Cognitive Improvement (cognitive + improvement)

Distribution by Scientific Domains


Selected Abstracts


THE ROLE OF TUMOR NECROSIS FACTOR-ALPHA IN COGNITIVE IMPROVEMENT AFTER PEROXISOME PROLIFERATOR-ACTIVATOR RECEPTOR GAMMA AGONIST PIOGLITAZONE TREATMENT IN ALZHEIMER'S DISEASE

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 5 2010
Haruo Hanyu MD
No abstract is available for this article. [source]


Neurocognition and its influencing factors in the treatment of schizophrenia,effects of aripiprazole, olanzapine, quetiapine and risperidone

HUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 2 2010
M. Riedel
Abstract Background To examine influencing variables of neurocognition in patients with schizophrenia and to predict cognition during antipsychotic treatment. Methods Data were obtained from patients with an acute episode of schizophrenia participating in two double-blind and one open label trial comparing the effects of different atypical antipsychotics on cognition. In total, 129 patients were enrolled in this analysis. Cognitive function was assessed at admission, week 4 and 8. Efficacy and tolerability were assessed weekly using the Positive and Negative Syndrome Scale (PANSS) and the Simpson Angus Sale (SAS). Patients were treated with aripirazole, olanzapine, quetiapine and risperidone. Regression analysis including mixed effect models was performed. Results A significant improvement in all cognitive domains was observed from baseline to week 8. Regarding the antipsychotic treatment applied quetiapine seemed to achieve the most favourable cognitive improvement. Negative and depressive symptoms, the patient's age and the concomitant and antipsychotic treatment applied were observed to significantly influence and predict neurocognition. Conclusion The results may indicate that schizophrenia is a static disorder with trait and state dependent cognitive components especially in the memory domains. The influence of negative and depressive symptoms should be considered in daily clinical routine. Copyright © 2010 John Wiley & Sons, Ltd. [source]


What is mild cognitive impairment?

ACTA NEUROLOGICA SCANDINAVICA, Issue 2003
Variations in definitions, evolution of nondemented persons with cognitive impairment
Numerous studies have endeavoured to explore the nature of cognitive impairment in nondemented elderly persons. Comparison of this literature is hampered by huge variations in criteria and methodology. Despite these limitations, there are repeated reports that nondemented persons with cognitive impairment have a higher chance of progressing to dementia. Evidence also indicates higher mortality in cognitively impaired persons but there is also a chance of improvement in cognition over time. The current paper provides an overview of the various concepts and criteria proposed for cognitive impairment in nondemented persons, discusses some of the problems with current research in this field, and presents some of the findings concerning the evolution of cognitive impairment in relation to dementia, mortality and cognitive improvement. [source]


Schizophrenia: genetics, prevention and rehabilitation

ACTA NEUROPSYCHIATRICA, Issue 3 2009
Paolo Olgiati
Objective:, Genetic factors are largely implicated in predisposing to schizophrenia. Environmental factors contribute to the onset of the disorder in individuals at increased genetic risk. Cognitive deficits have emerged as endophenotypes and potential therapeutic targets for schizophrenia because of their association with functional outcome. The aims of this review were to analyse the joint effect of genetic and environmental (G×E) factors on liability to schizophrenia and to investigate relationships between genes and cognitive endophenotypes focusing on practical applications for prevention and rehabilitation. Methods:, Medline search of relevant studies published between 1990 and 2008. Results:, In schizophrenia, examples of G×E interaction include the catechol- O -methyl transferase (COMT) (Val158Met) polymorphism, which was found to moderate the onset of psychotic manifestations in response to stress and to increase the risk for psychosis related to cannabis use, and neurodevelopmental genes such as AKT1 (serine-threonine kinase), brain-derived neurotrophic factor (BDNF), DTNBP1 (dysbindin) and GRM3 (metabotropic glutamate receptor 3), which were associated with development of schizophrenia in adulthood after exposure to perinatal obstetric complications. Neurocognitive deficits are recognised as core features of schizophrenia that facilitate the onset of the disorder and have a great impact on functional outcome. Neurocognitive deficits are also endophenotypes that have been linked to a variety of genes [COMT, neuregulin (NRG1), BDNF, Disrupted-In-Schizophrenia 1 (DISC1) and dysbindin] conferring susceptibility to schizophrenia. Recently, it has emerged that cognitive improvement during rehabilitation therapy was under control of COMT (Val158Met) polymorphism. Conclusion:, This review could indicate a pivotal role of psychiatric genetics in prevention and rehabilitation of schizophrenic psychoses. [source]


Do statins slow down Alzheimer's disease?

JOURNAL OF CLINICAL PHARMACY & THERAPEUTICS, Issue 3 2004
A review
Summary More than 4 million people suffer from Alzheimer's disease (AD) in the United States. The prevalence increases with age as the rate is 3% in those between 65 and 74 years compared with 47% among those over 85 years of age. Some epidemiological studies have reported a decrease in the incidence of AD with the use of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins). Other studies have shown statins to decrease A, peptides, but data regarding cognitive benefits is lacking in this patient population. There are also concerns that statins, which cross the blood,brain barrier may cause more side-effects, but more information is needed. Adverse events were either infrequently noted or not reported in most of the published studies, and at this time there is insufficient evidence to suggest the use of statins for cognitive improvements in patients with AD. [source]