Risk Of Impaired Cognitive Function Research Articles

Neighborhood disadvantage reduces cognitive reserve independent of neuropathologic change.

Individuals in socioeconomically disadvantaged neighborhoods exhibit increased risk for impaired cognitive function. Whether this association relates to the major dementia-related neuropathologies is unknown. This cross-sectional study included 469 autopsy cases from 2011 to 2023. The relationships between neighborhood disadvantage measured by Area Deprivation Index (ADI) percentiles categorized into tertiles, cognition evaluated by the last Mini-Mental State Examination (MMSE) scores before death, and 10 dementia-associated proteinopathies and cerebrovascular disease were assessed using regression analyses. Higher ADI was significantly associated with lower MMSE score. This was mitigated by increasing years of education. ADI was not associated with an increase in dementia-associated neuropathologic change. Moreover, the significant association between ADI and cognition remained even after controlling for changes in major dementia-associated proteinopathies or cerebrovascular disease. Neighborhood disadvantage appears to be associated with decreased cognitive reserve. This association is modified by education but is independent of the major dementia-associated neuropathologies.

Association between cortical thickness and cognitive ability in very preterm school-age children

Very preterm children, born before 32 weeks of gestation, are at risk for impaired cognitive function, mediated by several risk factors. Cognitive impairment can be measured by various neurodevelopmental assessments and is closely associated with structural alterations of brain morphometry, such as cortical thickness. However, the association between structural alterations and high-order cognitive function remains unclear. This study aimed to investigate the neurodevelopmental associations between brain structural changes and cognitive abilities in very preterm and full-term children. Cortical thickness was assessed in 37 very preterm and 24 full-term children aged 6 years. Cortical thickness analysis of structural T1-weighted images was performed using Advanced Normalization Tools. Associations between cortical thickness and the Wechsler Intelligence Scale for Children were evaluated by regression analysis based on ordinary least square estimation. Compared with full-term children, very preterm children showed significant differences in cortical thickness, variously associated with cognitive abilities in several brain regions. Perceptual reasoning indices were broadly correlated with cortical thickness in very preterm and full-term children. These findings provide important insights into neurodevelopment and its association with cortical thickness, which may serve as a biomarker in predictive models for neurodevelopmental diagnosis of high-order cognitive function.

Dietary Total Antioxidant Capacity and Cognitive Function in Older Adults in the United States: The NHANES 2011-2014.

Oxidative stress level takes part in the development of cognitive decline. However, the association between total antioxidant capacity (TAC) from diet and cognitive function is controversial. The aim of this study was to investigate the relationship between TAC and the cognitive function of older adults in the U.S. A cross-sectional study. National Health and Nutrition Examination Surveys database. 2712 older adults aged over 60 years. TAC was calculated from 8 antioxidative vitamins based on the reference values for vitamin C equivalent antioxidant capacity obtained from individuals' 24 h dietary recall. Four memory-related assessments were employed [Immediate Recall test (IRT), Delayed Recall test (DRT), Animal Fluency test (AFT), and Digit Symbol Substitution test (DSST)]. Among the 2712 participants, the median age was 68 years, and 50.4% were women. Participants in the group with higher TAC levels had relatively higher IRT, AFT and DSST scores (P=0.025, P=0.008, P<0.001, respectively). In adjusted weighted linear regression, log-transformed TAC was positively associated with AFT (β=1.10, 95%CI: 0.51, 1.70) and DSST (β=2.81, 95%CI: 1.16, 4.45). Compared with the first quartile, the participants in the second (Q2 vs. Q1, OR=0.66, 95%CI: 0.43,1.02) and fourth quartile (Q4 vs. Q1, OR=0.47, 95%CI:0.28, 0.78) of log-transformed TAC showed a decreased risk of impaired cognitive function (ICF) after adjusting for confounders. The dose-response analysis indicated a gradual descent in the risk of ICF as TAC increases. Diabetes mellitus (DM) mediated part of the effect of TAC on ICF. The relationship between TAC and ICF was more pronounced in subjects with DM (Q4 vs Q1, OR=0.36, 95%CI:0.17, 0.74). Our findings support that higher dietary antioxidant potential was related to a decreased risk of cognitive dysfunction, particularly in the subjects with DM who may have oxidative injury. DM was one of the factors mediating the effect of TAC on ICF.

The 2018 Japan Floods increased prescriptions of anti-dementia drugs among disaster victims: a retrospective cohort study based on a national health insurance database

BACKGROUND AND AIM: The occurrence of weather-related disasters is increasing with the progression of global climate change. Natural disasters increase the risk of impaired cognitive function of elderly victims. It is not clear what effects such natural disasters have on the prescriptions of drug treatment for dementia. Thus, we evaluated the effect of the 2018 Japan Floods, the second-largest water-related disaster in Japan, on the prescriptions of anti-dementia drugs (ADD) for elderly people. Methods: From the National Database of Health Insurance Claims, we extracted prescription data in Hiroshima, Okayama and Ehime prefectures for one year before and after the disaster. From the database, 1,710,119 people aged 65 years or over were selected as the study participants. Sex- and age-adjusted odds ratios (ORs) of victims for new ADD prescriptions were calculated using logistic regression models. A difference-in-difference analysis was conducted to take into account the trends for the ORs before the disaster. Furthermore, among continuous ADD users, the effects of disaster on the increasing trend for ADD prescriptions (daily dose or number of drug types) was also evaluated. Results: Of 1,710,119 people enrolled, 15,994 (0.9%) were recorded as a disaster-victims, and 112,289 (6.6%) were prescribed ADD. Among original non-users, victims were more likely to start using ADD after the disaster than non-victims [adjusted OR=1.33 (95% CI:1.16–1.52)]. Among continuous users, an increasing trend for ADD prescriptions was more often observed for victims than non-victims [1.61 (1.13–2.31)]. These associations were maintained even after considering the pre-disaster trend of ADD use. Conclusions: The natural disaster results in an increased number of users of anti-dementia medications. Special attention to such neurological shifts and welfare support is needed for elderly victims of a large-scale natural disaster.

Greater adolescent cognitive ability is linked to lower risk of cognitive impairment in later life

AbstractBackgroundThere have been few investigations of the role that adolescent cognitive ability might play in predicting who will later develop cognitive impairment. This is due, in part, to a lack of cohorts with early‐life cognitive assessment who have been followed to later adulthood. We capitalized on the 1960 Project Talent high school cohort to assess whether higher adolescent cognitive ability predicted lower risk of impaired cognitive function in older adulthood. A subsample of twin and non‐twin siblings allowed for assessment of whether these associations are due to shared family and genetic factors.MethodData come from the 1960 Project Talent (PT) baseline data collection (n&gt;360,000) and two follow‐ups: the Project Talent Twin &amp; Sibling (PTTS; n=2,491) Study and the Project Talent Aging Study (PTAS; n=6,421). The 1960 data collection assessed performance in multiple cognitive abilities (see Table 1). In 2018, participants/proxies reporting 2 or more symptoms of cognitive impairment on the AD8 Dementia Screener were classified as having a positive screen. Binary logistic generalized estimating equations assessed odds of a positive AD8 screen as a function of 1960 cognitive abilities. Models included age, race, sex, adolescent family SES, and adult educational attainment covariates. Co‐sibling control models examined whether associations remained when accounting for shared family and genetic characteristics.ResultsCovariate‐adjusted models indicated that each 1 SD higher adolescent cognitive ability predicted lower odds of a positive AD8 screen in later life for most ability domains (e.g., general cognitive ability OR = 0.86 (95% CI = 0.76, 0.98), see Table 1); associations were attenuated somewhat with inclusion of adult educational attainment in models. Preliminary co‐sibling control analyses indicated the persistence and strengthening of this association (OR = 0.57 (95% CI = 0.36, 0.91)).ConclusionFindings indicate that greater performance in multiple cognitive domains in adolescence predicts lower risk of cognitive impairment over 5 decades later. A co‐sibling control analysis indicated that the link between adolescent general cognitive ability and later‐life cognitive impairment is not simply due to shared family background and genetic factors. Ongoing analyses are assessing whether this is true for other cognitive domains and other indicators of cognitive function.

Fetal growth restriction impairs hippocampal neurogenesis and cognition via Tet1 in offspring.

Fetal growth restriction (FGR) increases the risk for impaired cognitive function later in life. However, the precise mechanisms remain elusive. Using dexamethasone-induced FGR and protein restriction-influenced FGR mouse models, we observe learning and memory deficits in adult FGR offspring. FGR induces decreased hippocampal neurogenesis from the early post-natal period to adulthood by reducing the proliferation of neural stem cells (NSCs). We further find a persistent decrease of Tet1 expression in hippocampal NSCs of FGR mice. Mechanistically, Tet1 downregulation results in hypermethylation of the Dll3 and Notch1 promoters and inhibition of Notch signaling, leading to reduced NSC proliferation. Overexpression of Tet1 activates Notch signaling, offsets the decline in neurogenesis, and enhances learning and memory abilities in FGR offspring. Our data indicate that a long-term decrease in Tet1/Notch signaling in hippocampal NSCs contributes to impaired neurogenesis following FGR and could serve as potential targets for the intervention of FGR-related cognitive disorders.

Incident Impaired Cognitive Function in Sarcopenic Obesity: Data From the National Health and Aging Trends Survey

ObjectivesThe prevalence of obesity with sarcopenia is increasing in adults aged ≥65 years. This geriatric syndrome places individuals at risk for synergistic complications that leads to long-term functional decline. We ascertained the relationship between sarcopenic obesity and incident long-term impaired global cognitive function in a representative US population. DesignA longitudinal, secondary data set analysis using the National Health and Aging Trends Survey. SettingCommunity-based older adults in the United States. ParticipantsParticipants without baseline impaired cognitive function aged ≥65 years with grip strength and body mass index measures. MethodsSarcopenia was defined using the Foundation for the National Institutes of Health Sarcopenia Project grip strength cut points (men <35.5 kg; women <20 kg), and obesity was defined using standard body mass index (BMI) categories. Impaired global cognition was identified as impairment in the Alzheimer's Disease-8 score or immediate/delayed recall, orientation, clock-draw test, date/person recall. Proportional hazard models ascertained the risk of impaired cognitive function over 8 years (referent = neither obesity or sarcopenia). ResultsOf the 5822 participants (55.7% women), median age category was 75 to 80, and mean grip strength and BMI were 26.4 kg and 27.5 kg/m2, respectively. Baseline prevalence of sarcopenic obesity was 12.9%, with an observed subset of 21.2% participants having impaired cognitive function at follow-up. Compared with those without sarcopenia or obesity, the risk of impaired cognitive function was no different in obesity alone [hazard ratio (HR) 0.98; 95% confidence interval (CI) 0.82–1.16]), but was significantly higher in sarcopenia (HR 1.60; 95% CI 1.42–1.80) and sarcopenic obesity (HR 1.20; 95% CI 1.03–1.40). There was no significant interaction term between sarcopenia and obesity. ConclusionsBoth sarcopenia and sarcopenic obesity are associated with an increased long-term risk of impaired cognitive function in older adults.

Correlation Between Cognitive Function Impairment and Chronic Kidney Disease With a Low Glomerular Filtration Rate at Sanglah Hospital Denpasar

BACKGROUND: Chronic kidney disease is a condition of chronic kidney damage with abnormal structure and function of the kidneys that lasts more than 3 months, accompanied or not by a decrease in glomerular filtration rate. Organic kidney disease leaves accumulated organic waste that cannot be removed by the kidneys. Furthermore, several biochemical and metabolic mechanisms such as chronic inflammation and oxidative stress can cause executive disorders.&#x0D; AIM: The aim of the study was to find out an increased risk of impaired cognitive function in patients with chronic kidney disease with a low glomerular filtration rate in Sanglah Hospital.&#x0D; METHOD: This study uses a retrospective case–control analytic observational study design. We included all patients with chronic kidney disease in Sanglah Hospital in December 2017–January 2018. This study involved 46 subjects with chronic kidney disease who met eligibility criteria, classified as a case group with cognitive impairment and a control group without cognitive impairment.&#x0D; RESULTS: Each decrease in glomerular filtration rate &lt; 30 ml/min/173 m2 in patients with chronic renal failure correlates with an increased incidence of cognitive impairment of around 15–25%. The risk of chronic kidney disease patients with glomerular filtration rate &lt; 30 ml/min/1.73 m2 decreased cognitive function 13 times compared to subjects with glomerular filtration rate &gt; 30 ml/min/ 1.73 m2.&#x0D; CONCLUSION: Low glomerular filtration rate correlate with increased risk of cognitive impairment.

Electroretinography may reveal cognitive impairment among a cohort of subjects at risk of a major psychiatric disorder

IntroductionAlmost a third of the offspring of parents diagnosed with schizophrenia or bipolar disorder could develop a mental disorder or related symptoms. The objectives of this study were to test the existence of two distinct subgroups of youth at-risk, according to their retinal response to luminance measured with electroretinography (ERG), and to relate the resulting cluster memberships with the cognitive clusters previously reported. MethodologyA clustering analysis was performed with ERG measurements in 107 at-risk offspring. Each subgroup was compared to a healthy control group of 203 individuals. The ERG subgroup memberships were then associated with the cognitive clusters. ResultsA two-cluster solution was obtained: HR-Cluster1 (n=53) showed a control-like ERG profile and HR-Cluster2 (n=54) showed reduced rod amplitudes and prolonged cone latencies of the b-wave. Subjects in the HR-Cluster2 were 2.7 times more likely to belong to the most detrimental cognitive subgroup than subjects in the HR-Cluster1 (49% Vs 18%). ConclusionAt-risk offspring showed two distinct ERG profiles: a control-like and an altered profile. A higher risk of impaired cognitive function was observed in subjects with the altered ERG profile, suggesting the ERG as a potential biomarker of susceptibility to mental illness among youth at risk.

Indole-3 acetic acid increased risk of impaired cognitive function in patients receiving hemodialysis

Patients receiving hemodialysis (HD) have a higher risk of cognitive impairment and dementia than the general population. The accumulation of uremic toxins in the brain causes uremic encephalopathy, however, limited data exists to elucidate the effect of protein-bound uremic toxins on cognitive function. Here we investigate the effect of indole-3 acetic acid (IAA) and hippuric acid (HA), two different protein-bound uremic toxins from amino acid derivatives, on cognitive function by Silico and in a clinical study. Prevalent HD patients were enrolled in two independent hospitals. Serum IAA and HA were measured using mass spectrometry. Cognitive performance was measured using Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), and Cognitive Abilities Screening Instrument (CASI) by trained psychologists. Using silico data to predict the effect of blood-brain barrier penetration was performed. The silico data demonstrated that IAA and HA had positive blood-brain barrier penetration ability. Amongst the 230 HD patients, serum IAA was associated with poor MMSE score (β= -0.90, 95% CI -1.61 to -0.19) and poor CASI score (β= -3.29, 95% CI -5.69 to -0.88) in stepwise multiple linear regression analysis. In logistic regression model, Serum IAA was also associated with cognitive impairment based on MMSE definition (OR, 1.96, 95% CI 1.10, 3.5) and CASI definition (OR, 2.09, 95% CI 1.21, 3.61). There was no correlation between Serum HA levels and cognitive function status. In conclusion, IAA, not HA, was associated with cognitive impairment in HD patients. Further large scale and prospective studies are needed to confirm our findings.

Brain-derived neurotrophic factor modulates neuronal network structure and dynamics in striatal cultures: Implications for Huntington's disease

Almost a third of the offspring of parents diagnosed with schizophrenia or bipolar disorder could develop a mental disorder or related symptoms. The objectives of this study were to test the existence of two distinct subgroups of youth at-risk, according to their retinal response to luminance measured with electroretinography (ERG), and to relate the resulting cluster memberships with the cognitive clusters previously reported.A clustering analysis was performed with ERG measurements in 107 at-risk offspring. Each subgroup was compared to a healthy control group of 203 individuals. The ERG subgroup memberships were then associated with the cognitive clusters.A two-cluster solution was obtained: HR-Cluster1 (n=53) showed a control-like ERG profile and HR-Cluster2 (n=54) showed reduced rod amplitudes and prolonged cone latencies of the b-wave. Subjects in the HR-Cluster2 were 2.7 times more likely to belong to the most detrimental cognitive subgroup than subjects in the HR-Cluster1 (49% Vs 18%).At-risk offspring showed two distinct ERG profiles: a control-like and an altered profile. A higher risk of impaired cognitive function was observed in subjects with the altered ERG profile, suggesting the ERG as a potential biomarker of susceptibility to mental illness among youth at risk.

Physically Active Diabetics Report Lower Rates of Impaired Cognitive Function—Findings from the 2012 National Health Interview Survey

Background: Diabetics are known to be at increased risk for impaired cognitive function (ICF). Some studies have suggested this risk may be reduced through physical activity. We examined associations among age, obesity, leisure time physical activity (LPA), and ICF in a large sample of U.S. diabetics. Methods: A secondary data analysis was conducted using data from the 2012 National Health Interview Survey (NHIS), which collects self-reported data on a variety of health-related constructs (n=32866). A logistic regression was used to investigate the associations between diabetes, obesity, LPA and ICF across three age groups: young adults (YA):18 to 38 year; middle-aged adults (MA):39-59 year; and older adults (OA): 60+ year. Results: All MAs (OR: 2.18 CI95%: 1.78-2.66) and OAs (OR: 3.62 CI95%: 3.02-4.35) in the total sample were more likely to report experiencing ICF than YAs. Obese YAs and MAs, but not OA, reported a slightly higher rate of ICF compared with non-obese peers within their age groups. Diabetes was strongly associated with ICF among YAs (OR: 3.25 CI95%:2.10- 5.01), MAs (OR: 3.57 CI95%:2.77- 4.61), and OAs (OR: 1.67 CI95%:1.41- 1.99). However, among diabetics, individuals who met weekly PA goals (guidelines from Office of Disease Prevention and Health Promotion) reported significantly lower rates of ICF, in all age groups: Among diabetic YAs 1.71% (CI95%: 0.16 -3.26%) of goal achievers reported ICF compared to 9.79% (CI95%: 5.84-13.73%) in inactive diabetic peers*. Among MAs it was 5.32% (CI95%: 3.11-7.53%) compared to 14.58% (CI95%: 11.64-17.52%)*; and among OAs it was 5.57% (CI95%: 3.78-7.37%) compared to 12.04% (CI95%: 10.33-13.75%)*. *: p&amp;lt;p=0.001. Conclusion: These findings support the hypothesis that both aging and diabetes increase risk of ICF. Obese YAs and MAs had slightly higher rates of ICF. Among diabetic individuals in all age groups, meeting PA guidelines was associated with significantly lower rates of ICF. Disclosure Z. Fu: None. M. Komelski: None. A. Kumar: None.

Prescribing antiepileptic drugs to women of reproductive age

The notion that use of antiepileptic drugs by pregnant women increases the risk for major congenital malformations is not new, but the oversimplification of grouping all antiepileptic drugs together into the same risk category is outdated. Data have accumulated to show the differential risks for major congenital malformations, with the highest risk consistently associated with in-utero valproate exposure. 1 Hernandez-Diaz S Smith CR Shen A et al. Comparative safety of antiepileptic drugs during pregnancy. Neurology. 2012; 78: 1692-1699 Crossref PubMed Scopus (399) Google Scholar The Neurodevelopmental Effects of Antiepileptic Drugs study also concluded that the highest risk for impaired cognitive function at 6 years of age occurs in the children of women who took valproate during pregnancy compared with other antiepileptic drug monotherapies. 2 Meador KJ Baker GA Browning N et al. Fetal antiepileptic drug exposure and cognitive outcomes at age 6 years (NEAD study): a prospective observational study. Lancet Neurol. 2013; 12: 244-252 Summary Full Text Full Text PDF PubMed Scopus (526) Google Scholar Reports from pregnancy registries have also revealed that the teratogenic risk for valproate is dose dependent, 3 Harden CL Meador KJ Pennell PB et al. Practice parameter update: management issues for women with epilepsy—focus on pregnancy (an evidence-based review): teratogenesis and perinatal outcomes: report of the Quality Standards Subcommittee and Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology and American Epilepsy Society. Neurology. 2009; 73: 133-141 Crossref PubMed Scopus (274) Google Scholar and it was tempting for physicians to not worry about the level of the so-called safe antiepileptic drugs, such as lamotrigine. However, a landmark paper in 2011 by the investigators of the EURAP international registry, 4 Tomson T Battino D Bonizzoni E et al. Dose-dependent risk of malformations with antiepileptic drugs: an analysis of data from the EURAP epilepsy and pregnancy registry. Lancet Neurol. 2011; 10: 609-617 Summary Full Text Full Text PDF PubMed Scopus (549) Google Scholar reporting on 3909 pregnancies exposed to the four most common antiepileptic drug monotherapies (carbamazepine, valproate, lamotrigine, and phenobarbital), showed that not only did the antiepileptic drug choice matter in determining the relative risk of major congenital malformations, but also the dose at conception, even for lamotrigine despite having the lowest risk. Comparative risk of major congenital malformations with eight different antiepileptic drugs: a prospective cohort study of the EURAP registryDifferent antiepileptic drugs and dosages have different teratogenic risks. Risks of major congenital malformation associated with lamotrigine, levetiracetam, and oxcarbazepine were within the range reported in the literature for offspring unexposed to antiepileptic drugs. These findings facilitate rational selection of these drugs, taking into account comparative risks associated with treatment alternatives. Data for topiramate and phenytoin should be interpreted cautiously because of the small number of exposures in this study. Full-Text PDF

Strong Association between Plasma Dipeptidyl Peptidase-4 Activity and Impaired Cognitive Function in Elderly Population with Normal Glucose Tolerance.

Objective: Inflammation, oxidative stress, and decreased glucagon-like peptide-1 (GLP-1) are risk factors for cognitive impairment. Dipeptidyl peptidase-4 (DPP4) was identified as a novel adipokine capable of enhancing these risk factors. Hence, we investigated the relationship between plasma DPP4 activity and impaired cognitive function in elderly Chinese population with normal glucose tolerance (NGT).Methods: We performed a cross-sectional study using data from 1229 elderly participants (60 years or older) in Guilin. Plasma DPP4 activity, oxidative stress parameters, fasting active GLP-1, and inflammatory markers were measured in all participants. Impaired cognitive function was diagnosed according to the National Institute on Aging-Alzheimer’s Association workgroups criteria.Results: Participants in the upper quartile of plasma DPP4 activity had higher C-reactive protein (CRP), interleukin-6 (IL-6), 8-iso-PGF2a, nitrotyrosine, and lower GLP-1 and Montreal Cognitive Assessment (MoCA) scores compared with those in the lowest quartile (P < 0.001). The odds ratios (ORs) for increased CRP, IL-6, 8-iso-PGF2a, nitrotyrosine, and decreased active GLP-1 were higher with increasing DPP4 quartiles after adjustment for confounders (all P < 0.001). In the highest DPP4 quartile, impaired cognitive function risk was higher (OR, 2.26; 95% confidence interval, 1.36–3.76) than in the lowest quartile after adjustment for potential confounders. The risk for impaired cognitive function increased more with higher levels of DPP4 activity, nitrotyrosine and 8-iso-PGF2a (P < 0.05), but not with higher IL-6, CRP or lower GLP-1.Conclusion: Plasma DPP4 activity is significantly and independently associated with impaired cognitive function, mainly executive, in elderly Chinese population with NGT. The underlying mechanisms for this association may be partly attributed to the effect of DPP4 on oxidative stress. Plasma DPP4 activity might serve as a risk biomarker or therapeutic target for the prevention and treatment of impaired cognitive function.

The Influence of Exercise on Cognitive Performance in Normobaric Hypoxia.

Although previous reports indicate that exercise improves cognitive function in normoxia, the influence of exercise on cognitive function in hypoxia is unknown. The purpose of this study was to determine if the impaired cognitive function in hypoxia can be restored by low to moderate intensity exercise. Sixteen young healthy men completed the ANAM versions of the Go/No-Go task (GNT) and Running Memory Continuous Performance Task (RMCPT) in normoxia to serve as baseline (B-Norm) (21% O2). Following 60 minutes of exposure to normobaric hypoxia (B-Hypo) (12.5% O2), these tests were repeated at rest and during cycling exercise at 40% and 60% of adjusted Vo2max. At B-Hypo, the % correct (p≤0.001) and throughput score (p≤0.001) in RMCPT were significantly impaired compared to B-Norm. During exercise at 40% (p=0.023) and 60% (p=0.006) of adjusted Vo2max, the throughput score in RMCPT improved compared to B-Hypo, and there was no significant difference in throughput score between the two exercise intensities. Mean reaction time also improved at both exercise intensities compared to B-Hypo (p≤0.028). Both peripheral oxygen saturation (Spo2) and regional cerebral oxygen saturation (rSo2) significantly decreased during B-Hypo (p≤0.001) and further decreased at 40% (p≤0.05) and 60% (p≤0.039) exercise. There was no significant difference in Spo2 or rSo2 between two exercise intensities. These data indicate that low to moderate exercise (i.e., 40%-60% adjusted Vo2max) may attenuate the risk of impaired cognitive function that occurs in hypoxic conditions.

Serum folate, vitamin B12 and cognitive impairment in Chilean older adults.

To analyse the relationship between serum folate (SF), vitamin B12 and impaired cognitive function in the Chilean elderly. We analysed the relationships between impaired cognitive function and age, SF (µg/l) and vitamin B12 (pg/ml) with Student's t test, as well as between impaired cognitive function and gender, educational level, residence area, diabetes and hypertension with the χ 2 test. Multiple logistic regressions with interactions were estimated to assess the impact of SF on impaired cognitive function according to these methods. Chile. Older adults (>65 years, n 1051), drawn from representative households of a national prevalence study, assessed using the Modified Mini Mental Status Examination (MMMSE). Individuals with altered MMMSE scores (≤13 points) were sequentially assessed using the Pfeffer Functional Activities Questionnaire (PFAQ). Multivariate models using the MMMSE demonstrated an increased risk of impaired cognitive function for seniors who had hypertension, diabetes and higher vitamin B12 levels. SF and its square (SF2) were statistically significant, indicating that this predictor of impaired cognitive function displays a U-shaped distribution. The interaction between SF and vitamin B12 was not statistically significant. Models using the MMMSE plus PFAQ suggested that urban residence decreased the risk of impaired cognitive function, whereas male gender, older age, vitamin B12 levels and hypertension increased this risk. The variables SF and SF2 and the SF × vitamin B12 interaction were statistically significant (P<0.05). The risk of impaired cognitive function depended on different combinations of SF and vitamin B12 levels. When SF was low, a one-unit increase in SF (1 µg/l) diminished the risk. When SF was elevated, a further increase in SF raised the risk, especially at low vitamin B12 levels. The relationship between folate, vitamin B12 and impaired cognitive function warrants further study.

Influence of nutrition and socioeconomic status on intellectual development in school children

Background: The nutritional adequacy is one of the determinants of quality of human resources everywhere. Malnutrition is the root cause for the death of 6 million children each year in developing countries. Nutritional deficiency is correlated with an increased risk of impaired cognitive function in children. Aims and Objective: To assess the role of nutrition and socioeconomic status on the development of IQ in school children. Materials and Methods: A cross-sectional, observational study was carried out in 200 primary school children aged 5–9 years of both the sexes. The children were grouped into five nutritional grades. The IQ was calculated using Kamat’s psychological tests for all the children. Results: The degree of malnutrition shows a definite reduction in IQ development, which is statistically significant. The study showed that declined socioeconomic status further decreases the development of IQ in school children. Conclusion: The study concluded that the nutritional status and the socioeconomic status significantly decline the mental and physical growth of children.

Impaired Cognitive Functioning in Patients with Tyrosinemia Type I Receiving Nitisinone

To examine cognitive functioning in patients with tyrosinemia type I treated with nitisinone and a protein-restricted diet. We performed a cross-sectional study to establish cognitive functioning in children with tyrosinemia type I compared with their unaffected siblings. Intelligence was measured using age-appropriate Wechsler Scales. To assess cognitive development over time, we retrieved sequential IQ scores in a single-center subset of patients. We also evaluated whether plasma phenylalanine and tyrosine levels during treatment was correlated with cognitive development. Average total IQ score in 10 patients with tyrosinemia type I receiving nitisinone was significantly lower compared with their unaffected siblings (71 ± 13 vs 91 ± 13; P = .008). Both verbal and performance IQ subscores differed (77 ± 14 vs 95 ± 11; P < .05 and 70 ± 11 vs 87 ± 15; P < .05, respectively). Repeated IQ measurements in a single-center subset of 5 patients revealed a decline in average IQ score over time, from 96 ± 15 to 69 ± 11 (P < .001). No significant association was found between IQ score and either plasma tyrosine or phenylalanine concentration. Patients with tyrosinemia type I treated with nitisinone are at risk for impaired cognitive function despite a protein-restricted diet.

Inflammation-initiating illnesses, inflammation-related proteins, and cognitive impairment in extremely preterm infants.

Neonatal inflammation is associated with perinatal brain damage. We evaluated to what extent elevated blood levels of inflammation-related proteins supplement information about the risk of impaired early cognitive function provided by inflammation-related illnesses. From 800 infants born before the 28th week of gestation, we collected blood spots on days 1, 7 and 14, for analysis of 25 inflammation-related proteins, and data about culture-positive bacteremia, necrotizing enterocolitis (Bell stage IIIb), and isolated perforation of the intestine, during the first two weeks, and whether they were ventilated on postnatal day 14. We considered a protein to be persistently or recurrently elevated if its concentration was in the top quartile (for gestational age and day blood was collected) on two separate days one week apart. We assessed the children at 2 years of age with the Bayley Mental Development Index (MDI). The combinations of NEC and ventilation on day 14, and of bacteremia and ventilation on day 14 consistently provided information about elevated risk of MDI <55, regardless of whether or not a variable for an elevated protein concentration was included in the model. A variable for a persistently or recurrently elevated concentration of each of the following proteins provided additional information about an increased risk of MDI <55: CRP, SAA, IL-6, TNF-alpha, IL-8, MIP-1beta, ICAM-1, E-SEL, and IGFBP-1. We conclude that elevated blood concentrations of inflammation-related proteins provide information about the risk of impaired cognitive function at age 2 years that supplements information provided by inflammation-associated illnesses.

Clinical Interaction between Brain and Kidney in Small Vessel Disease

Patients with chronic kidney disease (CKD) are well known to have a higher prevalence of cardiovascular disease from epidemiological studies. Recently, CKD has also been shown to be related to neurological disorders, not only ischemic brain injury but also cognitive impairment. This cerebrorenal connection is considered to involve small vessel disease in both the kidney and brain, based on their hemodynamic similarities. Clinical studies suggest that markers for CKD such as estimated glomerular filtration rate (eGFR), proteinuria, and albuminuria may be helpful to predict brain small vessel disease, white matter lesions (WMLs), silent brain ischemia (SBI), and microhemorrhages. Recently, changes in the vascular system of the brain have been shown to contribute to the onset and progression of cognitive impairment, not only vascular dementia but also Alzheimer's disease. Patients with CKD are also reported to have higher risk of impaired cognitive function in the future compared with non-CKD subjects. These results indicate that CKD markers may be helpful to predict the future risk of neuronal disease.