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 Anesthesiology and cognitive impairment: a narrative review of current clinical literature

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Jillian C. Belrose ◽  
Ruediger R. Noppens
Keyword(s):  
Cognitive Impairment ◽  
General Anesthesia ◽  
Cognitive Dysfunction ◽  
Large Body ◽  
Postoperative Cognitive Dysfunction ◽  
Cognitive Disorders ◽  
Future Research ◽  
Main Body ◽  
Modifiable Factors ◽  
The Impact

Abstract Background The impact of general anesthesia on cognitive impairment is controversial and complex. A large body of evidence supports the association between exposure to surgery under general anesthesia and development of delayed neurocognitive recovery in a subset of patients. Existing literature continues to debate whether these short-term effects on cognition can be attributed to anesthetic agents themselves, or whether other variables are causative of the observed changes in cognition. Furthermore, there is conflicting data on the relationship between anesthesia exposure and the development of long-term neurocognitive disorders, or development of incident dementia in the patient population with normal preoperative cognitive function. Patients with pre-existing cognitive impairment present a unique set of anesthetic considerations, including potential medication interactions, challenges with cooperation during assessment and non-general anesthesia techniques, and the possibility that pre-existing cognitive impairment may impart a susceptibility to further cognitive dysfunction. Main body This review highlights landmark and recent studies in the field, and explores potential mechanisms involved in perioperative cognitive disorders (also known as postoperative cognitive dysfunction, POCD). Specifically, we will review clinical and preclinical evidence which implicates alterations to tau protein, inflammation, calcium dysregulation, and mitochondrial dysfunction. As our population ages and the prevalence of Alzheimer’s disease and other forms of dementia continues to increase, we require a greater understanding of potential modifiable factors that impact perioperative cognitive impairment. Conclusions Future research should aim to further characterize the associated risk factors and determine whether certain anesthetic approaches or other interventions may lower the potential risk which may be conferred by anesthesia and/or surgery in susceptible individuals.

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 Inflammation and Insulin Resistance as Risk Factors and Potential Therapeutic Targets for Alzheimer’s Disease

2021 ◽  
Vol 15 ◽  
Author(s):  
Angeles Vinuesa ◽  
Carlos Pomilio ◽  
Amal Gregosa ◽  
Melisa Bentivegna ◽  
Jessica Presa ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Insulin Resistance ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Brain Aging ◽  
Therapeutic Targets ◽  
Low Grade ◽  
Increased Risk ◽  
The Impact

Overnutrition and modern diets containing high proportions of saturated fat are among the major factors contributing to a low-grade state of inflammation, hyperglycemia and dyslipidemia. In the last decades, the global rise of type 2 diabetes and obesity prevalence has elicited a great interest in understanding how changes in metabolic function lead to an increased risk for premature brain aging and the development of neurodegenerative disorders such as Alzheimer’s disease (AD). Cognitive impairment and decreased neurogenic capacity could be a consequence of metabolic disturbances. In these scenarios, the interplay between inflammation and insulin resistance could represent a potential therapeutic target to prevent or ameliorate neurodegeneration and cognitive impairment. The present review aims to provide an update on the impact of metabolic stress pathways on AD with a focus on inflammation and insulin resistance as risk factors and therapeutic targets.

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.

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.

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.

Insulin and cognitive function in humans: experimental data and therapeutic considerations

2005 ◽  
Vol 33 (5) ◽  
pp. 1037-1040 ◽  
Author(s):  
M.W.J. Strachan
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Function ◽  
Memory Function ◽  
Experimental Studies ◽  
Epidemiological Studies ◽  
Therapeutic Benefit ◽  
Systemic Absorption ◽  
Intravenous Insulin ◽  
People With Dementia ◽  
The Impact

Data from experimental studies in animals and from epidemiological studies in humans suggest a link between insulin and cognitive performance. Do these results translate into clinical and therapeutic benefit for people with cognitive impairment? Insulin injected peripherally can readily cross the blood–brain barrier. Intravenous insulin can improve aspects of cognitive function in healthy adults and in individuals with Alzheimer's dementia. Moreover, intravenous insulin increases concentrations of a long form of β-amyloid protein, Aβ42. One potential confounding factor with these data, however, is the need for co-administration of glucose with the insulin to maintain euglycaemia as glucose itself can facilitate memory function. Administration of insulin via the intranasal route is scientifically (and therapeutically) more attractive because the insulin goes directly to the cerebrospinal fluid, with minimal systemic absorption; this obviates the need for a glucose infusion. Intranasal insulin may improve some aspects of memory in healthy individuals, but has yet to be studied in people with cognitive impairment. TZDs (thiazolidinediones) reduce peripheral insulin concentrations by enhancing insulin sensitivity. In adults with Type II (non-insulin-dependent) diabetes, TZD therapy improves memory function, but so does sulphonylurea therapy (which elevates peripheral insulin concentrations). Improved memory is linked to lower blood glucose concentrations, rather than altered insulin levels. However, major trials are currently under way examining the impact of TZDs in people with dementia.

scholarly journals A comparative study for evaluation of cognitive function in type-II diabetes mellitus patients and non-diabetics

2018 ◽  
Vol 7 (4) ◽  
pp. 738
Author(s):  
Dulcie Celia A. ◽  
Ezhil Ramya J. ◽  
Sriviruthi B.
Keyword(s):  
Diabetes Mellitus ◽  
Cognitive Impairment ◽  
Cognitive Function ◽  
Type Ii Diabetes ◽  
Type Ii Diabetes Mellitus ◽  
Control Group ◽  
Diabetic Patients ◽  
Type Ii ◽  
Duration Of Diabetes ◽  
The Impact

Background: To evaluate the impact of type-II diabetes mellitus on cognitive function and to assess the factors associated with impaired function.Methods: This prospective study compared 100 type-II diabetic people attending the diabetic clinic of Tirunelveli Medical College Hospital with another 100 membered control group. The study group was selected randomly between the age group of 45-65 years. A neuro-cognitive assessment was done using Standardized Mini Mental State Examination (SMMSE), which is a simple and reliable screening test. This scale has 12 questions with time limits to assess orientation, memory, calculation, language, attention and construction. Magnitude and severity of cognitive decrement were analysed along with the possible factors affecting it.Results: Mean age of the study population was 54.6±7.24 years. Cognitive impairment was noted among 62 of cases and 48 of the control group, which means a 14% higher prevalence of cognitive impairment among the type 2 diabetics. The association of development of cognitive impairment and duration of diabetes mellitus was significant statistically (p value = 0.025443; p<0.05). Other demographic variables like gender, education and domicile were also seen to affect the results.Conclusions: Mild to moderate cognitive impairment was found significantly higher among the type-II diabetics than the non-diabetics. The cognitive impairment was found to be associated with the duration of diabetes. Hence the routine screening of cognition by SMMSE should be done in all type-II diabetic patients.

scholarly journals A healthy body, a healthy mind: long-term impact of diet on mood and cognitive function

2001 ◽  
Vol 60 (1) ◽  
pp. 135-143 ◽  
Author(s):  
Peter J. Rogers
Keyword(s):  
Risk Factors ◽  
Fatty Acids ◽  
Cognitive Impairment ◽  
Cognitive Function ◽  
Polyunsaturated Fatty Acids ◽  
Cognitive Decline ◽  
Alternative Hypothesis ◽  
Neuronal Cell ◽  
The Impact ◽  
Long Chain

Certain dietary risk factors for physical ill health are also risk factors for depression and cognitive impairment. Although cholesterol lowering has been suggested to increase vulnerability to depression, there is better support for an alternative hypothesis that intake of n-3 long-chain polyunsaturated fatty acids can affect mood (and aggression). Possible mechanisms for such effects include modification of neuronal cell membrane fluidity and consequent impact on neurotransmitter function. Stronger evidence exists concerning a role for diet in influencing cognitive impairment and cognitive decline in older age, in particular through its impact on vascular disease. For example, cognitive impairment is associated with atherosclerosis, type 2 diabetes and hypertension, and findings from a broad range of studies show significant relationships between cognitive function and intakes of various nutrients, including long-chain polyunsaturated fatty acids, antioxidant vitamins, and folate and vitamin B12. Further support is provided by data on nutrient status and cognitive function. Almost all this evidence, however, comes from epidemiological and correlational studies. Given the problem of separating cause and effect from such evidence, and the fact that cognitive impairment and cognitive decline (and depression) are very likely to be significant factors contributing to the consumption of a poor diet, greater emphasis should now be placed on conducting intervention studies. An efficient approach to this problem could be to include assessments of mood and cognitive function as outcome measures in studies designed primarily to investigate the impact of dietary interventions on markers of physical health.

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