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The evidence regarding a potential link of low-to-moderate iodine deficiency, selenium status, and cadmium exposure during pregnancy with neurodevelopment is either contradicting or limited. We aimed to assess the prenatal impact of cadmium, selenium, and iodine on children's neurodevelopment at 4 years of age. The study included 575 mother—child pairs from the prospective \"Rhea\" cohort on Crete, Greece. Exposure to cadmium, selenium and iodine was assessed by concentrations in the mother's urine during pregnancy (median 13 weeks), measured by ICPMS. The McCarthy Scales of Children's Abilities was used to assess children's general cognitive score and seven different sub-scales. In multivariable-adjusted regression analysis, elevated urinary cadmium concentrations (≥0.8 μg/L) were inversely associated with children's general cognitive score [mean change: —6.1 points (95 % CI — 12; —0.33) per doubling of urinary cadmium; corresponding to ~0.4 SD]. Stratifying by smoking status (p for interaction 0.014), the association was restricted to smokers. Urinary selenium was positively associated with children's general cognitive score [mean change: 2.2 points (95 % CI —0.38; 4.8) per doubling of urinary selenium; ~0.1 SD], although the association was not statistically significant. Urinary iodine (median 172 μg/L) was not associated with children's general cognitive score. In conclusion, elevated cadmium exposure in pregnancy of smoking women was inversely associated with the children's cognitive function at pre-school age. The results indicate that cadmium may adversely affect neurodevelopment at doses commonly found in smokers, or that there is an interaction with other toxicants in tobacco smoke. Additionally, possible residual confounding cannot be ruled out.

Patients with 22q11 deletion syndrome (22q11DS) have a high prevalence of psychiatric disorders and intellectual disability. At present the neurobiology underlying psychopathology in 22q11DS is still not understood. In the present study, we analyzed urinary serotonergic, dopaminergic and noradrenergic markers in 67 adults with 22q11DS. Levels of serotonin and the catecholamine metabolite homovanillic acid were significantly lower in the 22q11DS subjects compared to healthy controls. Within the 22q11DS group, levels of dopamine, homovanillic acid, norepinephrine, vanillyl mandelic acid and serotonin positively correlated with Full Scale Intelligence Quotient scores. Our results suggest that cognitive deficits in 22q11DS are associated with abnormal function of several neurotransmitters.

Post-operative cognitive dysfunction (POCD), especially in elderly patients, has been reported in many studies. Although increasing age, duration of anesthesia, postoperative infections, and respiratory complications were regarded as the risk factors for POCD, no extracerebral diagnostic biomarkers have been identified as indicators of POCD. Ninety-five patients, ages 65–80 years, scheduled for major orthopedic or abdominal surgery were enrolled. Twenty-two patients aged between 20 and 40 years undergoing the same procedures served as controls. Subjects received neuropsychological tests one-day prior and one week post procedure. To determine the presence of POCD, the criteria were used as described in most previous studies. Morning urine samples were obtained one day before surgery and on day 1, day 2 and day 7 post operatively. Urine formaldehyde was determined with high-performance liquid chromatography. The urine formaldehyde level of all patients with and without POCD increased on the first 2 days after surgery. But the formaldehyde concentration (on day 7) in patients with POCD was significantly higher than that in patients without POCD ( p  < 0.01). In the young control group, no patient was diagnosed with POCD. Although the changes in urine formaldehyde of young patients during perioperative period were similar to those in elderly patients without POCD, the formaldehyde concentrations measured at four time points were all significantly lower than those in elderly patients ( p  < 0.05). Levels of urine formaldehyde were elevated in the perioperative period, with the highest levels at day 7 in patients with POCD. This suggests that the increase on day 7 may provide a new physiologic marker along with neuropsychological assessments to assist in the diagnosis of POCD.

Oxidative stress has been associated with mild cognitive impairment (MCI) and Alzheimer’s disease (AD). However, little is known about oxidative stress in postoperative cognitive dysfunction (POCD) in aging. The aim of this study was to investigate urinary excretion rate of 8-isoprostane:creatinine (U8-isoPG:Cr) and malonaldehyde:creatinine (UMDA:Cr) to predict short-term POCD in elderly patients undergoing general and orthopedic surgery. 72 patients aged above 65 years were enrolled in this prospective observational study. Each patient underwent cognitive testing to determine POCD performed by an investigator before surgery and 1 week after surgery. Morning urine was collected at baseline, 1, 2, and 7 days postoperatively. U8-isoPG was performed using enzymelinked immunosorbent assay (ELISA), and UMDA levels were measured by chemiluminescence detection. Creatinine levels were also analyzed if differences in the oxidative biomarkers were observed in the urine creatinine concentration. (1). Of 72 patients who completed cognitive testing, postoperative cognitive dysfunction was detected in 29.2 % (n = 21) of patients in 7 days. (2) U8-isoPG:Cr levels in 7 days postoperatively were significantly higher in POCD patients compared with the non-POCD group ( p  = 0.01). When measuring change from baseline, U8-isoPG:Cr levels were higher than that of control groups ( p  = 0.01). (3) UMDA:Cr levels were significantly elevated in 1 and 2 days postoperatively in both groups ( p  < 0.05). U8-isoPG:Cr level seems to be a valuable marker to detect lipid peroxidation early in POCD patients. However, it will also be important to take into account or reduce potential confounders to improve the identification of changes in the status of oxidative stress as a marker for POCD.

Background: Oxidative stress has been implicated in the pathogenesis of Alzheimer’s disease (AD). The pathobiological changes related to AD occur long before the overt clinical symptoms. The plasma lipid peroxidation enzyme F2-isoprostane has been suggested as a biomarker to detect the progression from mild cognitive impairment (MCI) to AD. Objective: To test whether plasma and urine F2-isoprostane was diagnostic for dementia in living people. Methods: Plasma and urine were collected from 222 Religious Orders Study participants with a clinical diagnosis of no cognitive impairment, MCI or AD at time of fluid collection. Isoprostane levels were determined using gas chromatography/mass spectroscopy. Results: Plasma and urine F2-isoprostane levels did not differ between the three clinical groups. Postmortem neuropathologic diagnosis of subjects who died during the course of the study was not associated with baseline blood or plasma F2-isoprostane levels. Conclusions: In living people, plasma or urine isoprostane levels were not sensitive enough to discriminate between individuals with a clinical diagnosis of no cognitive impairment, MCI or AD.

No abstract available Copyright © 2012 S. Karger AG, Basel [PUBLICATION ABSTRACT]

Dependent cocaine users consistently display cognitive deficits but cognitive performance of recreational cocaine users has rarely been investigated. To examine whether cognitive performance is impaired in relatively pure recreational and dependent cocaine users. The cognitive performance of recreational (n = 68) and dependent cocaine users (n = 30) was compared with the performance of stimulant-naive controls (n = 68) employing an extensive neuropsychological test battery. Moreover, the impact of attention-deficit hyperactivity disorder (ADHD) symptoms, craving and early age at onset was analysed. Dependent cocaine users display broad cognitive impairments in the domains of attention, working memory, declarative memory and executive functions. The performance of recreational cocaine users in all four domains was intermediate between that of controls and dependent users and they displayed significant deficits foremost in the domains of attention and working memory. In addition, ADHD symptoms, craving and age at onset were important modulators of cognitive function in cocaine users. Cognitive deficits occur at a recreational and non-dependent level of cocaine use. Cocaine use and ADHD seem to have mutually aggravating effects on cognitive impairment.

As a component of thyroid hormones, iodine is essential for fetal brain development. Although the UK has long been considered iodine replete, increasing evidence suggests that it might now be mildly iodine deficient. We assessed whether mild iodine deficiency during early pregnancy was associated with an adverse effect on child cognitive development. We analysed mother–child pairs from the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort by measuring urinary iodine concentration (and creatinine to correct for urine volume) in stored samples from 1040 first-trimester pregnant women. We selected women on the basis of a singleton pregnancy and availability of both a urine sample from the first trimester (defined as ≤13 weeks' gestation; median 10 weeks [IQR 9–12]) and a measure of intelligence quotient (IQ) in the offspring at age 8 years. Women's results for iodine-to-creatinine ratio were dichotomised to less than 150 μg/g or 150 μg/g or more on the basis of WHO criteria for iodine deficiency or sufficiency in pregnancy. We assessed the association between maternal iodine status and child IQ at age 8 years and reading ability at age 9 years. We included 21 socioeconomic, parental, and child factors as confounders. The group was classified as having mild-to-moderate iodine deficiency on the basis of a median urinary iodine concentration of 91·1 μg/L (IQR 53·8–143; iodine-to-creatinine ratio 110 μg/g, IQR 74–170). After adjustment for confounders, children of women with an iodine-to-creatinine ratio of less than 150 μg/g were more likely to have scores in the lowest quartile for verbal IQ (odds ratio 1·58, 95% CI 1·09–2·30; p=0·02), reading accuracy (1·69, 1·15–2·49; p=0·007), and reading comprehension (1·54, 1·06–2·23; p=0·02) than were those of mothers with ratios of 150 μg/g or more. When the less than 150 μg/g group was subdivided, scores worsened ongoing from 150 μg/g or more, to 50–150 μg/g, to less than 50 μg/g. Our results show the importance of adequate iodine status during early gestation and emphasise the risk that iodine deficiency can pose to the developing infant, even in a country classified as only mildly iodine deficient. Iodine deficiency in pregnant women in the UK should be treated as an important public health issue that needs attention. None.

It has been reported that disordered Cu metabolism is associated with several neurodegenerative diseases, including Alzheimer’s disease (AD) and Parkinson’s disease (PD). However, the underlying mechanism is still unclear. In this study, 4-week-old male mice were exposed to Cu by free-drinking water for three months. Then, the effects of Cu on cognitive functions in mice were tested by Morris water maze tests, and the potential mechanisms were investigated by the ELISA, immunochemistry, TUNEL, and Western blot tests. It was found that Cu exacerbates learning and memory impairment, and leads to Cu-overload in the brain and urine of mice. The results showed that Cu induces neuronal degeneration and oxidative damage, promotes the expression of apoptosis-related protein Bax, cuproptosis-related proteins FDX1 and DLAT and the proteotoxic stress marker HSP70, and decreases Fe-S cluster proteins. In addition, Cu affects the pre-synaptic and post-synaptic regulatory mechanisms through inhibiting the expression of PSD-95 and SYP. Cu also suppresses phosphorylation levels in CREB and decreases the expression of BDNF and TrkB in the mouse hippocampus. In conclusion, Cu might mediate cuproptosis, damage synaptic plasticity and inhibit the CREB/BDNF pathway to cause cognitive dysfunction in mice.

This study aims to identify neuropsychiatric manifestations in neurological Wilson disease (NWD), and their correlation with MRI changes and glutamate excitotoxicity. Forty-three consecutive patients with NWD from a tertiary care teaching hospital were evaluated prospectively who fulfilled the inclusion criteria. The neuropsychiatric evaluation was done using Neuropsychiatric Inventory (NPI) battery that assesses 12 domains including delusion, hallucination, agitation/aggression, dysphoria/depression, anxiety, euphoria, apathy, disinhibition, irritability, aberrant motor activity, appetite change, and abnormal nighttime behavior. Cranial MRI was done using a 3 T machine, and locations of signal changes were noted including the total number of MRI lesions. Serum glutamate level was measured by a fluorescence microplate reader. Abnormal NPI in various domains and total NPI scores were correlated with MRI lesions, serum and urinary copper, and glutamate level. The median age of the patients was 16 years. Forty-one (48.8%) patients had cognitive impairment and 37 (86%) had movement disorder. Neurobehavioral abnormality was detected in all—commonest being agitation (90.7%) followed by appetite change (81.4%), elation (74.4%), irritability (69.8%), anxiety (67.4%), depression (65.1%), apathy (44.2%), night time abnormal behavior (32.6%), aberrant motor behavior (20.9%), delusions (16.3%), and hallucination (18.6%). The thalamic lesion was associated with depression, globus pallidus with depression and anxiety, caudate with anxiety and agitation, brainstem with irritability, and frontal cortex with apathy. Serum glutamate level was higher in NWD. NPI sum score correlated with MRI load and glutamate level. Varying severity of neurobehavioral abnormalities are common in the patients with NWD and correlate with the location of MRI lesion and glutamate level.