects in presynaptic vesicle proteins, but not synaptic plasma membrane proteins in AD and that defects correlate with cognitive dysfunction in this disease.

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PubMed2004

Use of angiotensin-converting enzyme inhibitors and variations in cognitive performance among patients with heart failure.

AIMS: Cognitive dysfunction is a prevalent condition among patients with heart failure, and is independently associated with disability and mortality. Angiotensin-converting enzyme (ACE)-inhibitors might increase cerebral blood flow in subjects with heart failure. Our aim was to assess whether starting treatment with ACE-inhibitors might improve cognition in patients with heart failure. METHODS AND RESULTS: Analyses involved 12 081 subjects, 1220 of whom had a verified diagnosis of heart failure, enrolled in a multi-centre pharmaco-epidemiology survey. None of these participants received ACE-inhibitors before hospitalization. Among participants with heart failure, cognitive performance improved in 30% of 446 participants who started ACE-inhibitors, but only in 22% of remaining patients (P=0.001). Among participants without heart failure, cognition improved in 19% of those receiving ACE-inhibitors, and in 18% of untreated patients (P=0.765). Use of ACE-inhibitors among patients with heart failure was associated with improving cognition (odds ratio=1.57; 95% CI 1.18-2.08) also in the multivariable regression modelling, independently of baseline or discharge blood pressure levels. The probability of improving cognitive performance was higher for dosages above the median values, as compared with lower doses (odds ratios=1.90 and 1.42; P for trend=0.001), and increased with duration of treatment (odds ratios for the lower, middle, and upper tertiles=1.25, 1.34, and 1.59; P for trend=0.007). CONCLUSION: Treatment with ACE-inhibitors might selectively improve cognitive performance in patients with heart failure. However, up-titration of these agents might be required to yield the greatest benefit.

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PubMed2005

The relationships among cognition, motivation, and emotion in schizophrenia: how much and how little we know.

This article summarizes a workshop discussion focused on the current state of our understanding of the ways in which cognitive dysfunction in schizophrenia is related to, influenced by, or even leads to disturbances in areas such as emotion, motivation, and stress, as well as areas in need of further research. A major emphasis in the workshop discussion was the critical importance of motivation and its potential influence on cognitive function and learning in schizophrenia. As such, the members of the workshop suggested a number of questions regarding motivation that need further research, including (1) the definition and measurement of different components of motivation; (2) the relationship between intrinsic motivation and incentive drive and hedonic processing; (3) the integrity of motivational processes, incentive drive, and hedonic processing in schizophrenia; (4) the influence of cognitive deficits on motivational disturbances in schizophrenia; (5) the influence of antipsychotic medication on incentive drive and hedonic processing in schizophrenia; and (6) the relationships among cognitive function, stress, and the processing of aversive stimuli.

Antipsychotic Agents↗