scholarly journals Cognitive Enhancement Therapy in Schizophrenia

2020 ◽  
Vol 9 (1) ◽  
pp. 7
Author(s):  
Zain Budi Syulthoni ◽  
I Gusti Ngurah Gunadi
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Function ◽  
Social Cognitive ◽  
Cognitive Enhancement ◽  
Late Onset ◽  
Rehabilitation Program ◽  
The Impact ◽  
Additional Therapy ◽  
The Brain ◽  
Back To Work

Schizophrenia is a chronic, severe, and debilitate mental disorder that causing disability. Factors that causing disability is cognitive impairment. Cognitive impairment caused by disturbance in neurodevelopmental process of the brain that related to Dopaminergic, GABA-ergic, and Acethylcholinergic pathway. Cognitive Enhancement Therapy is additional therapy to recovery the cognitive function. CET facilitated repairmenin socio and non-socio cognitive function, encourage patient behaviour related social condition, develop patient understanding of schizophrenia and the impact on cognitive impair- ment, and rehabilitation program that characterised of an experiential and exercise to repair the non-social cognitive function (attention, memmory, and problem solving). CET shows improvement in early or late onset of schizophrenia. Pa- tients who got CET can back to work. Now, CET is used for early intervention in cognitive impairment in Schizophrenia. CET was also developed in patients with Schizoaffective, Schizophrenia comorbid with drug abuse, and patientswith au- tism. Hopefully, the improvement onquality of life patient with schizophrenia can achieve with combination pharmacother- apy and Cognitive Enhancement Therapy.

The Oxford Handbook of Adult Cognitive Disorders

2019 ◽  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Function ◽  
Neurodevelopmental Disorders ◽  
Brain Aging ◽  
Cognitive Disorders ◽  
Diverse Range ◽  
Medical Specialties ◽  
Psychiatric Illnesses ◽  
Medical Disorders ◽  
The Impact

The prevalence of cognitive impairment caused by neurodegenerative diseases and other neurologic disorders associated with aging is expected to rise dramatically between now and year 2050, when the population of Americans aged 65 or older will nearly double. Cognitive impairment also commonly occurs in other neurologic conditions, as well as in non-neurologic medical disorders (and their treatments), idiopathic psychiatric illnesses, and adult neurodevelopmental disorders. Cognitive impairment can thus infiltrate all aspects of healthcare, making it necessary for clinicians and clinical researchers to have an integrated knowledge of the spectrum of adult cognitive disorders. The Oxford Handbook of Adult Cognitive Disorders is meant to serve as an up-to-date, scholarly, and comprehensive volume covering most diseases, conditions, and injuries resulting in impairments in cognitive function in adults. Topics covered include normal cognitive and brain aging, the impact of medical disorders (e.g., cardiovascular, liver, pulmonary) and psychiatric illnesses (e.g., depression and bipolar disorder) on cognitive function, adult neurodevelopmental disorders (e.g., Down Syndrome, Attention Deficit/Hyperactivity Disorder), as well as the various neurological conditions (e.g., Alzheimer’s disease, chronic traumatic encephalopathy, concussion). A section of the Handbook is also dedicated to unique perspectives and special considerations for the clinicians and clinical researchers, covering topics such as cognitive reserve, genetics, diversity, and neuroethics. The target audience of this Handbook includes: (1) clinicians, particularly psychologists, neuropsychologists, neurologists (including behavioral and cognitive neurologists), geriatricians, and psychiatrists (including neuropsychiatrists), who provide clinical care and management for adults with a diverse range of cognitive disorders; (2) clinical researchers who investigate cognitive outcomes and functioning in adult populations; and (3) graduate level students and post-doctoral trainees studying psychology, clinical neuroscience, and various medical specialties.

scholarly journals Prospective Associations of Erythrocyte Composition and Dietary Intake of n-3 and n-6 PUFA with Measures of Cognitive Function

Nutrients ◽  
2018 ◽  
Vol 10 (9) ◽  
pp. 1253 ◽  
Author(s):  
Sherman Bigornia ◽  
Tammy Scott ◽  
William Harris ◽  
Katherine Tucker
Keyword(s):  
Cognitive Impairment ◽  
Executive Function ◽  
Cognitive Function ◽  
Dietary Intake ◽  
Puerto Rican ◽  
Cognitive Domain ◽  
Health Study ◽  
Individual Species ◽  
Dietary Pufa ◽  
The Impact

Polyunsaturated fatty acid (PUFA) consumption is recommended as part of a healthy diet, but evidence of the impact of individual species and biological concentrations on cognitive function is limited. We examined prospective associations of PUFA erythrocyte composition and dietary intake with measures of cognitive function among participants of the Boston Puerto Rican Health Study (aged 57 years). Erythrocyte and dietary PUFA composition were ascertained at baseline and associated with 2-year scores on the Mini-Mental State Exam (MMSE) (n = 1032) and cognitive domain patterns derived from a battery of tests (n = 865), as well as with incidence of cognitive impairment. Erythrocyte and dietary n-3 PUFA were not significantly associated with MMSE score. However, total erythrocyte and dietary n-3 very-long-chain fatty acids (VLCFA), and intake of individual species, were associated with better executive function (P-trend < 0.05, for all). There was evidence that greater erythrocyte n-6 eicosadienoic acid concentration was associated with lower MMSE and executive function scores (P-trend = 0.02). Only erythrocyte arachidonic acid (ARA) concentration predicted cognitive impairment (Odds Ratio = 1.26; P = 0.01). Among Puerto Rican adults, we found that n-3 VLCFA consumption may beneficially impact executive function. Further, these findings provide some evidence that n-6 metabolism favoring greater ARA tissue incorporation, but not necessarily dietary intake, could increase the risk of cognitive impairment.

scholarly journals Chemerin-induced macrophages pyroptosis in fetal brain tissue leads to cognitive disorder in offspring of diabetic dams

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Zhaoxia Liang ◽  
Luyang Han ◽  
Dianjianyi Sun ◽  
Yanmin Chen ◽  
Qi Wu ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Brain Tissue ◽  
Abdominal Cavity ◽  
Behavioral Changes ◽  
Dependent Manner ◽  
Diabetes In Pregnancy ◽  
The Impact ◽  
The Brain ◽  
In Pregnancy ◽  
Brain Tissues

Abstract Background Chemerin is highly expressed in the serum, placenta tissue, and umbilical cord blood of diabetic mother; however, the impact of chemerin on cognitive disorders of offspring from mothers with diabetes in pregnancy remains unclear. Methods A diabetic phenotype in pregnant mice dams was induced by streptozocin (STZ) injection or intraperitoneal injection of chemerin. Behavioral changes in offspring of diabetic dams and nondiabetic controls were assessed, and changes in chemerin, two receptors of chemerin [chemerin receptor 23 (ChemR23) and chemokine (C-C motif) receptor-like 2 (CCRL2)], macrophages, and neurons in the brain tissue were studied to reveal the underlying mechanism of the behavioral changes. Results Chemerin treatment mimicked the STZ-induced symptom of maternal diabetes in mice along with the altered behavior of offspring in the open field test (OFT) assay. In the exploring process for potential mechanism, the brain tissues of offspring from chemerin-treated dams were observed with an increase level of macrophage infiltration and a decrease number of neuron cells. Moreover, an increased level of NOD-like receptor family pyrin domain containing 3 (NLRP3) and apoptosis-associated speck-like (Asc) protein as well as pyroptosis [characterized by increased active caspase-1 content and secretion of cytokines such as interleukin (IL) 1 beta (IL-1β) and IL-18] more activated in macrophages is also observed in the brain of these diabetic dam’s offspring, in the presence of ChemR23. In vitro, it was found that pyroptosis activation was increased in macrophages separated from the abdominal cavity of normal mice, after chemerin treatment. However, depletion of CCRL2 decreased the level of chemerin in the brain tissues of diabetic dams’ offspring; depletion of ChemR23 decreased macrophage pyroptosis, and depletion of either receptor reversed chemerin-mediated neurodevelopmental deficits and cognitive impairment of offspring of diabetic pregnant dams. Conclusions Chemerin induced diabetic pregnant disease and CCRL2 were required to enrich chemerin in the brain of offspring. Aggregation of chemerin could lead to macrophage recruitment, activation of pyroptosis, the release of inflammatory cytokines, a decrease in the number of neurons, and cognitive impairment in offspring in a ChemR23-dependent manner. Targeting CCRL2 and/or ChemR23 could be useful for treating neuropsychological deficits in offspring of dams with diabetes in pregnancy.

scholarly journals P1240EVALUATION OF COGNITIVE FUNCTION IN HEMODIALYSIS PATIENTS USING MAGNETIC RESONANCE SPECTROSCOPY: FIVE YEARS FOLLOW UP RESULTS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Shigeru Owada ◽  
Aki Hirayama ◽  
Teruhiko Maeba
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Function ◽  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
Future Research ◽  
Resonance Spectroscopy ◽  
Brain Metabolites ◽  
Dialysis Patients ◽  
Cont Group ◽  
The Brain

Abstract Background and Aims In Japan, the elderly population is increasing remarkably, and dialysis patients are aging as usual. According to statistics from the Japanese Society for Dialysis Therapy, at the end of 2017, the incidence of HD patients is estimated to be 3 per 1,000 population, and by the end of 2020, the average age will be over 70 years. Therefore, early diagnosis of cognitive impairment is an important issue. With the aging of dialysis patients, the number of cases showing cognitive dysfunction increase in addition to the decline of physical strength. The problem of the onset of dementia involves many difficulties in medical treatment and nursing. Magnetic resonance spectroscopy (MRS) has been progressing from 1970s to evaluate neurological functions by measuring metabolites in the brain non-invasively. There are few reports using MRS for dialysis patients. In this study, we investigated the brain metabolites of hemodialysis (HD) patients with or without cognitive impairments using MRS and evaluated its usefulness for the diagnosis of cognitive disorder. Method A Toshiba MR device of 1.5 T was used. PRESS sequence was used to acquire water-suppressed 1H-MRS. Timing was TR/TE 2000/25 ms. Three kinds of brain metabolites, namely N-acethylaspartate (NAA), creatine (Cr) and mioinositol (MI) in the posterior cingulate gyrus were measured for 25 healthy adults (Cont group, 44±16 y.o.) and 84 HD patients (HD group, 74±11 y.o.), and ratios of NAA/Cr, MI/Cr and MI/NAA were calculated. The concentration of each metabolite was analyzed using LC model. HD patients were classified into three groups, namely normal cognitive function group (HD-N, n=25, 72±16 y.o.), mild cognitive impairment (HD-M, n=29, 74±9 y.o.) and dementia (HD-D, n=30, 79±8 y.) using MMSE test. Also, sequential changes of the brain metabolites were evaluated for 13 patients with worse cognitive function prospectively. Results HD patients showed a significant decrease of NAA and increases of MI and MI/NAA ratios compared to those of Cont group, suggesting that some metabolic abnormalities were inducted in HD. With a detailed classification of cognitive function in HD patients, NAA/Cr ratios were 1.69±0.17, 1.57±0.15, 1.71±0.20 and 1.54±0.22 in Cont, HD-N, HD-M and HD-D groups, respectively, and was significantly lower even in HD-N group than that of Cont group. MI/Cr ratios were 0.78±0.21, 0.90±0.21, 0.95±0.28 and 1.02±0.27 in Cont, HD-N, HD-M and HD-D groups, respectively, and those of HD-N/-M/-D were significantly higher than that of Cont group. Also, the value of HD-D was significantly higher than those in the other groups. MI/NAA ratios were 0.46±0.13, 0.56±0.17, 0.54±0.16 and 0.66±0.15, in Cont, HD-N, HD-M and HD-D groups, respectively. Again, those of HD-N/-M/-D were significantly higher than that of Cont group. HD-D group was highest among the HD patients. In the prospective study, dementia progressed in 10 of 13 HD patients who were observed more than 5 years. The MI/NAA ratio increased in the patients with dementia progression (from 0.58±0.11 to 1.24±0.17) while that value of the patients without dementia progression showed no changes (from 0.51±0.14 to 0.55±0.18). Conclusion These result suggest that the measurement of metabolic fluctuation in the brain using MRS is useful for the diagnosis of cognitive function in HD patients. The MI/NAA value is a strong candidate for a predictive biomarker of dementia progression. In the future, research and development of measurements of various parts of the brain and their integration to show changes in the whole brain are desired.

scholarly journals Dementing brain processes in patients with Wilson’s disease and multiple sclerosis (pathogenesis and treatment approaches)

2019 ◽  
Keyword(s):  
Multiple Sclerosis ◽  
Cognitive Impairment ◽  
Wilson’S Disease ◽  
Early Stage ◽  
Critical Mass ◽  
Wilson's Disease ◽  
Biological Aging ◽  
Cognitive Mechanisms ◽  
The Impact ◽  
The Brain

This article discusses various aspects of dementing processes in patients with Wilson’s disease (WD) and multiple sclerosis (MS), followed by a discussion of current pathogenetic treatment methods for these patients. A comprehensive clinical and laboratory study showed that the pathogenesis and staged development of the dementing process in patients with WD and MS largely coincides with those in patients with Alzheimer's disease and depends on three groups of factors: genetic predisposition, natural (biological) aging, and endo and exogenous pathogenic factors effects on the brain. Therefore, on the basis of the data presented by us, as well as literature data, it allows us to state that dementia is an organic pathophysiological syndrome of destruction of the critical mass of structural-functional blocks and systems of cognitive mechanisms of the brain. Each individual has his own, genetically determined, critical mass of cognitive mechanisms. Like any false system, this one is ultimately subject to both natural (slow) decay and pathological (accelerated) decay due to the death of neurons both in the type of apoptosis and in the type of necrosis. Thus, in patients with WD and MS, the pathogenetic process always involves structures sooner or later that ensure the functioning of the cognitive functions of the brain and lead to the development of their defects, therefore, therapy should be prescribed for the treatment of these patients. Dementia should be treated at its early stage, at the stage of cognitive impairment (CI). The general principles of managing patients with CI are the determination of the etiopathogenetic cause underlying the development of cognitive impairment, the reduction in the degree and prevention of the progression of cognitive deficit and the impact, if possible, on risk factors. Also, at all stages of cognitive deficiency, treatment of concomitant somatic diseases and correction of the emotional state are relevant. Therefore, timely prescribed comprehensive, pathogenetically substantiated personified therapy helps prevent irreversible consequences and improves the quality of life of patients.

scholarly journals Exercise-Linked Irisin Prevents Mortality and Enhances Cognition in a Mice Model of Cerebral Ischemia by Regulating Klotho Expression

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Zhao Jin ◽  
Zongze Zhang ◽  
Jianjuan Ke ◽  
Yanlin Wang ◽  
Huisheng Wu
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Function ◽  
Cerebral Ischemia ◽  
Enzyme Linked Immunosorbent Assay ◽  
Ros Generation ◽  
Mice Model ◽  
Stroke Patients ◽  
Neuroprotective Effects ◽  
Protein Expressions ◽  
The Impact

Irisin, which can be released in the hippocampus after physical exercise, is demonstrated to have beneficial effects on neurovascular diseases. This study investigated the impact of exercise linked-irisin on mortality and cognition in a mice model of cerebral ischemia and further explored its underlying mechanism. The cerebrospinal concentrations of irisin and klotho from ischemic stroke patients were measured with an enzyme-linked immunosorbent assay (ELISA). The cognitive function of mice was evaluated by a series of behavioural experiments. The expressions of klotho, MnSOD, and FOXO3a in the hippocampus of mice were detected by Western blot. Superoxide production in the brain tissue of mice was evaluated with the dihydroethidium (DHE) dying. The results demonstrated that stroke patients showed a positive correlation between their CSF irisin concentration and klotho concentration. In addition, when mice subjected to cerebral ischemia, their cognitive function was impaired, the protein expressions of klotho, MnSOD, and FOXO3a downregulated, and the production of reactive oxygen species (ROS) increased compared with the sham group. After pretreatment with exogenous irisin, improved cognitive impairment, upregulated protein expressions of klotho, MnSOD, and FOXO3a, and reduced ROS generation were observed in mice with MCAO. However, the neuroprotective effects of irisin compromised with the evidence of severe cognitive impairment, decreased protein expressions of MnSOD and FOXO3a, and increased ROS production in klotho knockout mice. Thus, our results indicated that exercise-linked irisin could prevent mortality and improve cognitive impairment after cerebral ischemia by regulating klotho expression.

Cognitive Functions under Anti-HER2 Targeted Therapy in Cancer Patients: A Scoping Review

2020 ◽  
Vol 20 ◽  
Author(s):  
Javier García-Sánchez ◽  
María D. Torregrosa ◽  
Omar Cauli
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Function ◽  
Cancer Patients ◽  
Cognitive Functions ◽  
Uterine Cancer ◽  
Cochrane Library ◽  
Acute Administration ◽  
Breast Cancer Patients ◽  
Her 2 ◽  
The Impact

Background and Objective: Pharmacological therapy targeting the HER2 protein is one of the major breakthroughs in the treatment of cancer patients overexpressing HER2 who have increased survival rates. Despite improved survival, it is important to determine the less frequent adverse effects in order to tailor treatments more personalized to the patients’ features. The possible impact of cancer treatments on cognitive functions is huge, and the effects of anti-HER 2 therapies on this issue have not been reviewed and are the objective of this study. Results: Analysis of PubMed, Scopus, Cochrane library and Web of Science databases revealed six studies performed in breast and serous uterine cancer patients analyzing cognitive function under chemotherapy regimens including anti-HER2 drugs. Four of these studies reported small to significant worsening of cognitive function following chemotherapy regimens containing trastuzumab (the most widely used anti-HER2 drug). In neoadyuvant settings, and in breast cancer patients, treatment with the new anti-HER-2 drug trastuzumab emtansine seems to induce less cognitive impairment than therapeutic regimens containing chemotherapy and trastuzumab. Acute administration of trastuzumab induced cognitive impairment in gastric cancer mice models, confirming its ability to alter cognitive function in patients,. Conclusions: More studies analyzing the impact of anti-HER2 therapy on cognitive function are necessary at preclinical and clinical levels in order to personalize pharmacological treatment and offers cancer patients a better quality of life.

scholarly journals The impact of diet-based glycaemic response and glucose regulation on cognition: evidence across the lifespan

2017 ◽  
Vol 76 (4) ◽  
pp. 466-477 ◽  
Author(s):  
Sandra I. Sünram-Lea ◽  
Lauren Owen
Keyword(s):  
Blood Glucose ◽  
Cognitive Function ◽  
Brain Function ◽  
Healthy Lifestyle ◽  
Glucose Deprivation ◽  
Glucose Regulation ◽  
Glycaemic Response ◽  
Glucose Levels ◽  
The Impact ◽  
The Brain

The brain has a high metabolic rate and its metabolism is almost entirely restricted to oxidative utilisation of glucose. These factors emphasise the extreme dependence of neural tissue on a stable and adequate supply of glucose. Whereas initially it was thought that only glucose deprivation (i.e. under hypoglycaemic conditions) can affect brain function, it has become apparent that low-level fluctuations in central availability can affect neural and consequently, cognitive performance. In the present paper the impact of diet-based glycaemic response and glucose regulation on cognitive processes across the lifespan will be reviewed. The data suggest that although an acute rise in blood glucose levels has some short-term improvements of cognitive function, a more stable blood glucose profile, which avoids greater peaks and troughs in circulating glucose is associated with better cognitive function and a lower risk of cognitive impairments in the longer term. Therefore, a habitual diet that secures optimal glucose delivery to the brain in the fed and fasting states should be most advantageous for the maintenance of cognitive function. Although the evidence to date is promising, it is insufficient to allow firm and evidence-based nutritional recommendations. The rise in obesity, diabetes and metabolic syndrome in recent years highlights the need for targeted dietary and lifestyle strategies to promote healthy lifestyle and brain function across the lifespan and for future generations. Consequently, there is an urgent need for hypothesis-driven, randomised controlled trials that evaluate the role of different glycaemic manipulations on cognition.

scholarly journals Hypertension and the Brain: A Risk Factor for More Than Heart Disease

2016 ◽  
Vol 42 (3-4) ◽  
pp. 255-262 ◽  
Author(s):  
Anja Meissner
Keyword(s):  
Risk Factor ◽  
Cognitive Impairment ◽  
Cognitive Decline ◽  
Small Vessel Disease ◽  
Current Knowledge ◽  
White Matter Lesions ◽  
Cerebrovascular Complications ◽  
Cerebrovascular Function ◽  
The Impact ◽  
The Brain

Background: Cerebral small vessel disease (cSVD), a common risk factor for cognitive impairment, involves unspecific arteriopathy characterized by hypertrophy and endothelial dysfunction that alter cerebrovascular function and auto-regulation of cerebral blood flow (CBF). Microbleedings, subcortical lacunar infarctions and diffuse areas of white matter lesions resulting from vascular injury are associated with reduced cognitive function mostly characterized by difficulties in learning and retention, attention deficits, gait disorders or depression. In recent years, it has become evident that vascular risk factors contribute to the development of cSVD and associated vascular cognitive impairment (VCI). Among them, hypertension emerged as such a major modifiable risk factor since the brain presents an early target for organ damage due to changes in blood pressure (BP). Subsequently both high and, especially in the elderly, low BP have been linked to cognitive decline, which initiated controversial discussions about BP control as a potential therapeutic strategy to achieve optimal brain perfusion and thus, reduce the occurrence of cSVD and cognitive dysfunction. Yet, recent randomized controlled trials examined the impact of anti-hypertensive therapy on cognitive performance with conflicting results. Summary: In light of the current knowledge, it becomes apparent that there is an urgent need to understand the mechanisms underlying hypertension-induced cerebrovascular complications in order to identify effective therapeutic targets to prevent and most importantly also reverse cognitive decline mediated through hypertension. Key Message: This review summarizes the current knowledge of cSVD pathogenesis as well as possible links to hypertension-mediated cerebrovascular complications. By pointing out knowledge gaps, it aims to spur future studies in search of specific targets helping to prevent therapy failures and decelerate the rapidly progressing neuro-degeneration of patients suffering from cerebrovascular diseases emanating from hypertension.

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