Predictors Of Cognitive Impairment Research Articles

Protocol for a construct and clinical validation study of MyCog Mobile: a remote smartphone-based cognitive screener for older adults

IntroductionAnnual cognitive screening in older adults is essential for early detection of cognitive impairment, yet primary care settings face time constraints that present barriers to routine screening. A remote cognitive...

Predictors of cognitive impairment and its association with mortality in maintenance hemodialysis patients: A prospective follow-up study

Objective: To determine predictors of cognitive impairment (CI) and its association with mortality in maintenance haemodialysis (MHD) patients.
 Methods: This prospective follow up study was conducted at HD Department, Mayo Hospital, Lahore from September, 2021 to November, 2022. All patients undergoing MHD for more than three months and having age between 18-65 years were included while those with dialysis duration less than three months, history of neuropsychiatric illness was excluded. Cognitive function was assessed using British Columbia Cognitive Complaints Inventory (BC-CCI) questionnaire. CI was defined on Likert scale as mild, moderate, and severe. Patients were followed up to one year regarding outcome measures.
 Results: One hundred and four patients were included in the study. Mean age was 45.86±11.11 years and Diabetes Mellitus (DM) was the most common cause of End Stage Renal Disease (ESRD) in 39(37.5%) patients. CI was found in 86(82.7%) patients in following order of severity: mild 61(58.7%), moderate 19(18.3%) and severe 6(5.9%). Increasing age (≥50 years), gender (female), Diabetes Mellitus (DM), unemployment and education <10th grade were found as significant predictors of CI (p<0.05). Significant positive correlations of CI score with age (r=0.338, p<0.001) and MHD duration (r=0.211, p=0.032) were found. However, the CI was not significantly associated with mortality (p=0.302).
 Conclusion: CI was common in MHD patients. Factors affecting CI were increasing age, female gender, DM, unemployment and low education level. CI was not associated with mortality in MHD patients.
 doi: https://doi.org/10.12669/pjms.40.5.7836
 How to cite this: Anees M, Pervaiz MS, Aziz S, Elahi I. Predictors of cognitive impairment and its association with mortality in maintenance hemodialysis patients: A prospective follow-up study. Pak J Med Sci. 2024;40(5):---------. doi: https://doi.org/10.12669/pjms.40.5.7836
 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Chronic Active Lesions and Larger Choroid Plexus Explain Cognition and Fatigue in Multiple Sclerosis.

Chronic inflammation may contribute to cognitive dysfunction and fatigue in patients with multiple sclerosis (MS). Paramagnetic rim lesions (PRLs) and choroid plexus (CP) enlargement have been proposed as markers of chronic inflammation in MS being associated with a more severe disease course. However, their relation with cognitive impairment and fatigue has not been fully explored yet. Here, we investigated the contribution of PRL number and volume and CP enlargement to cognitive impairment and fatigue in patients with MS. Brain 3T MRI, neurologic evaluation, and neuropsychological assessment, including the Brief Repeatable Battery of Neuropsychological Tests and Modified Fatigue Impact Scale, were obtained from 129 patients with MS and 73 age-matched and sex-matched healthy controls (HC). PRLs were identified on phase images of susceptibility-weighted imaging, whereas CP volume was quantified using a fully automatic method on brain three-dimensional T1-weighted and fluid-attenuated inversion recovery MRI sequences. Predictors of cognitive impairment and fatigue were identified using random forest. Thirty-six (27.9%) patients with MS were cognitively impaired, and 31/113 (27.4%) patients had fatigue. Fifty-nine (45.7%) patients with MS had ≥1 PRLs (median = 0, interquartile range = 0;2). Compared with HC, patients with MS showed significantly higher T2-hyperintense white matter lesion (WM) volume; lower normalized brain, thalamic, hippocampal, caudate, cortical, and WM volumes; and higher normalized CP volume (p from <0.001 to 0.040). The predictors of cognitive impairment (relative importance) (out-of-bag area under the curve [OOB-AUC] = 0.707) were normalized brain volume (100%), normalized caudate volume (89.1%), normalized CP volume (80.3%), normalized cortical volume (70.3%), number (67.3%) and volume (66.7%) of PRLs, and T2-hyperintense WM lesion volume (64.0%). Normalized CP volume was the only predictor of the presence of fatigue (OOB-AUC = 0.563). Chronic inflammation, with higher number and volume of PRLs and enlarged CP, may contribute to cognitive impairment in MS in addition to gray matter atrophy. The contribution of enlarged CP in explaining fatigue supports the relevance of immune-related processes in determining this manifestation independently of disease severity. PRLs and CP enlargement may contribute to the pathophysiology of cognitive impairment and fatigue in MS, and they may represent clinically relevant therapeutic targets to limit the impact of these clinical manifestations in MS.

Prediction of cognitive impairment using higher order item response theory and machine learning models.

Timely detection of cognitive impairment (CI) is critical for the wellbeing of elderly individuals. The MyCog assessment employs two validated iPad-based measures from the NIH Toolbox® for Assessment of Neurological and Behavioral Function (NIH Toolbox). These measures assess pivotal cognitive domains: Picture Sequence Memory (PSM) for episodic memory and Dimensional Change Card Sort Test (DCCS) for cognitive flexibility. The study involved 86 patients and explored diverse machine learning models to enhance CI prediction. This encompassed traditional classifiers and neural-network-based methods. After 100 bootstrap replications, the Random Forest model stood out, delivering compelling results: precision at 0.803, recall at 0.758, accuracy at 0.902, F1 at 0.742, and specificity at 0.951. Notably, the model incorporated a composite score derived from a 2-parameter higher order item response theory (HOIRT) model that integrated DCCS and PSM assessments. The study's pivotal finding underscores the inadequacy of relying solely on a fixed composite score cutoff point. Instead, it advocates for machine learning models that incorporate HOIRT-derived scores and encompass relevant features such as age. Such an approach promises more effective predictive models for CI, thus advancing early detection and intervention among the elderly.

Serum level of YWHAG as a diagnostic marker of cognitive impairment in Parkinson's disease patients.

Identifying reliable biomarkers for early detection and prediction of cognitive impairment in Parkinson's disease (PD) is crucial for optimal patient care. This study set out to investigate the potential of YWHAG as a diagnostic biomarker for cognitive impairment in PD. We enrolled a total of 331 PD patients and selected 241 patients that met the criteria for cognitive impairment analysis. The patients were classified into three groups: PD-NC: PD patients with normal cognition, PD-MCI: PD patients with mild cognitive impairment, and PD-D: PD patients with dementia. ELISA was employed to assess YWHAG expression, as well as the neurofilament light chain (NfL). Additionally, cognitive impairment was evaluated using MoCA scores. Correlation analysis and receiver operating curve analysis (ROC) were performed to clarify the relationship between YWHAG expression and cognitive impairment. Our findings revealed a significant upregulation of YWHAG expression in both the PD-MCI and PD-D groups compared to the PD-NC group. This observation aligned with the elevated expression of NfL in the PD-MCI and PD-D groups. YWHAG and NfL expression levels displayed negative correlations with MoCA scores and positive associations with age. Furthermore, ROC curve analysis demonstrated the diagnostic efficacy of YWHAG expression in distinguishing individuals with PD-NC, PD-MCI, and PD-D. Our findings indicate that YWHAG could serve as a promising biomarker for cognitive impairment in PD. The upregulation of YWHAG expression in PD-MCI and PD-D groups, its association with cognitive impairment, and its correlations with MoCA scores and NfL levels support its potential clinical utility.

HEARING LOSS AS A MODIFIABLE RISK FACTOR FOR DEMENTIA IN UK BIOBANK

Abstract Age-related hearing loss is a predictor of cognitive impairment and dementia. The mechanisms of the observed associations are unclear but could involve depletion of cognitive reserve, the occupation of cognitive resources, and lack of sensory input to the brain. Hearing loss may therefore represent a preventable or treatable causative risk factor for dementia. Indeed, many studies report on lower rates of cognitive decline among hearing aid users when compared to non-users. However, most investigations to date have been observational or with relatively short follow-ups, thus precluding clear interpretations of the underlying mechanism. In our study using UK Biobank data with n=502,386 participants followed up from ~2008 to 2021, we emulate a randomised clinical trial to probe the role of initiating the use of hearing aids in people with conductive hearing loss or with self-reported hearing difficulties in the diagnosis dementia. Diagnosis of dementia was ascertained through hospital and death records, and self-reports in such a way as to increase the positive predictive value. Among participants with hearing loss or hearing difficulties, 2,914 (2.1%) were diagnosed with dementia, compared to 4,982 (1.4%) in those without hearing loss or hearing difficulties. Additional results on the relationship between hearing aid use and dementia, and stratified analyses by sex/gender and ethnicity will be presented. We discuss the modifiability of hearing loss and recommend studies with longer follow-ups to determine the efficacy of hearing loss interventions in reducing the risk of cognitive decline and dementia.

Association of cognitive impairment and arterial hypertension

Impaired cognitive function (CF) is a common manifestation of brain damage as a target organ of arterial hypertension (AH). The presence of hypertension in middle age increases the risk of developing cognitive impairment (CI) and dementia in old age. At the same time, changes in certain indicators characteristic of AH may serve as predictors of CI and dementia in the future. The review presents data on the effects of endothelial dysfunction and increased arterial stiffness on CF. The small number of papers on the effects of hypertension in middle-aged people on the development of CI emphasizes the importance of investigating this topic, as the incidence of CI in young and middle-aged people has increased in recent years.

Thalamic Atrophy, Duration of Illness, and Years of Education are the Best Predictors of Cognitive Impairment in Multiple Sclerosis

Thalamic Atrophy, Duration of Illness, and Years of Education are the Best Predictors of Cognitive Impairment in Multiple Sclerosis

Developing a DNAm Surrogate to Predict Cognitive Functioning among Older Adults

AbstractBackgroundBlood‐based epigenetic measures are being developed and used to predict aging‐related health outcomes. Specifically, researchers have developed “epigenetic clocks” based on predictions of chronological age and age‐related health declines by DNA methylation. However, these markers are meant to predict aging per se and are not disease specific. Recently, scholars have developed “DNAm surrogates” to predict specific outcomes. This methodological technique has yet to be applied to cognitive functioning despite its potential to improve prediction of cognitive health in later life and provide insight into the role of biological aging.MethodThis study developed a novel DNAm surrogate measure for cognitive functioning (DNAmCogScore) based on an elastic net approach linking using 833,865 CpG sites predicting the Telephone Interview Cognitive Status score (TICS) available in the Health and Retirement Study (HRS), a nationally representative sample of older adults in the United States. Additionally, we evaluate the association of this DNAm surrogate and other neuropathology biomarkers. We used used ridge regression to create DNAmCogScore with 50% of the sample for training and 50% for testing (N = 2009 for each subsample). The Irish Longitudinal Study of Aging (TILDA) will be used for validation (results forthcoming).ResultWe find a positive association and modest predictive value between DNAmCogScore and TICS (see Figure 1, r = .4). Table 1 shows the strong associations with the DNAmCogScore and demographic characteristics. Overall, we find a strong positive coefficient between DNAmCogScore with attenuation after controlling for demographic characteristics, from 1.12 in Model 1 to .20 in Model 3, but remaining statistically significant throughout. Table 3 shows modest negative correlations between DNAmCogScore and NfL, pTau181, and GFAP (ranging from ‐.24 to ‐.36) and no correlation with AB42:40.ConclusionThis study is among the first to create a DNA methylation surrogate measure of cognitive functioning. Our measure is associated with cognitive functioning, even after adjusting for key demographic characteristics. And it has the expected association with other more neuropathology biomarkers. Overall, it suggests that changes in DNA methylation may be a molecular‐level mechanisms by which biological aging impacts cognitive health, and this measure may provide useful prediction of cognitive impairment before the onset of symptoms.

Usefulness of Serum Translocator Protein as a Potential Predictive Biochemical Marker of Three-Month Cognitive Impairment After Acute Intracerebral Hemorrhage: A Prospective Observational Cohort Study.

Translocator protein (TSPO) is a biomarker of neuroinflammation and brain injury. This study aimed to ascertain the potential of serum TSPO as a predictor of cognitive impairment after acute intracerebral hemorrhage (ICH). In this prospective observational cohort study, 276 patients with supratentorial ICH were randomly assigned to two groups (184 patients in the study group and 92 in the validation group) in a 2:1 ratio. Serum TSPO levels were gauged at admission, and cognitive status was assessed using the Montreal Cognitive Assessment Scale (MoCA) post-stroke 3 months. A MoCA score of < 26 was considered indicative of cognitive impairment. Serum TSPO levels were inversely correlated with MoCA scores (ρ=-0.592; P<0.001). Multivariate linear regression analysis showed that serum TSPO levels were independently associated with MoCA scores (β, -0.934; 95% confidence interval (CI), -1.412--0.455; VIF, 1.473; P<0.001). Serum TSPO levels were substantially higher in patients with cognitive impairment than in the remaining patients (median, 2.7 versus 1.6 ng/mL; P<0.001). Serum TSPO levels were linearly correlated with the risk of cognitive impairment under a restricted cubic spline (P=0.325) and independently predicted cognitive impairment (odds ratio, 1.589; 95% CI, 1.139-2.216; P=0.016). Subgroup analysis showed that the relationship between serum TSPO levels and cognitive impairment was not markedly influenced by other parameters, such as age, sex, drinking, smoking, hypertension, diabetes mellitus, body mass index, and dyslipidemia (all P for interaction > 0.05). The model, which contained serum TSPO, National Institutes of Health Stroke Scale scores and hematoma volume, performed well under the receiver operating characteristic curve, calibration curve and decision curve, and using the Hosmer-Lemeshow test. This model was validated in the validation group. Serum TSPO level upon admission after ICH was independently associated with cognitive impairment, substantializing serum TSPO as a reliable predictor of post-ICH cognitive impairment.

HLA-C*07:01 and HLA-DQB1*02:01 protect against white matter hyperintensities and deterioration of cognitive function: A population-based cohort study

BackgroundNeuroinflammation and aberrant immune regulation are increasingly implicated in the pathophysiology of white matter hyperintensities (WMH), an imaging marker of cerebrovascular pathologies and predictor of cognitive impairment. The role of human leukocyte antigen (HLA) genes, critical in immunoregulation and associated with susceptibility to neurodegenerative diseases, in WMH pathophysiology remains unexplored. MethodsWe performed association analyses between classical HLA alleles and WMH volume, derived from MRI scans of 38 302 participants in the UK Biobank. To identify independent functional alleles driving these associations, we conducted conditional forward stepwise regression and lasso regression. We further investigated whether these functional alleles showed consistent associations with WMH across subgroups characterized by varying levels of clinical determinants. Additionally, we validated the clinical relevance of the identified alleles by examining their association with cognitive function (n = 147 549) and dementia (n = 460 029) in a larger cohort. FindingsFour HLA alleles (DQB1*02:01, DRB1*03:01, C*07:01, and B*08:01) showed an association with reduced WMH volume after Bonferroni correction for multiple comparisons. Among these alleles, DQB1*02:01 exhibited the most significant association (β = −0.041, 95 % CI: −0.060 to −0.023, p = 1.04 × 10−5). Forward selection and lasso regression analyses indicated that DQB1*02:01 and C*07:01 primarily drove this association. The protective effect against WMH conferred by DQB1*02:01 and C*07:01 persisted in clinically relevant subgroups, with a stronger effect observed in older participants. Carrying DQB1*02:01 and C*07:01 was associated with higher cognitive function, but no association with dementia was found. InterpretationOur population-based findings support the involvement of immune-associated mechanisms, particularly both HLA class I and class II genes, in the pathogenesis of WMH and subsequent consequence of cognitive functions.

Depressive Symptomatology as a Predictor of Cognitive Impairment: Evidence from the Korean Longitudinal Study of Aging (KLOSA), 2006-2020.

Depressive symptoms are recognized as risk factors for cognitive impairment with intricate underlying biological mechanisms. We explored the link between depressive symptoms and cognitive impairment onset; we also assessed how this association is influenced by educational levels. This study included 5843 individuals aged ≥45 years, comprising 27,908 observations from 2006 to 2020. Based on repeated measurements of each participant, we estimated the association between depressive symptoms and cognitive impairment onset after a 2-year follow-up by using generalized estimating equations. The incidence rate was 9.4% among those individuals without depressive symptoms, which was in contrast with a rate of 21.0% among those individuals experiencing depressive symptoms. The odds ratio (OR) (95% confidence interval [CI]) for the association between depressive symptoms and cognitive impairment onset in the overall sample was 1.61 (1.47-1.76). This association was more pronounced among individuals with higher educational levels. Specifically, the OR (95% CI) of the association between depressive symptoms and cognitive impairment was highest among individuals with a college education (2.60 [1.78-3.81]), and the association was lowest among individuals with elementary or no education levels (1.45 [1.28-1.63]). Our findings highlight the idea that although individuals with higher educational backgrounds exhibit a diminished risk of cognitive impairment, the detrimental impacts of depressive symptoms on cognitive performance are particularly more pronounced within this group.

Serum levels of 25-OH vitamin D levels predict cognitive impairments among acute coronary syndrome patients.

The cognitive impairment after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS) has become a crucial clinical concern that cannot be ignored. However, studies on the early warning factors of cognitive impairment after PCI are still insufficient. This study reviewed the postoperative cognitive function of 284 patients who underwent PCI in our hospital from June 2019 to June 2022. During the 21-day follow-up, all participants included in the analysis were divided into the cognitive impairment (CI) group (n = 82) and the noncognitive impairment (NCI) group (n = 186) according to their Montreal cognitive assessment (MoCA) scale. Participants' serum 25(OH)D3 levels on admission and serum neuron-specific enolase (NSE), glial fibrillary acidic protein (GFAP) and S100β levels were measured 21 days after surgery. Age more than 65 years, hypertension, operation time longer than 60 min, left ventricular ejection fraction less than 50% and serum 25(OH)D3 less than 31.41 ng/ml were the risk factors for cognitive dysfunction in ACS patients 21 days after PCI. Serum levels of 25(OH)D3, NSE, S100β and GFAP were significantly higher in patients with cognitive impairment than in patients without cognitive impairment. Postoperative serum NSE, S100β and GFAP levels were significantly negatively correlated with serum 25(OH)D3 levels at admission. The serum 25(OH)D3 level is a risk factor and predictor of cognitive impairment in patients with ACS after PCI.

Cognitive impairment and dementia in young onset Parkinson's disease.

Patients with young-onset Parkinson's disease (YOPD) have a slower progression. Our aim was to analyze the change in cognitive function in YOPD compared to patients with a later onset and controls. Patients with Parkinson's disease (PD) and controls from the COPPADIS cohort were included. Cognitive function was assessed with the Parkinson's Disease Cognitive Rating Scale (PD-CRS) at baseline (V0), 2-year ± 1month (V2y), and 4-year ± 3months follow-up (V4y). Regarding age from symptoms onset, patients were classified as YOPD (< 50years) or non-YOPD (≥ 50). A score in the PD-CRS < 81 was defined as cognitive impairment (CI): ≤ 64 dementia; 65-80 mild cognitive impairment (MCI). One-hundred and twenty-four YOPD (50.7 ± 7.9years; 66.1% males), 234 non-YOPD (67.8 ± 7.8years; 59.3% males) patients, and 205 controls (61 ± 8.3years; 49.5% males) were included. The score on the PD-CRS and its subscore domains was higher at all visits in YOPD compared to non-YOPD patients and to controls (p < 0.0001 in all analysis), but no differences were detected between YOPD patients and controls. Only non-YOPD patients had significant impairment in their cognitive function from V0 to V4y (p < 0.0001). At V4y, the frequency of dementia and MCI was 5% and 10% in YOPD compared to 25.2% and 22.3% in non-YOPD patients (p < 0.0001). A lower score on the Parkinson's Disease Sleep Scale at baseline was a predictor of CI at V4y in YOPD patients (Adjusted R2 = 0.61; OR = 0.965; p = 0.029). Cognitive dysfunction progressed more slowly in YOPD than in non-YOPD patients.

Predictor of cognitive impairment: metabolic syndrome or circadian syndrome

BackgroundIt was reported that metabolic syndrome increases the risk for cognitive impairment and circadian rhythm may influence cognition behavior. Identifying the potential risk factors is essential to screen individuals with neuronal dysfunction, neuronal loss, and cognitive decline and prevent cognitive impairment and dementia development.MethodsWe clarified participants by the presence of metabolic syndrome (MetS) and circadian syndrome (CircS) and employed three multivariable Generalized Estimating Equation (GEE) models to control the potential confounding factors and estimate the β values for cognitive function using as referents those had neither MetS nor CircS at baseline. The cognitive function consists of episodic memory and executive function was estimated via the modified Telephone Interview for Cognitive Status (TICS) every two years until 2015.ResultsThe mean age of the participants was 58.80 (8.93) years and 49.92% (male). The prevalence of MetS and CircS was 42.98% and 36.43%, respectively. 1,075 (11.00%) and 435 (4.45%) participants had either MetS or CircS alone and 3,124 (31.98%) had both CircS and MetS. Participants with both MetS and CircS compared with normal had a significantly decreased cognitive function score during the 4-years cohort (β = -0.32, 95% CI: -0.63, -0.01) with the complete model, as well as among participants who suffered from CircS alone (β = -0.82, 95% CI: -1.47, -0.16), while not among participants with MetS alone (β = 0.13, 95% CI: -0.27, 0.53). Specifically, compared with the normal population a significantly lower score was discovered in the episodic memory (β = -0.51, 95% CI: -0.95, -0.07), while slightly lower in executive function (β = -0.33, 95% CI: -0.68, -0.01) among individuals with CircS alone.ConclusionsIndividuals with CircS alone or both MetS and CircS have a high risk of cognitive impairment. The association was even stronger in participants with CircS alone than those with both MetS and CircS, suggesting CircS probably have a stronger association with cognitive functioning than MetS and could be a better predictor for cognitive impairment.

Frequency, pattern and predictors of cognitive impairments in patients with Parkinson's disease using the Community Screening Instrument for Dementia.

Parkinson's disease (PD) is a chronic neurodegenerative disorder complicated by cognitive dysfunctions which are associated with increased caregiver burden, pressure on community health facilities, and mortality in affected patients. Most of the data concerning cognitive dysfunctions in PD are from studies conducted in Europe and North America, but there is paucity of data from Sub-Saharan Africa. The objective of this study is to determine the frequency, pattern and predictors of cognitive impairments amongst patients with Parkinson's disease. This was a cross sectional case control study carried out at a tertiary health facility in South-south Nigeria. Participants with PD were consecutively recruited from the neurology outpatient clinics. Demographic and disease-specific data were obtained with the use of a pre-tested questionnaire. Cognitive performance of thirty patients with PD were compared with thirty demographically matched controls using the Community Screening Instrument for Dementia (CSID). CSID was already validated among Nigerians. The frequency of cognitive impairment using the CSID was 50% for PD patients (3.3% for controls). Poor cognitive performance was observed across several cognitive domains including language, executive dysfunction, psychomotor speed, and constructional apraxia among PD patients. The independent predictors of the overall cognitive impairment in patients with PD determined by logistic regression analysis include recall deficiency (p = 0.007), impairment with naming (p = 0.044), apraxia (p = 0.003), Hoen&Yahr staging (p = 0.046), UPDRS score (p = 0.015) and age at presentation (p = 0.014). Cognitive impairments occur more frequently in patients with PD compared to controls. This study also demonstrated the predictive role of severity of disease based on Hoehn &Yahr staging and UPDRS score, and presence of recall deficiency, poor naming ability and apraxia.

Cognitive impairment in Neuromyelitis Optica Spectrum Disorder: A retrospective study using the Brief International cognitive Assessment for Multiple Sclerosis (BICAMS)

Background Neuromyelitis Optica Spectrum Disorder (NMOSD) is an inflammatory disease of the central nervous system. The study aimed to characterize the neuropsychological profile of NMOSD by comparing them with multiple sclerosis (MS) patients and healthy controls. Method Sixty-four participants were included:19 NMOSD, 27 MS, and 18 healthy controls. The neuropsychological protocol included the Portuguese version of Montreal Cognitive Assessment, the Brief International Cognitive Assessment for Multiple Sclerosis (BICAMS), Verbal Fluency (phonemic and semantic), the Hospital Anxiety and Depression Scale, and the Expanded Disability Status Scale for clinical groups. Results NMOSD patients had significant lower cognitive performance when compared to HC mainly in information processing speed, concentration, language processing, and in executive functions (cognitive flexibility, sustained, and divided attention). No significant differences were observed between NMOSD and MS patients. Three predictors for cognitive impairment, according to BICAMS criteria, were found: depression, disease duration, and the level of disability. Conclusion The neuropsychological profile found in the present study for NMOSD is consistent with the previous findings. Information regarding the predictors of cognitive impairment in both diseases and their different associations are important for future research and for guiding interventions more suitable for the neuropsychological needs of affected patients.

Eye Movement Latency Coefficient of Variation as a Predictor of Cognitive Impairment: An Eye Tracking Study of Cognitive Impairment.

Studies demonstrated impairment in the control of saccadic eye movements in Alzheimer's disease (AD) and people with mild cognitive impairment (MCI) when conducting the pro-saccade and antisaccade tasks. Research showed that changes in the pro and antisaccade latencies may be particularly sensitive to dementia and general executive functioning. These tasks show potential for diagnostic use, as they provide a rich set of potential eye tracking markers. One such marker, the coefficient of variation (CV), is so far overlooked. For biological markers to be reliable, they must be able to detect abnormalities in preclinical stages. MCI is often viewed as a predecessor to AD, with certain classifications of MCI more likely than others to progress to AD. The current study examined the potential of CV scores on pro and antisaccade tasks to distinguish participants with AD, amnestic MCI (aMCI), non-amnesiac MCI (naMCI), and older controls. The analyses revealed no significant differences in CV scores across the groups using the pro or antisaccade task. Antisaccade mean latencies were able to distinguish participants with AD and the MCI subgroups. Future research is needed on CV measures and attentional fluctuations in AD and MCI individuals to fully assess this measure's potential to robustly distinguish clinical groups with high sensitivity and specificity.

Could olfactory identification be a prognostic factor in detecting cognitive impairment risk in the elderly?

Aging contributes to the deterioration of the olfactory system in humans. Several studies indicate that the olfactory identification test alone may function as a screening test for olfactory dysfunction and they are more feasible to apply in clinical practice. Olfactory identification may be a predictor for cognitive impairment. Multiple studies have considered the use of odor identification as a measure to identify the conversion from normality to mild cognitive impairment or dementia. The objectives were (i) to elucidate the associations between cognitive status and olfactory identification performance in aging; (ii) understand the predictive value of olfactory capacity in identifying subjects with cognitive impairment risk; and (iii) to study how cognitive status and olfactory identification relate with other variables of wellness in aging, such as functional capabilities and clinical measures. For this purpose, a group of 149 participants (77.15 ± 7.29 years; 73 women of 76.7 ± 8 years and 76 men of 77.6 ± 6.52 years) were recruited and were subjected to a sociodemographic questionnaire, a psychological screening tool of general cognitive status, an olfactory identification evaluation, and clinical measures. The participants were divided into groups based on their cutoff scores of previous scientific reports about the Spanish version of Montreal Cognitive Assessment. Our results indicate an age-associated decline in olfactory identification ability and intensity of odor perception. The predictive ability of olfactory identification scores for the risk of mild and severe impairment is around 80%. Olfactory identification decreases with cognitive function. Performance in odor identification is associated with impairment of episodic memory and executive functions. These findings further our current understanding of the association between cognition and olfaction, and support olfactory assessment in screening those at higher risk of dementia.

Предикторы когнитивных нарушений при мальформациях коркового развития

Введение. Мальформации коркового развития (МКР) – большая гетерогенная группа заболеваний, характеризующаяся нарушением формирования коры головного мозга. Клинические проявления представлены эпилепсией, когнитивными и двигательными нарушениями. Цель. Установить факторы, определяющие развитие когнитивных нарушений (КН) у детей с МКР. Материалы и методы. Проанализированы данные о 115 пациентах с МКР: 61 – мужского пола, 54 – женского пола. Средний возраст пациентов составил 11,0 [IQR: 7,0; 16,0] года. В зависимости от варианта мальформации были сформированы следующие группы: 56 (48,7%) человек имели фокальную кортикальную дисплазию, 4 (3,5%) – гемимегалэнцефалию, 22 (19,1%) – гетеротопию, 12 (10,4%) – лиссэнцефалию и 21 (18,2%) – полимикрогирию. Результаты. Интеллектуальная недостаточность была диагностирована у 62 (53,9%) пациентов: у 24 (20,9%) – легкая, у 17 (14,8%) – умеренная, у 10 (8,7%) – тяжелая и у 11 (9,6%) – глубокая. Согласно результатам однофакторного анализа установлена зависимость развития КН от таких факторов, как ранний возраст дебюта эпилепсии (рМанна-Уитни=0,001), частота приступов (рМанна-Уитни=0,042), наличие инфантильных спазмов (рХи-квадрат&lt;0,001) и эпилептического статуса в анамнезе (рХи-квадрат=0,022), фармакорезистентное течение эпилепсии (рХи-квадрат&lt;0,001), наличие интериктальной диффузной эпилептиформной активности (рХи-квадрат=0,001), наличие продолженной эпилептиформной активности в фазу медленного сна (рХи-квадрат=0,047), сопутствующие церебральные аномалии по данным нейровизуализации (рХи-квадрат=0,014), микроцефалия (рХи-квадрат&lt;0,001), сопутствующие двигательные нарушения (рХи-квадрат&lt;0,001) и расстройство аутистического спектра (рХи-квадрат&lt;0,001). Последующий многофакторный анализ продемонстрировал зависимость КН лишь от таких независимых признаков, как возраст начала эпилепсии (р=0,019; AOR=0,83; 95% CI [0,71–0,96]), наличие инфантильных спазмов (р=0,095; AOR=6,59; 95% CI [1,72–60,6]) и атипичных абсансов (р=0,034; АOR=6,50; 95% CI [1,15–36,7]), фармакорезистентное течение эпилепсии (р=0,003; АOR=8,25; 95% CI [2,04–33,4]) и вариант МКР (р=0,01; AOR=0,21; 95% CI [0,06–0,68]). AUC составила 0,88±0,03 (95% ДИ 0,82–0,95). Чувствительность и специфичность прогностической модели при пороговом значении cut-off 47,52% составили 81,5% и 83,0% соответственно. Заключение. Установленные предикторы развития КН при МКР демонстрируют зависимость когнитивных функций от варианта МКР и особенностей течения эпилепсии. В терапевтическом плане нет возможности влиять на вариант МКР, в отличие от возможностей терапии эпилепсии. Раннее хирургическое лечение и контроль над эпилептическими приступами могут способствовать предотвращению значимого когнитивного дефицита. Introduction. Malformations of cortical developmental (MCD) constitute a large heterogeneous group of diseases characterized by impaired formation of the cerebral cortex. Clinical manifestations are represented by epilepsy, cognitive and motor disorders. Purpose. To establish predictors of cognitive impairment in children with MCD. Materials and methods. Data on 115 patients with MCD were analyzed, including 61 male and 54 female. The mean age of the patients was 11.0 [IQR: 7.0; 16.0] years. Depending on the type of MCD, the following groups were formed: 56 (48.7%) children had focal cortical dysplasia, 4 (3.5%) had hemimegalencephaly, 22 (19.1%) had heterotopia, 12 (10.4%) had lissencephaly, and 21 (18.2%) had polymicrogyria. Results. An intellectual disability was diagnosed in 62 (53.9%) patients: mild in 24 (20.9%), moderate in 17 (14.8%), severe in 10 (8.7%), and profound in 11 (9.6%). According to the results of the univariate analysis, cognitive impairment depended on such factors as early age of epilepsy onset (pMann-Whitney=0.001), frequency of seizures (pMann-Whitney=0.042), the history of infantile spasms (pChi-square&lt;0.001) and epileptic status (pChi-square=0.022), drug-resistant epilepsy (pChi-square&lt;0.001), interictal diffuse epileptiform activity (pChi-square=0.001), CSWS (pChi-square=0.047), concomitant cerebral neuroimaging abnormalities (pChi-square=0.014), microcephaly (pChi-square&lt;0.001), concomitant movement disorders (pChi-square&lt;0.001) and autism spectrum disorder (pChi-square&lt;0.001). Subsequent multivariate analysis demonstrated the dependence of cognitive impairment only on such independent signs as the age of epilepsy onset (p=0.019; AOR=0.83; 95% CI [0.71–0.96]), the history of infantile spasms (p=0.095; AOR=6.59; 95% CI [1.72–60.6]), the presence of atypical absences (p=0.034; AOR=6.50; 95% CI [1.15–36.7]), drug-resistant epilepsy (p=0.003; AOR=8.25; 95% CI [2.04–33.4]) and type of MCD (p=0.01; AOR=0.21; 95% CI [0.06–0.68]). AUC was 0.88±0.03 (95% CI 0.82–0.95). The sensitivity and specificity of the predictive model at the cut-off threshold of 47.52% were 81.5% and 83.0%, respectively. Conclusion. The established predictors demonstrate the dependence of cognitive function on the variant of MCD and features of the course of epilepsy. Therapeutically, there is no way to influence the variant of MCD, unlike therapeutic options for epilepsy. Early surgical treatment and control of epileptic seizures may help to prevent significant cognitive deficits.