Cognitive Impairment In Adults Research Articles

Mitochondrial dysfunction is associated with cognitive impairment in adults with OSA without dementia

Study objectivesIncreased reactive oxygen species associated with loss of mitochondrial function affect synaptic activity, which is an important mechanism underlying cognitive decline. This study assesses the role of mitochondrial proteins in neuron-derived exosomes (NDEs) on cognitive impairment in patients with obstructive sleep apnea (OSA) without dementia. MethodsAnalyses were conducted in 268 study participants with complete polysomnography data, cognitive tests, and important clinical data available. NDEs were isolated immunochemically for enzyme-linked immunosorbent assay quantification of mitochondrial proteins, i.e., humanin and mitochondrial open reading frame of the 12S rRNA-c (MOTS-c), and synaptic protein, i.e., neurogranin (NRGN). A mediation analysis of the relationship between sleep parameters and cognition was performed using humanin, MOTS-c, and NRGN values as a mediating factor. Twenty-two patients with moderate to severe OSA who received CPAP therapy were followed up, and humanin, MOTS-c and NRGN levels were reassessed after 1 year of treatment. ResultsAll participants were divided into the OSA + MCI group (n = 91), OSA-MCI group (n = 89), MCI group (MCI without OSA) (n = 38) and control group (normal cognitive state without OSA) (n = 50). The mean CD63-normalized NDE levels of humanin, MOTS-c, and NRGN in the OSA + MCI group were higher than those in the OSA-MCI and control groups. The NDE levels of humanin, MOTS-c, and NRGN in the MCI group were lower than those in controls. The odds of cognitive impairment in patients with OSA were higher with higher NDE levels of humanin, MOTS-c, and NRGN (odds ratio (OR): 2.100, 95 % confidence interval (CI): 1.646–2.679, P < 0.001; OR: 5.453, 95 % CI: 3.112–9.556, P < 0.001; OR: 3.115, 95 % CI: 2.163–4.484, P < 0.001). The impaired cognitive performance was associated with higher NDE levels of humanin (β: 0.505, SE: 0.048, P < 0.001), MOTS-c (β: 0.580, SE: 0.001, P < 0.001), and NRGN (β: 0.585, SE: 0.553, P < 0.001). The relationship between sleep parameters (mean SaO2 and T90) and MoCA scores was mediated by the NDE levels of humanin, MOTS-c, and NRGN with the proportion of mediation varying from 35.33 % to 149.07 %. Receiver operating characteristic curve revealed an area under the curve of 0.905 for humanin, 0.873 for MOTS-c, and 0.934 for NRGN to predict MCI in OSA patients without dementia. Increased humanin, MOTS-c, and NRGN levels significantly decreased after CPAP treatment. ConclusionsMitochondrial dysfunction is implicated in cognitive impairment in OSA patients without dementia, and mainly mediates the association between intermittent hypoxia and cognitive impairment in adults with OSA without dementia. Mitochondrial dysfunction can be partially reversible by CPAP treatment. Mitochondrial proteins can be used as markers of cognitive impairment in patients with OSA.

Assessment of Cognitive Impairment in Adults Living with HIV

Assessment of Cognitive Impairment in Adults Living with HIV

MRI hypoperfusion as a determinant of cognitive impairment in adults with Moyamoya angiopathy.

In Moyamoya angiopathy (MMA), mechanisms underlying cognitive impairment remain debated. We aimed to assess the association of cognitive impairment with the degree and the topography of cerebral hypoperfusion in MMA. A retrospective analysis of neuropsychological and perfusion MRI data from adults with MMA was performed. Ischemic and haemorrhagic lesion masks were created to account for cerebral lesions in the analysis of cerebral perfusion. Whole brain volume of hypoperfused parenchyma was outlined on perfusion maps using different Tmax thresholds from 4 to 12 s. Regional analysis produced mean Tmax values at different regions of interest. Analyses compared perfusion ratios in patients with and without cognitive impairment, with multivariable logistic regression analysis to identify predictive factors. Cognitive impairment was found in 20/48 (41.7%) patients. Attention/processing speed and memory were equally impaired (24%) followed by executive domain (23%). After adjustment, especially for lesion volume, hypoperfused parenchyma volume outlined by Tmax > 4 s or Tmax > 5 s thresholds was an independent factor of cognitive impairment (OR for Tmax > 4 s = 1.06 [CI 95% 1.008-1.123]) as well as attention/processing speed (OR for Tmax > 4 s = 1.07 [CI 95% 1.003-1.133]) and executive domains (OR for Tmax > 5 s = 1.08 [CI 95% 1.004-1.158]). Regarding cognitive functions, patients with processing speed and flexibility impairment had higher frontal Tmax compared to other ROIs and to patients with normal test scores. Cerebral hypoperfusion emerged as an independent factor of cognitive impairment in MMA particularly in attention/processing speed and executive domains, with a strong contribution of frontal areas. Considering this association, revascularization surgery could improve cognitive impairment.

Neonatal hypoxia impairs serotonin release and cognitive functions in adult mice

Children who experienced moderate perinatal asphyxia (MPA) are at risk of developing long lasting subtle cognitive and behavioral deficits, including learning disabilities and emotional problems. The prefrontal cortex (PFC) regulates cognitive flexibility and emotional behavior. Neurons that release serotonin (5-HT) project to the PFC, and compounds modulating 5-HT activity influence emotion and cognition. Whether 5-HT dysregulations contribute to MPA-induced cognitive problems is unknown. We established a MPA mouse model, which displays recognition and spatial memory impairments and dysfunctional cognitive flexibility. We found that 5-HT expression levels, quantified by immunohistochemistry, and 5-HT release, quantified by in vivo microdialysis in awake mice, are reduced in PFC of adult MPA mice. MPA mice also show impaired body temperature regulation following injection of the 5-HT1A receptor agonist 8-OH-DPAT, suggesting the presence of deficits in 5-HT auto-receptor function on raphe neurons. Finally, chronic treatment of adult MPA mice with fluoxetine, an inhibitor of 5-HT reuptake transporter, or the 5-HT1A receptor agonist tandospirone rescues cognitive flexibility and memory impairments. All together, these data demonstrate that the development of 5-HT system function is vulnerable to moderate perinatal asphyxia. 5-HT hypofunction might in turn contribute to long-term cognitive impairment in adulthood, indicating a potential target for pharmacological therapies.

Impaired synaptic plasticity and decreased excitability of hippocampal glutamatergic neurons mediated by BDNF downregulation contribute to cognitive dysfunction in mice induced by repeated neonatal exposure to ketamine.

Repeated exposure to ketamine during the neonatal period in mice leads to cognitive impairments in adulthood. These impairments are likely caused by synaptic plasticity and excitability damage. We investigated the precise role of brain-derived neurotrophic factor (BDNF) in the cognitive impairments induced by repeated ketamine exposure during the neonatal period. We evaluated the cognitive function of mice using the Morris water maze test and novel object recognition test. Western blotting and immunofluorescence were used to detect the protein levels of BDNF. Western blotting, Golgi-Cox staining, transmission electron microscopy, and long-term potentiation (LTP) recordings were used to assess synaptic plasticity in the hippocampus. The excitability of neurons was evaluated using c-Fos. In the intervention experiment, pAdeno-CaMKIIα-BDNF-mNeuronGreen was injected into the hippocampal CA1 region of mice to increase the level of BDNF. The excitability of neurons was enhanced using a chemogenetic approach. Our findings suggest that cognitive impairments in mice repeatedly exposed to ketamine during the neonatal period are associated with downregulated BDNF protein level, synaptic plasticity damage, and decreased excitability of glutamatergic neurons in the hippocampal CA1 region. Furthermore, the specific upregulation of BDNF in glutamatergic neurons of the hippocampal CA1 region and the enhancement of excitability can improve impaired synaptic plasticity and cognitive function in mice. BDNF downregulation mediates synaptic plasticity and excitability damage, leading to cognitive impairments in adulthood following repeated ketamine exposure during the neonatal period.

Features of the clinical and neuroimaging picture in patients with early-onset Alzheimer's disease

The most common cause of severe cognitive impairment in adults is Alzheimer's disease (AD). Depending on the age of onset, AD is divided into early (<65 years) and late (≥65 years) forms. Early-onset AD (EOAD) is significantly less common than later-onset AD (LOAD) and accounts for only about 5-10% of cases. However, its medical and social significance, as a disease leading to loss of ability to work and legal capacity, as well as premature death in patients aged 40-64 years, is extremely high. Patients with EOAD compared with LOAD have a greater number of atypical clinical variants - 25% and 6-12.5%, respectively, which complicates the differential diagnosis of EOAD with other neurodegenerative diseases. However, the typical classical amnestic variant predominates in both EOAD and LOAD. Also, patients with EOAD have peculiarities according to neuroimaging data: when performing MRI of the brain, patients with EOAD often have more pronounced parietal atrophy and less pronounced hippocampal atrophy compared to patients with LOAD. The article pays attention to the features of the clinical and neuroimaging data in patients with EOAD; a case of a patient with EOAD is presented.

Utility of the Brief Assessment of Cognitive Health (BACH) computerized screening tool in identifying MS-related cognitive impairment

BackgroundCurrent guidelines recommend that individuals with MS are screened annually for processing speed deficits, often using the Symbol Digit Modalities Test (SDMT). However, given the heterogeneity of cognitive deficits in individuals with MS, other screening measures that assess a range of cognitive domains are necessary. The current cross-sectional study aimed to examine the ability of the computerized, self-administered Brief Assessment of Cognitive Health (BACH) screening measure to detect the presence of cognitive impairment in adults with MS as determined by performance on a standard neuropsychological test battery. MethodsSeventy-two individuals with MS completed the BACH and a comprehensive neuropsychological test battery. Receiver operating characteristic (ROC) analyses were conducted to investigate the ability of the BACH to identify cognitively impaired and cognitively intact individuals. ROC analyses were also conducted to compare the ability of the SDMT to discriminate between cognitively intact and cognitively impaired groups as a comparison with the BACH. ResultsCognitive impairment was observed in 56 % of the sample. The BACH showed acceptable ability to discriminate between cognitively intact and cognitively impaired groups (AUC = 0.78). Additionally, the BACH was able to adequately predict cognitive impairment in domains other than processing speed (AUC = 0.71). The SDMT also demonstrated adequate utility in identifying individuals with cognitive impairment (AUC = 0.73); however, the SDMT was not able to adequately predict cognitive impairment in domains other than processing speed (AUC = 0.56). ConclusionThe BACH showed adequate ability to detect cognitive impairment in individuals with MS. The BACH was able to identify impairments across various assessed cognitive domains, including individuals with and without processing speed deficits.

Cerebrovascular reactivity in Alzheimer's disease signature regions is associated with mild cognitive impairment in adults with hypertension.

Vascular risk factors contribute to cognitive decline suggesting that maintaining cerebrovascular health could reduce dementia risk. The objective of this study is to evaluate the association of cerebrovascular reactivity (CVR), a measure of brain blood vessel elasticity, with mild cognitive impairment (MCI) and dementia. Participants were enrolled in the Systolic Blood Pressure Intervention Trial Memory and Cognition in Decreased Hypertension (SPRINT-MIND) magnetic resonance imaging substudy. Baseline CVR in Alzheimer's disease (AD) signature regions were primary variables of interest. The occipital pole and postcentral gyrus were included as control regions. Higher AD composite CVR was associated with lower MCI risk. No significant associations between inferior temporal gyrus, occipital pole, or postcentral gyrus CVR and MCI risk, or any regional CVR-combined risk associations were observed. CVR in AD signature regions is negatively associated with occurrence of MCI, implicating CVR in AD signature regions as a potential mechanism leading to cognitive impairment.

Association between cardiovascular risk factors and cognitive impairment in adults aged 60 years or older from Chile: a cross-sectional study

BackgroundFew studies in Latin America have examined the association between cardiovascular risk factors and cognitive impairment (CI) in a nationally representative sample. Therefore, this study aimed to estimate the prevalence of CI in a nationally representative sample of adults aged 60 years or older from Chile and to investigate the association between cardiovascular risk factors and CI.MethodsData from the cross-sectional 2016–2017 National Health Survey of Chile, which included 2031 adults (63.7% women) was used. Body mass index, metabolic syndrome (blood pressure, triglycerides, fasting glucose or treatment for diabetics, waist circumference, and HDL cholesterol), risk of cardiovascular disease (history and measured variables, using the Framingham risk score), tobacco use, and physical activity were measured. CI was assessed using the Mini-Mental Status Examination (MMSE).ResultsOverall, the prevalence of CI was 12.2% at the national level. Significant differences in CI were observed by age, education level, risk of cardiovascular disease, and smoking. High risk of cardiovascular disease was associated with higher odds of CI (OR: 2.04; 95%CI: 1.20–3.45) compared to low risk. Smoking was significantly associated with a lower likelihood of CI (OR: 0.56; 95%CI: 0.36–0.87) compared to never smoking. Body mass index, metabolic syndrome, and physical activity were not associated with CI.ConclusionsThis study provided additional support for previous findings on the relationship between cognitive decline and an elevated risk of cardiovascular disease. Worse CI was associated with the group with the highest risk of cardiovascular disease, and the presence of lifestyle factors, such as obesity and physical inactivity, exacerbate this relationship, but not being a current smoker.

The mismatch negativity as an index of cognitive impairment in adults with Down syndrome

AbstractBackgroundPeople with Down syndrome (DS) have a high risk of developing Alzheimer’s disease (AD; Zis and Strydom 2018). The mismatch negativity (MMN) is an event‐related potential that can be used to index cognitive decline (Näätänen et al., 2011). Given its relative independence from attentional processes (Naatanen and Näätänen 1992), the MMN may be particularly useful when studying populations with intellectual disability, who may find sustained attention tasks challenging. We therefore investigated the MMN in people with DS and its association with cognitive abilities.MethodsMMN responses to a passive auditory oddball task were recorded from 27 adults with DS (aged 18 to 59) without any hearing impairments. Associations between MMN and age, as well as memory, language, IQ, and attention scores were examined.ResultsThe MMN was present only in young adults up to the age of 40 and the latency was prolonged. Attenuation of MMN amplitude was associated with poorer memory scores. Finally, longer MMN latencies were associated with increased inter‐individual performance variability and worse performance on memory, verbal, and general IQ tasks.ConclusionOverall, our results indicate that MMN amplitude may be associated with AD‐related memory loss, while increased MMN latency seems to reflect verbal abilities in people with DS. Furthermore, the association between MMN latency and inter‐individual performance variability may suggest the presence of AD‐driven white matter degenerations affecting the brian’s frontal lobe. Therefore, the MMN may represent a valuable tool for studying cognitive abilities and AD pathology in DS.

Modulation of Kynurenic Acid Production by N-acetylcysteine Prevents Cognitive Impairment in Adulthood Induced by Lead Exposure during Lactation in Mice.

Lead (Pb2+) exposure during early life induces cognitive impairment, which was recently associated with an increase in brain kynurenic acid (KYNA), an antagonist of NMDA and alpha-7 nicotinic receptors. It has been described that N-acetylcysteine (NAC) favors an antioxidant environment and inhibits kynurenine aminotransferase II activity (KAT II, the main enzyme of KYNA production), leading to brain KYNA levels decrease and cognitive improvement. This study aimed to investigate whether the NAC modulation of the brain KYNA levels in mice ameliorated Pb2+-induced cognitive impairment. The dams were divided into four groups: Control, Pb2+, NAC, and Pb2++NAC, which were given drinking water or 500 ppm lead acetate in the drinking water ad libitum, from 0 to 23 postnatal days (PNDs). The NAC and Pb2++NAC groups were simultaneously fed NAC (350 mg/day) in their chow from 0 to 23 PNDs. At PND 60, the effect of the treatment with Pb2+ and in combination with NAC on learning and memory performance was evaluated. Immediately after behavioral evaluation, brain tissues were collected to assess the redox environment; KYNA and glutamate levels; and KAT II activity. The NAC treatment prevented the long-term memory deficit exhibited in the Pb2+ group. As expected, Pb2+ group showed redox environment alterations, fluctuations in glutamate levels, and an increase in KYNA levels, which were partially avoided by NAC co-administration. These results confirmed that the excessive KYNA levels induced by Pb2+ were involved in the onset of cognitive impairment and could be successfully prevented by NAC treatment. NAC could be a tool for testing in scenarios in which KYNA levels are associated with the induction of cognitive impairment.

Screening for cognitive impairment in adults with sickle cell disease: a systematic review and meta-analysis

Neurovascular disease such as symptomatic stroke, silent brain infarcts and vascular cognitive impairment are common complications of sickle cell disease (SCD) that can have devastating consequences on quality of life, employment, and social functioning. Early recognition of neurovascular disease is a prerequisite for the timely optimization of medical care and to connect patients to adaptive resources. While cognitive impairment has been well described in children, currently available data are limited in adults. As a result, guidance on the optimal cognitive screening strategies in adults is scarce. We conducted a systematic review to identify the different screening tools that have been evaluated in SCD. A meta-analysis was performed to estimate the prevalence of suspected cognitive impairment in this population. In this qualitative synthesis, we present 8 studies that evaluated 6 different screening tools. Patient characteristics that impacted on cognitive screening performance included age, education level, and a prior history of stroke. We report a pooled prevalence of 38% [14-62%] of suspected cognitive impairment. We discuss the relative benefits and limitations of the different screening tools to help clinicians select an adapted approach tailored to their specific patients’ needs. Further studies are needed to establish and validate cognitive screening strategies in patients with diverse cultural and educational backgrounds.

51 Importance of Using Baseline Verbal Abilities When Interpreting the MOCA Test Performance

Objective:The Montreal Cognitive Assessment (MOCA) is widely used as a mental status screening test to detect cognitive impairment in adults over 55 years of age. Performance on this test ranges from 0 to 30. One point is given to individuals with 12 or lower years of education. This accommodation is based on the fact that low education may be a risk factor for dementia (Milani et al., 2018). However, studies suggest the one-point adjustment may not be sufficient to address the impact of low education on test performance (Malek-Ahmadi et al., 2015). The aim of this study is to compare the effects of educational achievement versus baseline verbal abilities on MOCA performance.Participants and Methods:Fifty patients (25 male; mean age=72.78, SD = 8.11; mean education=16.18, SD = 2.73) with cognitive concerns were referred to Massachusetts General Brigham. All underwent neuropsychological evaluation, including screening with the MOCA. Total MOCA scores were calculated. In this patient group, the MOCA scores ranged from 10 to 29 (mean=22, SD=5.129). Measures of literacy (Wechsler Test of Adult Reading or Test of Premorbid Functioning) were used to estimate baseline verbal abilities. Educational achievement was based on self-reported years of education.Results:Correlational analyses included the Total MOCA scores, measures of literacy, and years of education. Performance on the MOCA significantly correlated with measures of literacy, r(43)=.578, p&lt; .001, and a stepwise regression analysis revealed that literacy predicted performance on the MOCA, R2=.041, F(3,139)= 9.172, p&lt;.001. Years of education correlated with measures of literacy, r(44)=.494, p&lt; .001, but not with performance on the MOCA.Conclusions:Findings suggest that education-adjusted scoring on the MOCA may not be sufficient to “level the playing field” in terms of MOCA performance. Years of education had less of an effect on the Total MOCA scores than did baseline verbal abilities. It may be the case that literacy has a more robust effect on MOCA performance due to the inherent verbal nature of the MOCA. Data from this study highlight the importance of considering a patient’s baseline verbal abilities in the interpretation of their MOCA performance.

Prevalence and incidence of mild cognitive impairment in adults with diabetes in the United States

BackgroundLimited evidence exists about the prevalence and incidence of mild cognitive impairment (MCI) in individuals with diabetes in the U.S. We aimed to address such knowledge gaps using a nationally representative study dataset. MethodWe conducted a secondary analysis from the Health and Retirement Study (HRS) (1996–2018). The sample for examining the prevalence of MCI was14,988, with 4192 (28.0%) having diabetes, while the sample for the incidence was 21,824, with 1534 (28.0%) having diabetes. ResultsParticipants with diabetes had a higher prevalence of MCI than those without diabetes (19.9 % vs. 14.8 %; odds ratio [95 % confidence interval] (OR[95 %CI]): 1.468 [1.337, 1.611], p <.001). The incidence of MCI in participants with/without newly diagnosed diabetes was 42.9 % vs. 31.6 % after a mean 10-year follow-up, with the incidence rate ratio (IRR) [95 %CI] (1.314 [1.213, 1.424], p <.001). Newly diagnosed diabetes was associated with elevated risks of MCI compared with non-diabetes, with the uncontrolled hazard ratio (HR) [95 %CI] (1.498 [1.405, 1.597], p <.001). ConclusionsUsing a nationally representative study data in the U.S., participants with diabetes had a higher prevalence and incidence of MCI than those without diabetes. Findings show the importance of developing interventions tailored to the needs of individuals with diabetes and cognitive impairment.

A Life Course Approach to Understanding Cognitive Impairment in Adults with Type 2 Diabetes: A Narrative Literature Review

Diabetes is an independent risk factor for cognitive impairment, with the latter presenting challenges for diabetes self-management and glycemic control in individuals with type 2 diabetes. Predicated on the theory of unpleasant symptoms, the purpose of the current narrative review of the literature was to identify etiologic factors that influence cognitive impairment as a precursor to dementia in individuals with diabetes. Physiological, psychological, and situational factors were recognized as important life course components of cognitive impairment in later adulthood. Developing interventions targeting modifiable factors is warranted in preventing cognitive impairment in adults with diabetes.

Association between periodontitis and cognitive impairment in adults.

To summarize the data on association between periodontal diseases and cognitive impairment in adults this systematic review scrutinized various observational studies till September 2021. This review was carried out in accordance with the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA 2020) guidelines. The authors used PECO framework question,: population-Adults(18 years or older), exposure-adults suffering from periodontitis, comparator-adult group without periodontitis, outcome-adults at high risk for cognitive impairment. Search for the literature was conducted on PubMed, Web of Science, and Cumulative Index to Nursing and Allied Health Literature (CINAHL). Search was limited to human studies with no limitation to year of publication prior to September 2021. Search terms used were related to gingiva, oral bacteria like Porphyromonas gingivalis, gum inflammation, periodontitis, dementia, neuroinflammation, cognitive impairment, Alzheimer's disease, Parkinson disease. Following research, all the studies providing association between periodontal diseases and neurodegenerative diseases with quantitative measures were included in the study. Non-human studies, studies on patients below 18 year old, studies related to influence of treatment and in subjects already suffering from neurological disease were excluded. After removing duplicates, eligible studies were identified and data extracted by two reviewers to make ensure inter examiner reliability and to prevent data entry errors. Data from the studies were tabulated as study design, sample characteristics, diagnosis, exposure biomarkers/measures, outcomes and results. Methodological quality of studies was assessed by adapted Newcastle-Ottawa scale. Selection of study groups, comparability and exposure/outcome were used as parameters. Case-control and cohort studies were considered as high-quality studies if six or more stars were awarded out of nine maximum stars and four or more stars for cross-sectional studies out of six stars. Comparability among the groups was studied by taking into account primary factors for Alzheimer's disease such as age and sex and secondary factors like hypertension, osteoarthritis, depression, diabetes mellitus, and cerebrovascular disease. For cohort studies, 10 year follow up and dropout of <10% was considered to be successful. A total of 3693 studies were identified by two independent reviewers and finally 11 studies were included in the final analysis. Six cohort studies, three cross-sectional and two case-control studies were included after excluding remaining studies. Bias in studies was assessed by adapted Newcastle-Ottawa Scale. All included studies were of high methodological quality. Association between periodontitis and cognitive impairment was determined by using different criteria like International classification of disease, clinical measurement of periodontitis subjects, inflammatory biomarkers, microbes and antibodies. It was suggested that subjects with chronic periodontitis since 8 years or more, are at a higher risk of having dementia. Clinical measures of periodontal disease like probing depth, clinical attachment loss, alveolar bone loss were found to be positively associated with cognitive impairment. Inflammatory biomarkers and pre-existing elevated levels of serum IgG specific to periodontopathogens was reported to be associated with cognitive impairment. Within the limitations of the study, the authors concluded that though the patients with long-standing periodontitis are at greater risk for developing cognitive impairment by neurodegenerative diseases, the mechanism by which periodontitis can lead to cognitive impairment is still vague. Evidence suggests a strong association between periodontitis and cognitive impairment. Still further studies should be done to explore the mechanism involved.

Cognitive impairment in adults under compulsory psychiatric care: association with psychotic symptoms and high-dose antipsychotics

Background There is limited evidence on the association between cognitive function, psychotic symptoms and doses of antipsychotics in adults under compulsory psychiatric care. Aims We assessed (a) the degree of cognitive impairment in adults involuntarily hospitalised for compulsory psychiatric care and (b) correlation of Montreal Cognitive Assessment (MoCA) score with psychotic symptoms, polypharmacy and prescription of high-dose antipsychotics. Method This was a nationwide, cross-sectional study, conducted at the only referral state hospital for compulsory psychiatric care in Cyprus (December 2016–February 2018). Τhe MoCA was applied for the assessment of cognitive functioning. The Positive and Negative Syndrome Scale (PANSS) was applied for the assessment of psychotic symptoms. Results The sample comprised 187 men and 116 women. The mean MoCA score was 22.09 (reported scale range (RSR): 3–30); the mean PANSS general symptoms subscale score was 49.60 (RSR = 41–162). The participants who reported positive psychiatric history (mean 21.71, s.d. 5.37), non-adherence to pharmacotherapy (mean 21.32, s.d. 5.56) and prescription of high-dose antipsychotics (with medication prescribed as needed: mean 21.31, s.d. 5.70; without medication prescribed as needed: mean 20.71, s.d. 5.78) had lower mean MoCA scores compared with those who reported negative psychiatric history (mean 23.42, s.d. 4.51; P = 0.017), adherence to pharmacotherapy (mean 23.10, s.d. 6.61; P = 0.003) and no prescription of high-dose antipsychotics (with medication prescribed as needed: mean 22.56, s.d. 4.90; without medication prescribed as needed: mean 22.60 s.d. 4.94; P = 0.045–0.005), respectively. Mean MoCA score was mildly and inversely associated with total PANSS score (r = −0.15, P = 0.03), PANSS general (r = −0.18, P = 0.002) and PANSS negative (r = −0.16, P = 0.005) symptoms subscales, respectively. Conclusions Our findings support the evaluation of cognitive functioning in adults under compulsory psychiatric care via the MoCA tool, with focus on those prescribed high-dose antipsychotics, with positive mental health history and non-adherence to pharmacotherapy.

Blood Pressure, Incident Cognitive Impairment, and Severity of CKD: Findings From the Chronic Renal Insufficiency Cohort (CRIC) Study

Hypertension is a known risk factor for dementia and cognitive impairment. There are limited data on the relation of systolic blood pressure (SBP) and diastolic blood pressure (DBP) with incident cognitive impairment in adults with chronic kidney disease. We sought to identify and characterize the relationship among blood pressure, cognitive impairment, and severity of decreased kidney function in adults with chronic kidney disease. Longitudinal cohort study. 3,768 participants in the Chronic Renal Insufficiency Cohort (CRIC) Study. Baseline SBP and DBP were examined as exposure variables, using continuous (linear, per 10-mm Hg higher), categorical (SBP<120 [reference], 120 to 140,>140mm Hg; DBP<70 (reference), 70 to 80, > 80mm Hg) and nonlinear terms (splines). Incident cognitive impairment defined as a decline in Modified Mini-Mental State Examination (3MS) score to greater than 1 standard deviation below the cohort mean. Cox proportional hazard models adjusted for demographics as well as kidney disease and cardiovascular disease risk factors. The mean age of participants was 58±11 (SD) years, estimated glomerular filtration rate (eGFR) was 44mL/min/1.73m2 ± 15 (SD), and the median follow-up time was 11 (IQR, 7-13) years. In 3,048 participants without cognitive impairment at baseline and with at least 1 follow-up 3MS test, a higher baseline SBP was significantly associated with incident cognitive impairment only in the eGFR>45mL/min/1.73m2 subgroup (adjusted hazard ratio [AHR], 1.13 [95% CI, 1.05-1.22] per 10mm Hg higher SBP]. Spline analyses, aimed at exploring nonlinearity, showed that the relationship between baseline SBP and incident cognitive impairment was J-shaped and significant only in the eGFR>45mL/min/1.73m2 subgroup (P=0.02). Baseline DBP was not associated with incident cognitive impairment in any analyses. 3MS test as the primary measure of cognitive function. Among patients with chronic kidney disease, higher baseline SBP was associated with higher risk of incident cognitive impairment specifically in those individuals with eGFR>45mL/min/1.73m2. High blood pressure is a strong risk factor for dementia and cognitive impairment in studies of adults without kidney disease. High blood pressure and cognitive impairment are common in adults with chronic kidney disease (CKD). The impact of blood pressure on the development of future cognitive impairment in patients with CKD remains unclear. We identified the relationship between blood pressure and cognitive impairment in 3,076 adults with CKD. Baseline blood pressure was measured, after which serial cognitive testing was performed over 11 years. Fourteen percent of participants developed cognitive impairment. We found that a higher baseline systolic blood pressure was associated with an increased risk of cognitive impairment. We found that this association was stronger in adults with mild-to-moderate CKD compared with those with advanced CKD.

Association between urinary iodine excretion, genetic disposition and fluid intelligence in children, adolescents and young adults: the DONALD study

PurposeIodine deficiency increases the risk of cognitive impairment and delayed physical development in children. It is also associated with cognitive impairment in adults. Cognitive abilities are among the most inheritable behavioural traits. However, little is known about the consequences of insufficient postnatal iodine intake and whether the individual genetic disposition modifies the association between iodine intake and fluid intelligence in children and young adults.MethodsThe cultural fair intelligence test was used to assess fluid intelligence in the participants of the DONALD study (n = 238; mean age, 16.5 [SD = 7.7] years). Urinary iodine excretion, a surrogate iodine intake marker, was measured in 24-h urine. Individual genetic disposition (n = 162) was assessed using a polygenic score, associated with general cognitive function. Linear regression analyses were conducted to determine whether Urinary iodine excretion was associated with fluid intelligence and whether this association was modified by individual genetic disposition.ResultsUrinary iodine excretion above the age-specific estimated average requirement was associated with a five-point higher fluid intelligence score than that below the estimated average requirement (P = 0.02). The polygenic score was positively associated with the fluid intelligence score (β = 2.3; P = 0.03). Participants with a higher polygenic score had a higher fluid intelligence score.ConclusionUrinary iodine excretion above the estimated average requirement in childhood and adolescence is beneficial for fluid intelligence. In adults, fluid intelligence was positively associated with a polygenic score for general cognitive function. No evidence showed that the individual genetic disposition modifies the association between Urinary iodine excretion and fluid intelligence.

Peripheral and cerebral inflammation induced by repeated anesthesia and surgery do not cause impairment of learning and memory in middle‑aged mice.

Postoperative cognitive dysfunction is a postoperative complication of the central nervous system that reduces quality of life and increases mortality in perioperative patients, especially among elderly patients. Many studies have shown that the incidence of postoperative cognitive impairment in adults induced by one‑time anesthesia and surgery is very low, while multiple experiences of anesthesia and surgery can induce cognitive impairment in the developing brain. However, the effect of multiple experiences of anesthesia and surgery on cognitive function over a short period in middle‑aged mice, i.e., 6 to 8 months old, remains unclear. In this study, we explored whether the cognitive function of mice aged 6-8 months is impaired after multiple operations. Middle‑aged mice (6 to 8 months old) healthy male C57BL/6 mice underwent exploratory laparotomy under isoflurane anesthesia. Morris water maze testing was performed after the operations. Blood and brain samples were collected at 6 h, 24 h, and 48 h after the operations. Serum IL‑6, IL‑1, and S‑100β concentrations were detected by ELISA. The expressions of ChAT, AChE, and Aβ in the hippocampus were measured by western blot. Up‑regulation of Iba1 and GFAP, respectively, indicated activation of microglia and astrocytes in the hippocampus. Expression of Iba1 and GFAP was examined by immunofluorescence. The present results revealed that serum IL‑6, IL‑1β, and S‑100β concentrations were enhanced after multiple instances of anesthesia and surgery, and microglia and astrocytes in the hippocampus were activated. However, learning and memory were not impaired in the middle‑aged mice by multiple experiences of anesthesia and surgery. There were no changes in ChAT, AChE, and Aβ in the hippocampus after multiple experiences of anesthesia/surgery. Taken together, we suggest that although multiple anesthesia/surgery procedures can induce peripheral inflammation, neuroinflammation, and transient cerebral injury, it is insufficient to impair learning and memory in middle‑aged mice.