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PubMed2005

Animal models of cognitive dysfunction.

The increased life expectancy in industrialised countries in the last half century has also brought to a greater incidence of neurological disorders, including neurodegenerative diseases and developing in a rather long time. In this respect, Alzheimer's disease (AD), for the large incidence, and the dramatic loss of autonomy caused by its cognitive and behavioural symptoms represents one of the main challenges of modern medicine. Although AD is a typical human disease and probably includes several nosographic entities, the use of animal models may contribute to understand specific aspects of pathophysiology of the disease. The most widely used animal models are rodents and non-human primates. In this review different animal models characterised by impaired cognitive functions are analysed. None of the models available mimics exactly cognitive, behavioural, biochemical and histopathological abnormalities observed in neurological disorders characterised by cognitive impairment. However, partial reproduction of neuropathology and/or cognitive deficits of Alzheimer's disease (AD), vascular dementia and dementia occurring in Huntington's and Parkinson's diseases, or in other neurodegenerative disorders may represent a basis for understanding pathophysiological traits of these diseases and for contributing to their treatments.

Animals↗
PubMed2006

Delirium and cognitive dysfunction in the intensive care unit.

Delirium remains a non recognized, but highly prevalent, form of organ dysfunction in the intensive care unit (ICU). Intensive care physicians have begun to benefit from elucidation of risk factors for delirium in the ICU, some of which are modifiable, whereas others are not. In the last 5 years, a new tool for use in detecting delirium among critically ill patients has been adapted, validated, and found objectively reliable for use at the bedside by nonpsychiatrists. Moreover, that tool-the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU)-has enabled determination of the serious sequelae of delirium, including increased mortality, higher cost, longer length of hospital stay, failure of extubation, and burdensome long-term cognitive impairment. Although prevention and treatment options exist, little data guide current pharmacological approaches to delirium, and nonpharmacological approaches have yet to be fully adopted by ICUs. Ongoing trials will address some of these limitations, but large cohort studies within the ICU are needed to further clarify risk factors and to identify targets to modify the occurrence and course of delirium. Furthermore, consideration of a continuum may better elucidate the true magnitude of acute brain dysfunction in the ICU.

Aged↗
PubMed2000

The correlation between ventricular diameter measured by transcranial sonography and clinical disability and cognitive dysfunction in patients with multiple sclerosis.

CONTEXT: Magnetic resonance imaging (MRI) data suggest that the extent of brain atrophy in patients with multiple sclerosis (MS) is related to the severity of disease. OBJECTIVE: To evaluate whether ventricular diameter determined by transcranial sonography (TCS) is a marker of brain atrophy and is correlated with disability, cognitive performance, and mood. SUBJECTS AND METHODS: We examined 74 subjects with MS and 74 age- and sex-matched control subjects with TCS and assessed the transverse diameter of the third ventricle and the frontal horns of the lateral ventricles. Quantitative neurological examination was performed in subjects with MS using the Expanded Disability Status Scale. All subjects with MS underwent MRI, the Brief Repeatable Battery of Neuropsychological Tests for MS, and standardized tests for mood disorders. RESULTS: Transcranial sonographic measurements of ventricular diameter closely matched MRI measurements (Spearman rank correlation, r=0.7-0.9; P<.01). The ventricular diameters were significantly larger in subjects with MS than in healthy age- and sex-matched control subjects. The measurement of the diameter of the third ventricle obtained by TCS or MRI and the measurement of disability obtained with the Expanded Disability Status Scale were significantly correlated (Spearman rank correlation, r = 0.4; P<.01). The correlation between the diameter of the frontal horns and disability was substantially lower for both neuroimaging techniques. In addition, TCS and MRI data correlated significantly with the majority of neuropsychological tests; no correlation was found between the diameter of the ventricles and depression scales. CONCLUSION: As ventricular diameter is related to the status of disability and may also indicate disease progression, we propose measurement of the diameter of the third ventricle with TCS as a quick and easy surrogate marker for serial follow-up examinations in patients with MS.

Adult↗
PubMed2000

Impact of human immunodeficiency virus type-1-associated cognitive dysfunction on activities of daily living and quality of life.

We examined the impact of neuropsychological (NP) impairment on activities of daily living (ADLs) and quality of life in human immunodeficiency virus type-1 (HIV-1)-infected persons of low socioeconomic status (SES). Thirty-nine patients were stratified into one of three groups: cognitively normal (n = 13), mild cognitive impairment (n = 15), and moderate/severe impairment (n = 11). Quality of life was assessed with the Sickness Impact Profile and ADLs were evaluated via structured interview performed in the patient's residence. While there were no significant differences across groups on disease stage, drug use, depression, or estimated premorbid IQ, cognitively impaired patients were more likely to be unemployed and fail social planning and medication management tasks. Our study confirms a previously reported association between NP impairment and unemployment among HIV-1-infected patients. The data also extend this relationship to a low-SES sample with a high base rate of unemployment, and to instrumental activities of daily living other than work.

Journal Article↗
PubMed2005

Pharmacokinetics and metabolism studies on (3-tert-butyl-7-(5-methylisoxazol-3-yl)-2-(1-methyl-1H-1,2,4-triazol-5-ylmethoxy) pyrazolo[1,5-d][1,2,4]triazine, a functionally selective GABA(A) alpha5 inverse agonist for cognitive dysfunction.

(3-tert-Butyl-7-(5-methylisoxazol-3-yl)-2-(1-methyl-1H-1,2,4-triazol-5-ylmethoxy)pyrazolo[1,5-d][1,2,4]triazine (1) was recently identified as a functionally selective, inverse agonist at the benzodiazepine site of GABA(A) alpha5 receptors and enhances performance in animal models of cognition. The routes of metabolism of this compound in vivo in rat have been well characterised, the identities of the major metabolites are confirmed by synthesis and their biological profiles were evaluated. An unusual oxidation of the pyrazolo[1,5-d][1,2,4]triazine core to the corresponding pyrazolo[1,5-d][1,2,4]triazin-4(5H)-one scaffold by aldehyde oxidase has been observed.

Animals↗
PubMed2006

The allosteric potentiation of nicotinic acetylcholine receptors by galantamine ameliorates the cognitive dysfunction in beta amyloid25-35 i.c.v.-injected mice: involvement of dopaminergic systems.

Galantamine, a drug for Alzheimer's disease, is a novel cholinergic agent with a dual mode of action, which inhibits acetylcholinesterase and allosterically modulates nicotinic acetylcholine receptors (nAChRs), as a result stimulates catecholamine neurotransmission. In the present study, we investigated whether galantamine exerts cognitive improving effects through the allosteric modulation of nAChR in the intracerebroventricular beta amyloid (Abeta)(25-35)-injected animal model of Alzheimer's disease. Galantamine (3 mg/kg p.o.) significantly increased the extracellular dopamine release in the hippocampus of saline- and Abeta(25-35)-injected mice. The effects of nicotine on the extracellular dopamine release were potentiated by galantamine, but antagonized by mecamylamine, a nAChR antagonist. Abeta(25-35)-injected mice, compared with saline-injected mice, could not discriminate between new and familiar objects in the novel object recognition test and exhibited less freezing response in the fear-conditioning tasks, suggesting Abeta(25-35) induced cognitive impairment. Galantamine improved the Abeta(25-35)-induced cognitive impairment in the novel object recognition and fear-conditioning tasks. These improving effects of galantamine were blocked by the treatment with mecamylamine, SCH-23390, a dopamine-D1 receptor antagonist, and sulpiride, a dopamine-D2 receptor antagonist, but not by scopolamine, a muscarinic acetylcholine receptor antagonist. This study provides the first in vivo evidence that galantamine augments dopaminergic neurotransmission within the hippocampus through the allosteric potentiation of nAChRs. The improving-effects of galantamine on the Abeta(25-35)-induced cognitive impairment may be mediated through the activation of, at least in part, dopaminergic systems, and the enhancement of dopamine release may be one of multiple mechanisms underlying the therapeutic benefit of galantamine.

Amyloid beta-Peptides↗
PubMed2004

Postnatal development of prefrontal inhibitory circuits and the pathophysiology of cognitive dysfunction in schizophrenia.

The typical appearance of the clinical features of schizophrenia during late adolescence or early adulthood suggests that adolescence-related neurodevelopmental events may contribute to the pathophysiology of this disorder. Here the role that GABA-mediated inhibition in the dorsal lateral prefrontal cortex (DLPFC) plays in regulating working memory, a core cognitive process that matures late and that is disturbed in schizophrenia, is reviewed. Recent studies are summarized that demonstrate (1) that certain pre- and postsynaptic markers of GABA neurotransmission in the monkey DLPFC exhibit striking changes during adolescence, and (2) that these same markers are markedly altered in the DLPFC of subjects with schizophrenia. The implications of these findings for treatment and prevention strategies are discussed.

Adolescent↗
PubMed1989

Cognitive dysfunction following cardiac arrest.

Recent work that has been done in cardiopulmonary cerebral resuscitation has focused on the area of brain resuscitation and the prevention of neurologic deficits. The Glascow Coma Scale and Glascow-Pittsburgh Scale are useful clinical tools in the acute stages of survival; however, they fail to provide sufficient data relative to cognitive disturbances. The Levels of Cognitive Functioning Scale applied to the postcardiac arrest patient may be helpful in guiding therapeutic nursing interventions and nursing research in the Critical Care environment.

Brain↗
PubMed1988

Cognitive dysfunction and change in multiple sclerosis.

A cross-sectional study of 60 multiple sclerosis outpatients assessed neuropsychological variables in relation to age, duration of disease, and degree of disability. The test battery included subtests of the WAIS (Vocabulary, Similarities, and Digit Span);the Raven matrices; and memory tests (Wechsler Paired Associates, Benton Visual Retention). Results showed that cognitive functioning of MS patients varies considerably. There is a general mild decline that affects abstract reasoning and memory as the disease progresses. These deficits are usually not sufficient to impair occupational or social functioning. In addition, there is spotty deterioration in certain cognitive functions for some patients (17%). Only a small subsample (6.7%), however, showed global deterioration significant enough to be highlighted by an Index of Dementia that was developed for this investigation.

Adult↗
PubMed2003

Baseline and 8-OH-DPAT-induced release of acetylcholine in the hippocampus of aged rats with different levels of cognitive dysfunction.

During aging, neurotransmission systems such as the cholinergic and serotonergic ones are altered. Using rats aged 3 or 24-26 months, this study investigated whether the well-described 8-OH-DPAT-induced increase of hippocampal acetylcholine release was altered in aged rats and whether it may vary according to the magnitude of age-related cognitive deficits. Long-Evans female rats aged 24-26 months were classified as good or bad performers on the basis of their reference-memory performance in a Morris water-maze task. Subsequently, the efficiency of 5-HT(1A) receptor agonist 8-OH-DPAT (0.5 mg/kg, s.c.) in triggering hippocampal acetylcholine release was evaluated by in vivo microdialysis and high performance liquid chromatography analysis. Besides a reduced baseline release in aged rats and a correlation between the baseline release and probe-trial performance in all rats, the results demonstrated that 8-OH-DPAT produced a significant increase of hippocampal acetylcholine release (peak value) in all rats, whether aged or young. While significant in bad performers (+56%), this increase did not reach significance in good performers (+32%). The results suggest that (i) some aspects of cognitive alterations related to aging might be linked to the baseline release of acetylcholine in the hippocampus, and (ii) the cholinergic innervation of the hippocampus of aged rats responds almost normally to systemic activation of 5-HT(1A) receptors, and (iii) differential alterations of cholinergic/serotonergic interactions assessed by determination of the 8-OH-DPAT-induced release of acetylcholine in the hippocampus could not be linked with clarity to the cognitive status of aged rats.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2003

Chronic intermittent nicotine administration attenuates traumatic brain injury-induced cognitive dysfunction.

Traumatic brain injury (TBI) initiates immediate and secondary neuropathological cascades that can result in persistent neurological dysfunction. Previous studies from our laboratory have shown that experimental rat brain injury causes a rapid and persistent decrease in CNS alpha7* nicotinic cholinergic receptor (nAChr) expression. The purpose of this study was to investigate whether intermittent nicotine injections could improve cognitive performance in the Morris water maze (MWM) following experimental brain injury. Adult male rats were anesthetized and subjected to a 1.5 mm controlled cortical impact (CCI) injury of the somatosensory cortex. Animals received twice daily i.p. nicotine injections for 11 days prior to CCI, 11 days following CCI or during both pre- and post-surgical intervals. MWM training was initiated 12 days post-injury. In the training phase of cognitive testing, twice-daily nicotine treatment following injury attenuated trauma-induced deficits in the distance traveled to reach the escape platform. This group of animals also had improvements in several measures of the probe test, including time spent, distance traveled and total entries into the target quadrant. TBI caused significant deficits in alpha7* nAChr expression in several regions of the hippocampus and cerebral cortex, which were largely unaffected by intermittent nicotine treatment. However, nicotine treatment up-regulated [(3)H]-epibatidine binding to non-alpha7* nAChrs, attenuating TBI-induced deficits in receptor expression in several brain regions evaluated. These results suggest that nicotine is efficacious at attenuating CCI-induced cognitive deficits in a manner independent of changes in alpha7* nAChr expression, perhaps via up-regulation of non-alpha7* nAChrs.

Animals↗
PubMed2004

The relationship between type 2 diabetes and cognitive dysfunction: longitudinal studies and their methodological limitations.

Type 2 diabetes and dementia in the elderly are major public health problems. Cross-sectional studies have suggested that these two conditions may be inter-related, but the nature of this association is uncertain. Causation can only be established through studies with a longitudinal design, taking into account the many potential confounding factors in any study of cognition. A literature search has identified 10 studies (nine population-based and one of case-controlled design) that included a definable diabetic population and assessments of cognitive function at baseline and at follow-up. These 10 studies utilised a combination of domain-specific cognitive assessments and a clinical diagnosis of dementia in the assessment of cognitive function. Diabetes was associated with either an accelerated cognitive decline or an increased incidence of dementia in eight of nine of the population-based studies. One study demonstrated a relationship between diabetes and vascular cognitive impairment, but not with other types of dementia. No association between type 2 diabetes and cognitive decline was demonstrated in the case-controlled study. These studies provide compelling evidence to support the view that people with type 2 diabetes are at increased risk of developing cognitive impairment in comparison with the general population.

Cognition Disorders↗
PubMed2000

Cognitive dysfunction following thalamic stroke: a study of 16 cases and review of the literature.

The thalamus is a relay center for afferent sensory pathways that regulates and transmits peripheral stimulation to various representative areas of the cortex. Aphasia, neglect and anosognosia were also reported to occur after thalamic lesions, in the absence of cortical pathology. However, considerable controversy exists as to the pathogenetic mechanisms, and incidence of cognitive abnormalities following thalamic lesions. We present a series of sixteen consecutive stroke patients with thalamic stroke (n=12) or hemorrhage (n=4), admitted to a university based neurology department. Dysphasia was observed in seven of eight patients with left thalamic strokes (five in the territory of the tuberothalamic artery, two inferior-lateral thalamic lesions and one in the area supplied by the anterior choroidal artery). Neglect and anosognosia appeared in five of eight patients with right side thalamic insults (two each in the territories of the tuberothalamic and thalamogeniculate arteries and one in the area supplied by the posterior choroidal artery). These findings reconfirm those found in previous studies and suggest that the thalamus is part of an integral neuronal network concerned with cognitive functions.

Adult↗
PubMed1999

Cognitive dysfunction in schizophrenia and its importance to outcome: the place of atypical antipsychotics in treatment.

The neurocognitive impairment associated with schizophrenia has been well established. Such impairment may be present prior to the onset of the positive symptoms of schizophrenia and persist during periods of remission. Neurocognitive deficits predict multiple domains of outcome; treating such deficits is therefore regarded as highly important. Conventional antipsychotic agents do not appear to favorably affect cognitive function in schizophrenia. Indeed, their propensity to induce adverse effects such as extrapyramidal symptoms may further impair cognitive function. A growing body of evidence suggests that patients taking atypical antipsychotics perform better on some tests of neurocognitive ability than patients receiving conventional agents, with implications for adaptive functioning. The neurocognitive benefits of the atypical antipsychotic agents discussed in this article support their use as a first-line therapy for schizophrenia.

Adult↗
PubMed1990

Cognitive dysfunction in spinal cord injury patients: sensitivity of the Functional Independence Measure subscales vs neuropsychologic assessment.

The Functional Independence Measure (FIM) has been developed to provide an objective measure of functional gains during acute and chronic rehabilitation of disabled individuals, including those with spinal cord injury (SCI). A unique characteristic of the FIM, as compared with other functional scales, is that it reflects abilities in the areas of communication and social cognition. In order to examine the external validity of these subscales, 41 acute SCI patients were evaluated with the FIM just before discharge from acute rehabilitation. The subscale scores were compared to the results of a comprehensive, predominantly motor-free, neuropsychologic battery administered 74.8 +/- 5.3 days postinjury. Evaluation of scatter plots indicated that there were no relationships between any neuropsychologic test results and the discharge FIM social cognition or communication subscale scores. This was attributed to a ceiling effect in the FIM ratings. The results of this study suggest that the FIM cannot be a substitute for comprehensive neuropsychologic assessment in SCI patients.

Adult↗
PubMed1996

Negative symptoms, cognitive dysfunction, tardive akathisia and tardive dyskinesia.

This study examined the relationship of neuropsychological deficits and negative symptoms with tardive akathisia in chronic schizophrenic patients. Consecutive volunteers (n = 100) were recruited from Community Health Centres with a DSM-III-R diagnosis of schizophrenic disorder, chronic and on stable medication. Subjects were subgrouped into tardive akathisia (TA), tardive dyskinesia (TD) and control groups using four sets of criteria. Detailed single examinations were performed using the following measures: sociodemographic, illness-related and treatment-related variables, Negative Symptom Rating Scale (NSRS), Abnormal Involuntary Movement Scale (AIMS), Rating Scale for Extrapyramidal Side-Effects (EPSE), Akathisia Rating Scale, Barnes Akathisia Rating Scale, and a brief neuropsychological test battery. Group comparisons and logistic regression analyses were performed in order to test the significance of findings. TA ratings showed a significant association with NSRS subscale scores, and with some neuropsychological test scores (Symbol Digits Modalities Test, and to a lesser extent Trail Making Test and Finger Tapping Test). TD scores showed a consistent association with age, and a less consistent association with gender, and their association with NSRS subscale scores and neuropsychological dysfunction was positive but less significant. Higher EPSE scores predicted TA and limb truncal (LT) dyskinesia. In conclusion, TA showed a more significant association with some clinical indices of organic brain dysfunction than the oral-lingual-buccal-facial dyskinetic syndrome. Prospective studies are necessary to determine whether organicity is a vulnerability factor for TA. Both our data and the published literature suggest that the movement disorder seen in TA and TD is but one feature of complex syndromes that include motor and cognitive features.

Adult↗