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At least 19 recordsLinked to original sources
PubMed1979

Detection of cognitive deficits by a brief mental status examination: the Cognitive Capacity Screening Examination, a reappraisal and a review.

Results of a brief mental status questionnaire, the Cognitive Capacity Screening Examination (CCSE), were compared with the clinical evaluations of 59 patients on a neurology service. In 71% of the cases, the CCSE scores correctly indicated a cognitive deficit (true-positive) or the absence of one (true-negative); false-negative results were observed in 15% and questionable negative results were found in 10%. Abnormal neurologic physical signs were present in 90% of all patients with cognitive deficits. In this population, although positive CCSE scores were reliable, negative scores were often misleading. Mild diffuse intellectual dysfunction (dementia) and some discrete intellectual deficits (aphasia and anosognosia) went undetected. Cognitive deficits associated with major cerebral disease were unappreciated in nine patients. Caution is recommended in interpreting negative CCSE scores. Abbreviated screening devices are only a preliminary approach to mental status evaluation; this test requires further refinement.

Aged↗
PubMed1979

Emotional disturbance and cognitive deficits in hyperthyroidism.

Assessment of cognitive and emotional variables in 19 females with hyperthyroidism was made pretreatment, at 3 weeks, and after euthyroidism was established. A matched group of normal controls was similarly tested. Group differences on cognitive measures did not reach statistical significance, but cognitive deficits and symptoms of emotional disorder were significantly associated with the severity of thyroid toxicity previous to treatment. Measures of cognitive function and personality features moved towards control group values as euthyroidism was established. The implication of these findings is discussed in the context of a review of previous literature. The observed cognitive disturbance and emotional distress appear to be reflections of thyroid toxicity.

Age Factors↗
PubMed2026

Investigating the relationship between Toll-like receptor activity, low-grade inflammation, cognitive deficits, and antipsychotic drug dose in schizophrenia patients: a moderation analysis.

BACKGROUND: Schizophrenia (SZ) is a debilitating psychiatric disorder where patients experience cognitive decline. Antipsychotic drugs alleviate positive symptoms but do not improve cognitive performance. We previously demonstrated that Toll-like receptors (TLRs), involved in cytokine production, can predict cognitive deficits in SZ patients. In this study, we aim to investigate the potential moderating effects of antipsychotic drugs on the associations between cytokines, TLRs, and cognition. METHODS: In total, 280 participants (201 controls and 79 cases of SZ) were recruited in Ireland. Venous blood from the participants was stimulated with TLR ligands. Levels of cytokines were measured from plasma and post-blood stimulation. The participants were administered a battery of cognitive tasks using the Cambridge Neuropsychological Test Automated Battery and Wechsler Adult Intelligence Scale-IIIR. Olanzapine equivalents were calculated using the defined daily dose method. RESULTS: The results indicate that antipsychotic drug dose does not predict TLR activity or cognition, indicating that antipsychotic drug dose does not have a direct effect on cognition or TLR activity. However, the relationship between TLR4 activity and visual learning and memory is moderated by the antipsychotic drug dose (B&#xa0;=&#xa0;-0.065; p&#xa0;<&#xa0;0.001), where increasing doses have a decreasing impact on their relationship. CONCLUSIONS: Our data indicate that the dose of antipsychotic drugs alone cannot predict changes in cognitive performance and TLR4-activity. It also suggests that antipsychotic drug doses significantly affect TLR activity and its relationship with cognition. These effects are more pronounced on some domains than others. These findings open up new avenues for understanding the complex interplay between antipsychotic drugs, TLRs, and cognitive deficits in SZ.

Humans↗
PubMed1977

What have cognitive deficits to do with schizophrenic symptoms?

This paper considers possible relationships between cognitive deficits and symptomatology in schizophrenia. It is argued that a combination of defective filtering and slowness in response selection results in a state of information overload in acute schizophrenia. The methods by which normal subjects adapt to experimenter-induced overload may therefore be relevant to aspects of schizophrenic behaviour. The considerable intra- and inter-subject variability in symptomatology of schizophrenic patients may represent differeing adaptations to similar cognitive disturbance, such secondary abnormalities being prominent in chronic patients. Sections of the literature on acute-chronic differences are consistent with such a formulation, although one cannot infer intra-individual change from cross-sectional studies; there is a clear need for longitudinal investigations in this area. The preferred method of adaptation will be dependent on the severity of overload, the environment, and personality factors independent of the psychosis. The implications for the modification of schizophrenics' behavioural abnormalities by operant procedures are discussed.

Acute Disease↗
PubMed2026

Atomoxetine Versus Placebo for Cognitive Deficits in Stimulant Use Disorder: A Systematic Review.

BACKGROUND: Stimulant use disorder (StUD), particularly involving cocaine and amphetamines, is associated with significant cognitive impairments that impede recovery and increase relapse risk. Atomoxetine, a selective norepinephrine reuptake inhibitor, has been proposed as a potential treatment given its role in enhancing executive function and its established efficacy in attention-deficit/hyperactivity disorder (ADHD). This systematic review aimed to evaluate the efficacy, cognitive, and mood effects of atomoxetine compared with placebo in individuals with StUD. METHODS: A comprehensive literature search of PubMed, Cochrane CENTRAL, and Embase databases was conducted to identify randomized controlled trials (RCTs) evaluating atomoxetine for StUD. Eligible studies compared atomoxetine with placebo and assessed outcomes related to cognition (attention and response inhibition), stimulant use or abstinence, mood symptoms, and safety. Data were extracted and synthesized qualitatively due to methodological heterogeneity across studies. RESULTS: Nine RCTs met the inclusion criteria. Findings on cognitive outcomes were inconsistent: Some studies reported improvements in attentional bias and inhibitory control, while others showed no significant effects. Atomoxetine did not significantly reduce stimulant use, craving, or sustain abstinence compared with placebo. Limited mood-related benefits were observed, particularly among male participants, although results were variable. Across studies, atomoxetine was well tolerated, with most adverse events mild and transient. CONCLUSION: Despite a compelling neurobiological rationale and evidence of modest cognitive and mood benefits, atomoxetine has not demonstrated consistent efficacy as a monotherapy for StUD. Its favorable safety profile may warrant further investigation in carefully defined populations, such as individuals with comorbid ADHD or in combination with behavioral interventions.

Atomoxetine Hydrochloride↗
PubMed2026

Subchronic benzo[a]pyrene exposure disrupts APOE4-regulated lipid metabolism to induce Tau hyperphosphorylation and cognitive deficits.

BACKGROUND: Benzo[a]pyrene (B[a]P) is both a carcinogen and a potent neurotoxic pollutant. Despite growing evidence linking B[a]P to neurological dysfunction, the responsible mechanisms have not been elucidated. METHODS: Here, we employed human apolipoprotein E4 (hAPOE4) transgenic mice and APOE knockout (APOE-KO) mice to evaluate the influence of APOE on B[a]P-mediated neurotoxicity. hAPOE4 mice overexpress the human APOE4 isoform, whereas APOE-KO mice lack APOE expression; wild-type C57BL/6&#x202f;J mice served as controls. Animals received intraperitoneal injections of B[a]P at 0, 2.5, or 6.25&#x202f;mg/kg on alternate days for 3 months. Spatial memory and learning were examined via Morris Water Maze (MWM). Neuronal morphology, including dendritic branching and spine density in the CA1 region of the hippocampus and dentate gyrus (DG), was assessed using Golgi-Cox staining. Neurofibrillary tangles were detected by silver glycine staining. Tau, phosphorylated Tau (Ser199 and Ser396), and LRP1 were evaluated using Western blot and immunohistochemical analyses. Chromatin immunoprecipitation PCR (ChIP-PCR) was undertaken to examine the regulation of APOE4 expression by the aryl hydrocarbon receptor (AHR). In addition, both untargeted metabolomics and lipidomics analyses were conducted following B[a]P exposure. RESULTS: B[a]P led to pronounced impairments in mouse spatial memory and learning, shown by greater escape latency, less time in the target quadrant, and a decreased number of platform crossings in MWM tests. Structural analyses revealed a significant reduction in dendritic branching within the hippocampal CA1 and DG regions. These neurobehavioral and morphological deficits were most severe in hAPOE4 mice, which displayed greater cognitive impairment and more extensive dendritic loss than B[a]P-treated wild-type mice, indicating that APOE4 amplifies B[a]P-induced neurotoxicity. ChIP assays demonstrated that B[a]P modulates APOE4 transcription through AHR-dependent mechanisms. Additionally, metabolomics and lipidomics analyses revealed widespread B[a]P-induced metabolic remodeling, suggesting that disrupted lipid metabolism and altered neuronal membrane integrity may contribute to the observed neurotoxicity and cognitive dysfunction. CONCLUSION: Collectively, the results indicate that B[a]P-mediated neurotoxicity may be facilitated, at least in part, by APOE4-dependent dysregulation of lipid metabolic pathways.

Animals↗
PubMed1979

Cerebral hemispheric lateralization of cognitive deficits due to alcoholism.

Twenty chronic alcoholics and a group of matched control subjects were tested on verbal and visuospatial memory tasks in order to test directly the hypothesis that alcoholism disturbs cognitive functions subserved by the right hemisphere more than those subserved by the left hemisphere. The results provide some support for the hypothesis and indicate that information may be lost by pooling together test results from alcoholics which come from a mixture of verbal and nonverbal tasks.

Adult↗
PubMed1979

Cognitive deficit caused by regional depletion of dopamine in prefrontal cortex of rhesus monkey.

Depletion of dopamine in a circumscribed area of association cortex in rhesus monkeys produces an impairment in spatial delayed alternation performance nearly as severe as that caused by surgical ablation of the same area. This behavioral deficit can be pharmacologically reversed with dopamine agonists such as L-dopa and apomorphine. These data provide direct evidence that dopamine plays an important role in a specific cortical function.

Animals↗
PubMed1977

Two kinds of cognitive deficit associated with chronic schizophrenia.

The performance of 21 chronic schizophrenic patients was investigated on two tests of feature selection. It was found that patients with negative symptoms (muteness, withdrawal, etc.) were characterized by an extreme lack of persistence, but selected usual features; whereas patients with positive symptoms (hallucinations, delusions, etc.) had a normal degree of persistence, but selected unusual features.

Aged↗
PubMed1978

Age disorientation in chronic schizophrenia: the nature of the cognitive deficit.

In an interview survey of temporal orientation in chronic schizophrenia, patients with age disorientation (n = 77) were much less likely than patients without age disorientation (n = 222) to be able to give correct answers to simple questions about dates and the passage of time (e.g. their date of birth, the present year and the duration of their hospital stay). The age disorientated systematically under-estimate the present year and their duration of hospital stay; in individual patients the errors they make are consistent with their concept of their own age. "Time stands still" for these patients. However, there are patients in whom an incorrect appreciation of their own age co-exists with correct awareness of the present year. Between these patients and those for whom subjective time stands still, there appears to be a continuum of increasing temporal disorientation. This dimension may be a clinical correlate of intellectual impairment.

Age Factors↗
PubMed1979

Dopaminergic mechanisms and cognitive deficit in schizophrenia. A neurobiological model.

A hypothesis is briefly discussed proposing that schizophrenic symptoms are due to a breakdown in a mechanism by which conscious attention is limited and directed. It is shown that this mechanism can be modelled in terms of a simple nerve network in which every channel inhibits all the others. Failure of this inhibition would cause the defect hypothesised to occur in schizophrenia. It is shown that if dopamine is given a central role as transmitter in such a network then the various predictions about the biochemistry of schizophrenia that follow are not only consistent with the evidence for the 'dopamine theory' of schizophrenia, but also with much of the evidence held to be contrary to that theory. While not purporting to be an experimentally validated description of schizophrenia, this model goes beyond the single amine theories of schizophrenia and links dysfunctions in amine systems with specific behavioural control mechanisms. Given the current state of knowledge, such models can make only limited predictions about the biochemistry of schizophrenia. However, an attempt to link behavioural and biochemical systems in this way will be crucial for the development of viable animal models of schizophrenia.

Animals↗
PubMed1979

Transformational deficits in cognition of schizophrenic children.

This study examined schizophrenic children for cognitive deficits in logical thinking, symbolic imagery, and conservation. Evaluation revealed persistent failure of the aberrant subjects to achieve at the level of age expectancy. Comparison with nonpsychotic, institutionalized children demonstrated no effect due to institutionalization. By mid-teens not one of the subjects had accomplished formal operations and very few were able to master concrete operations. Implications for development and treatment were discussed.

Adolescent↗
PubMed2026

Duplication-based genetic dissection of the Down syndrome critical region reveals its complex functional organization.

Down syndrome (DS), associated with trisomy 21, is the most common genetic cause of developmental delay and intellectual disability, yet the specific dosage-sensitive genes and the associated genetic mechanisms underlying these phenotypes remain incompletely defined. Here, we applied an additive genetic strategy to dissect the Down syndrome critical region (DSCR) by generating 2 complementary mouse models using Cre/loxP-mediated chromosome engineering that together span the entire DSCR on mouse chromosome 16: Dp(16)5Yey, duplicating the Setd4-Kcnj6 interval, and Dp(16)6Yey, duplicating the Kcnj15-Mx2 interval. In addition, we engineered a third duplication model, Dp(16)7Yey, carrying a selective duplication of the Dyrk1a-Kcnj6 interval containing only these 2 genes. Building upon our previously reported results, cognitive behavioral analyses of these 3 models reveal a complex functional genetic architecture of the DSCR, including dosage-sensitive genetic elements, interactions among these elements, and their contributions to DS-associated cognitive deficits. Together, these findings highlight the complexity of dosage-dependent genetic interactions, which provide important insights into DSCR functional organization and have major implications for the development of effective therapeutic strategies for DS-associated cognitive deficits. In addition, these duplication mouse models represent valuable resources for further genetic dissection of DS phenotypes beyond cognition.

Animals↗