Predictors Of Cognitive Impairment Research Articles

The role of telomere length in predicting cognitive impairment in patients with cerebral atherosclerosis and diabetes mellitus

The purpose of the work was to investigate the relationship between telomere length and cognitive function and to identify predictors of cognitive impair­­ment in patients with cerebral atherosclerosis and DM. Materials and methods. 161 patients with stage I—III cerebral atherosclerosis were included in complex clinical and instrumental research.Patients were divided into 2 groups: I — with scores on the MMSE scale < 26 (moderate cognitive deficit, 26 patients), II — with scores on the MMSE scale ≥ 26 (mild cognitive deficit, 135patients). Both groups were comparable in age, sex ratio and telomerase activity (p < 0.05). All patients underwent conventional clinical, laboratory and instrumental (transthoracic echocardiography, electrocardiography, ultrasound Doppler of head and neck, magnetic resonance imaging of the brain) assessments. The relative length of the telomere was measured using a multiplex quantitative real-time polymerase chain reaction. Results and discussion. The analysis revealed that in patients of group I telomere length was statistically significantly shorter, patients were less educated, they had more pronounced situational anxiety, more pronounced thickening of complex intima-media in both carotid arteries, and on the Montreal Cognitive Assessment (MoCA) scale they had severe cognitive impairment (p < 0.05). Group II patients had longer telomeres, more education, and high personal anxiety.An inverse relationship has been established between cognitive decline and the thickness of the intima-media carotid artery complex and a direct relationship between telomere length and duration of education, regardless of the presence of type 2 DM. Conclusions. For patients with cerebral athero­sclerosis of different stages withDM, predictors of cognitive impairment are telomere length, thickness of the common carotid arteries and duration of education (AUC = 0.91; 95% CI 0.82—0.96).

Biopsychosocial Predictors of Cognitive Impairment in the Elderly: A Case-control Study

Background: Cognitive impairment is one of the most common diseases in the elderly. Several studies have already been conducted to identify related factors, but few have explored all the factors involved in the development of cognitive problems. Objective: The present study aimed to identify significant biopsychosocial predictors of cognitive impairment. Methods:: This case-control study was conducted on 535 elderly people referred to Shafa Clinic in the city of Tehran in 2017. The biological factors including serum cholesterol, fasting blood sugar, systolic and diastolic blood pressure, vitamin D, vitamin B12, serum folate, serum homocysteine, height, and weight were measured. The psychological variable in this study was a history of depression that was extracted from the medical records. Social network and social support were measured by LSNS-6 and MOS-SSS questionnaires. The SPSS version 25 was used to analyze the data. Results: The mean age of the control group was 68.4 years (SD = 5.89) and of the case group was 71.5 years (SD = 7.37). The results of multiple logistic regression analysis showed age (AOR=1.05; CI:1.089-1.016, p≤0.05,), Secondary education (AOR=0.51; CI:0.266-0.990, p&lt;0.05,), Tertiary education (AOR=0.41; CI:0.212-0.810, p&lt;0.01,), hypertension (AOR=2.16; CI:3.671-1.266, p&lt;0.01) homocysteine level (AOR=1.09; CI:1.147-1.045, p&lt;0.001,), Hypothyroidism (AOR=0.43; CI: 0.226 0.820, p&lt;0.001,), and depression (AOR=4.5; CI:7.163-2.822, p&lt;0.001) to be significant predictors of cognitive impairment. Conclusion: Results of this study showed that low education level, high blood pressure, high level of homocysteine and depression likely increase the risk of cognitive impairment; also, it was implied that timely screening can identify people at risk. The novelty of the present study is that it used a combination of the biopsychosocial factors to predict unique predictors of cognitive impairment.

Arterial stiffness acts synergistically with APOE genotype and amyloid status to predict cognitive impairment in non‐demented elderly

AbstractBackgroundVascular disease is a known contributor to cognitive impairment in the elderly, often associated with impairments in Executive Functions. Aortic‐femoral Pulse Wave Velocity (PWV) measures have been proposed as a non‐invasive measure of vascular risk. However, the predictive value for cognitive decline and interactions with amyloid biomarkers have received limited study.MethodsPWV was assessed in 129 non‐demented participants (108 cognitively normal and 21 mild cognitive impairment [MCI]) who underwent comprehensive medical and neuropsychological evaluation at the Shiley‐Marcos UCSD ADRC. PCA‐derived Domain Z‐Scores (relative to robust normal controls) were generated, representing Memory, Language, Visuospatial, Executive Functions, and Attention. Linear models examined if PWV significantly predicted each Domain Score and global cognition (the Mattis Dementia Rating Scale (DRS) total score), adjusting for age, sex, and education. In a subanalysis, history of hypertension, hypercholesterolemia, diabetes, stoke/TIA, CVD, atrial fibrillation, and current smoking status were each added to the model. Next, presence of an APOE ε4 allele was added and allowed to interact with PWV. Amyloid status was determined using CSF AB42/40 ratios in a subset of participants (n = 93), and its interaction with PWV was similarly tested.ResultsAfter adjusting for demographics, PWV predicted DRS scores (B=‐0.47, p=0.01), Memory Domain Scores (B=‐0.11, p=0.02), and Executive Domain Scores (B=‐0.10, p = 0.04, Figure 1). The pattern of results did not change when history of vascular risk factors was added to the models. When restricting to only cognitively normal participants, PWV significantly predicted only Executive Domain Scores (B=‐0.08, p = 0.03). Presence of an APOE e4 allele showed a significant interaction with PWV in predicting Memory (B=‐0.18, p=0.03, Figure 2). In the subsample with CSF data, the Memory Domain Score was predicted by the interaction of PWV with amyloid status (B = ‐0.30, p = 4.2x10‐4, Figure 3).ConclusionsArterial Stiffness measured through aortic‐femoral PWV is a predictor of cognitive impairment, especially in the Memory and Executive Function domains, and interacts with markers of Alzheimer’s disease (APOE and amyloid status), such that a stronger relationship is found in the amyloid/ε4 positive population.

Mapping the contribution of clinical risk factors and MRI‐based imaging features to cognitive impairment in community elders

AbstractBackgroundIt is still not clear about the clinical risk factors of cognitive impairment in community elderlies. Although many studies have investigated the association of imaging features with cognitive impairment, none has applied location‐specific information for the prediction.MethodWe included 609 stroke‐ and dementia‐free elderlies with comprehensive clinical information collected (Table 1). T1‐weighted (T1W) images, T2‐weighted images, FLAIR and diffusion tensor imaging (DTI) were acquired. T1W images were processed with AccuBrain to quantify brain volumes of anatomical structures (Table 2). White matter hyperintensities (WMHs) were automatically segmented using AccuBrain and normalized to standard space for the quantification of regional burden. Other small vessel disease features, including lacunes, cerebral microbleed and enlarged perivascular spaces (EPVS) were visually rated (Table 2). Peak width of skeletonized mean diffusivity (PSMD) was calculated on DTI sequence. These vascular imaging features and clinical variables were used predict Montreal Cognitive Assessment (MoCA) and Symbol Digit Modalities Test (SDMT) with support vector regression (SVR). We compared three prediction models here: (1) with clinical variables as predictors, (2) imaging features as predictors, and (3) the combination of clinical and imaging features as predictors. Different feature selection methods were attempted. Further statistical inference was performed with permutations to investigate independent contributing factors.ResultParticipant characteristics were shown in Table 3. When predicting MoCA or SDMT (Figure 1), Model 3 performed no better than Model 2 or 1, and Model 1 performed better than Model 2 (p&lt;0.001). In addition to age and education level, only average sitting systolic blood pressure presented significant independent contribution to MoCA, while for SDMT, no clinical variables had significant independent contribution (Table 4 and 5). The imaging features that had significant independent contribution included EPVS in basal ganglia, WMH volume in left superior corona radiata, and atrophy of right parietal lobe and insular for MoCA, and right insular atrophy for SDMT.ConclusionCombining clinical variables and MRI‐based features did not achieve better prediction of cognitive impairment than using either type of features alone. The highlighted predictors that presented independent contribution to MoCA or SDMT may help to understand the cognitive risk factors in community elderlies.

Cumulative cognitive deficits of Lewy body disease and Alzheimer’s disease neuropathology

AbstractBackgroundAlzheimer’s disease neuropathologic change (ADNC) may contribute to the emergence of dementia in patients with Lewy body disease (LBD) and may act synergistically with LBD. It is unclear to what extent LBD is a domain‐specific predictor of cognitive impairment in isolation and in combination with ADNC.MethodData from the National Alzheimer’s Coordinating Center database was obtained for 2,433 participants with antemortem longitudinal neuropsychological assessment and postmortem neuropathological assessment. We employed a novel measurement of cognitive impairment that incorporates information about the individual’s initial deviation from normative performance and decline over time. We compared domain‐specific cumulative cognitive deficits in LBD, ADNC, and combined LBD/ADNC at three pathologic stages of LBD (brainstem, limbic, and cerebral cortical).ResultThis study included 111 participants with LBD only, 741 participants with combined LBD/ADNC, 1,357 participants with ADNC only, and 224 healthy controls (HC). Limbic and cerebral cortical LBD groups exhibited similar executive/visuospatial deficits as combined ADNC and LBD impacting the limbic and cerebral cortical regions. The cerebral cortical LBD group demonstrated a significantly greater executive/visuospatial deficit relative to ADNC only. In contrast, ADNC and ADNC/LBD groups demonstrated significantly greater cumulative memory deficits relative to HC and LBD only groups, across all LBD pathologic stages.ConclusionThe results of the current study demonstrate that the impact of ADNC and LBD pathology on cognition differs based on the cognitive domain examined and the state of progression of LBD pathology. Limbic and cerebral cortical Lewy body pathologies impact executive/visuospatial functioning independent from the impact of ADNC. In contrast, a greater memory impairment is driven by ADNC, with relatively weaker deficits observed in the LBD only groups. These findings have relevance for predicting progression in Lewy body diseases. Further, detailed characterization of cognitive phenotypes of LBD is crucial for the development of effective disease‐modifying therapeutic trials.

Study of cognitive functions in major idiopathic interstitial pneumonias

BackgroundCognitive dysfunction in idiopathic interstitial pneumonia (IIP) is an important clinical co-morbidity that is associated with impaired lung function. The aim of the work is to assess cognitive function in major IIP and to find out the relation between cognitive dysfunction and the oxygenation parameters.ResultsFifty individuals were involved in the study; 30 patients with major IIP and 20 healthy individuals. Patients with IIP had significantly lower mini mental state examination (MMSE) score compared to the control group (P < 0.001). Wechsler Deterioration Index (WDI) revealed that 33.3% (n = 10) of the patients with IIP had sure cognitive impairment and 26.6% (n = 8) had ongoing cognitive deterioration. Patients with idiopathic pulmonary fibrosis (IPF) had lower cognitive function than other IIP.ConclusionThere is an impairment of cognitive function in patients with major IIP, particularly in IPF, as measured by WDI and MMSE. Further large studies are needed to assess the possible predictors of cognitive impairment and their effects on the patients’ outcome.

Being married/having an intimate partner/being has protective effects for mild cognitive impairment in acute coronary syndrome patients

Abstract Background Cardiovascular disease (CVD) is a leading cause of mortality and morbidity and is known to contribute to cognitive impairment, a condition common in CVD patients. Cognitive impairment (CI) is important to detect, manage and accommodate because it limits the capacity of CVD patients to learn about secondary prevention and engage in appropriate self-care including lifestyle change. Purpose Therefore this study aimed to determine the prevalence and predictors of cognitive impairment in acute coronary syndrome (ACS) patients during hospital admission. Methods ACS (myocardial infarction, unstable angina) inpatients (n=81) who did not have a neurocognitive diagnosis were recruited to a prospective descriptive study in 2019. Cognitive performance was assessed using the Montreal Cognitive Assessment (MoCA) and the Hopkins Verbal Learning Test (HVLT). Results The sample had an age mean of 63.49±10.86 (range 40–89) years, was mostly male (82.7%) and 50.6% were university educated. MI occurred in 56.8%, equally STEMI (28.4%) and nSTEMI (28.4%) with 70.4% treated by coronary intervention. The mean education adjusted MOCA score was 25.73±3.05 (range 18–31) and 48.1% were classified as having mild CI (18–26). The domain with the worst performance was delayed recall/memory domain at mean 2.58±1.77 (of potential 0–5 points). The mean unadjusted recall score on HVLT was 19.56±6.18 (range 0–32), the mean z-score −0.69±1.21 (range −4.59–1.87) and 40.7% were classified as having mild CI (age and education adjusted Z-score ≥−1). Mild CI was classified by both MOCA and HVLT (both adjusted) in 24.7%. Patients classified as having mild CI (MOCA) were significantly older (66.87 versus 60.36 years, p=0.006) and less likely and to be married or have an intimate partner (21% versus 32% p=0.039). When all factors were taken into account using multiple linear regression, higher MOCA scores in patients who were married/partnered (B=1.6) and lower scores with advancing age (B=−0.08). Conclusions Mild CI and decreased delayed recall is prevalent in ACS patients and patient education strategies need to be accommodate this. Being married/partnered may have protective effects, therefore additional support may need to be directed to single patients. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): National Heart Foundation of Australia Vanguard Award

Relationship between Cognition, levels of PTX-3, MBL and their polymorphisms: A systematic review

Introduction: Studies have suggested that pentraxin 3 (PTX3) and Mannose Binding Lectin (MBL) may interfere with cognitive processes. Objective: Identify data reported in the literature involving cognition, PTX3 and MBL. Materials and Methods: The research was done in five databases and the selection of studies was performed in two stages. The first involved review of titles and abstracts. Then the full articles were read and those that did not meet the eligibility criteria were excluded. Results: A total of 3,097 titles and abstracts were selected, but 3,089 were excluded. Finally, 8 articles were included in the review. The articles pointed out that high levels of PTX-3 could be predictors of cognitive impairment while high levels of MBL could have a protective effect on cognition. Conclusion: The current studies are still contradictory and inconclusive, but they lead us to reflect on possible genetic influences of innate immunity in the Central Nervous System. Further research involving the effects of PTX-3 and MBL and its variants on cognition are necessary.

Generalized form and duration of myasthenia gravis as predictors of cognitive impairment

We performed a clinical, neurological, neuropsychological and laboratory examination of 30 patients with a confirmed diagnosis of myasthenia gravis, aged 25 to 69 years (49.0 ± 14.6 years), 11 men and 19 women. Among the examined patients, the generalized form of myasthenia was diagnosed in 20 (66.7%) patients: 4 (20.0%) cases of severe and 16 (80.0%) of moderate forms. The ocular form of myasthenia was found in 10 (33.3%) cases. Neuropsychological testing revealed memory impairment in 15 (50.0%), attention – 11 (36.7%), emotional disturbances – 13 (43.3%) patients with myasthenia gravis. A significant decrease in the concentration of brain-derived neurotrophic factor (BDNF) in the blood serum of patients with myasthenia was noted, compared with the control group (p &lt; 0.01). When comparing the data of neuropsychological testing, the level of BDNF and the history of the disease, it was found that patients with a generalized form of myasthenia gravis and a disease duration of more than three years have a lower level BDNF, which has a reliable correlation with lower cognitive function scores.

Serum Uric Acid and High-Sensitivity C-Reactive Protein as Predictors of Cognitive Impairment in Patients with Cerebral Infarction

Background: Cognitive impairment induced by cerebral infarction has become a devastating health problem. More efficient predictors are required to evaluate the potential cognitive decline after cerebral infarction in clinic. Serum uric acid (UA) and high-sensitivity C-reactive protein (hs-CRP) are two factors reported to correlate with cognitive impairment. However, the understanding on serum UA and hs-CRP with cognitive dysfunction remains unclear. Methods: Serum UA and hs-CRP were evaluated in patients with cerebral infarction (n = 197) using single factor analysis and multivariate logistic regression analysis. Clinical and pathological characteristics were analyzed by logistic regression, respectively, and the results demonstrated the correlation between the pathological characteristics and the cognitive impairment post cerebral infarction. Montreal Cognitive Assessment (MoCA) was used to evaluate the patients’ cognitive function, and patients with a MoCA score <26 were recognized as with cognitive impairment. Results: Clinical characteristics related to cognitive impairment, including age, gender, blood pressure, serum UA, and hs-CRP were collected and analyzed. Serum UA and hs-CRP were identified to be potential predictors for post-stroke cognitive dysfunction, with higher serum UA levels correlated with better cognitive function and higher hs-CRP levels correlated with worse cognitive impairment. Conclusion: Serum UA and hs-CRP are two predictors for cognitive impairment post cerebral infarction.

Detection of cognitive decline in metabolic syndrome

Abstract Background Metabolic syndrome (MetS), a risk factor for many vascular conditions, may be a prodromal manifestation of vascular cognitive impairment. Diagnosing early stages of cerebrovascular pathology can lead to prevention and delay of the progression of pathological conditions such as vascular cognitive impairment. Methods The objective of the study was to investigate new biomarkers for early diagnosis of MetS and cognitive decline as a follow-up. A cardiological, neuropsychological and neurological study was conducted among 75 Bulgarian participants. Beta amyloid in the blood, procalcitonin (PCT), NT-proBNP as predictors of cognitive impairment in patients with metabolic syndrome were identified. Clinical, anthropometric, biochemical, neuropsychological, cognitive and statistical data processing. Plasma amyloid beta (Aβ) levels, procalcitonin, NT-proBNP in MetS were investigated in participants with MetS and in group of healthy people. Results In the present study, plasma levels of Aβ42 and Aβ40 were found to be reduced in MetS participants. Procalcitonin concentration was significantly higher in males than in females. NT-proBNP was significantly higher in females than in males (p &amp;lt; 0.001). Regression analysis showed a positive relationship between NT-proBNP and systolic blood pressure (p &amp;lt; 0.001) and fasting blood glucose (p &amp;lt; 0.05). An inverse relation between NT-proBNP and diastolic blood pressure, waist circumference, triglycerides, HDL- and LDL cholesterol was found. Conclusions There was a positive association between PCT levels, decreased levels of Aβ42 and Aβ40, as well as elevated NT-proBNP and cognitive impairment in people with MetC. A concentration of NT-proBNP of 60 pg / ml or greater could be an indicator of metabolic abnormalities and early cognitive decline. Key messages Metabolic syndrome may be a prodromal manifestation of vascular cognitive impairment. The use of new biomarkers for diagnosis can lead to preventing and slowing the progression of complications associated with MetS.

Weight Loss is a Preclinical Signal of Cerebral Amyloid Deposition and Could Predict Cognitive Impairment in Elderly Adults.

Higher late-life body mass index (BMI) was associated with reduced risk of Alzheimer's disease (AD), which might be explained by a reverse causal relationship. To investigate whether weight loss was a preclinical manifestation of AD pathologies and could be a predictor of cognitive impairment. A total of 1,194 participants (mean age = 73.2 [range: 54 to 91] years, female = 44.5%) from the Alzheimer's Disease Neuroimaging Initiative (ADNI) were grouped according to AD biomarker profile as indicated by amyloid (A) and tau (TN) status and clinical stage by clinical dementia rating (CDR). BMI across the biomarker-defined clinical stages was compared with Bonferroni correction. Pearson correlation analysis was performed to test the relationship between the amyloid change by PET and the BMI change. Multiple regression models were used to explore the influences of amyloid pathologies on BMI change as well as the effects of weight loss on longitudinal changes of global cognitive function. BMI was significantly decreased in AD preclinical stage (amyloid positive [A+] and CDR = 0) and dementia stage (A+/TN+ and CDR = 0.5 or 1), compared with the healthy controls (A-/TN-and CDR = 0, p < 0.005), while no significant differences were observed between preclinical AD and AD dementia. Amyloid PET change was inversely correlated with BMI change (p = 0.023, β= -14). Individuals in amyloid positive group exhibited faster weight loss (time×group interaction p = 0.019, β= -0.20) compared to the amyloid negative group. Greater weight loss predicted higher risk of developing cognitive disorders. Elders who experienced greater weight loss might belong to preclinical stage of AD and could be targeted for primary prevention of the disease.

Parkinson disease with mild cognitive impairment: Domain-specific cognitive complaints predict dementia.

The presence of subjective cognitive complaints (SCC) as a predictor of cognitive impairment in Parkinson´s disease (PD) has shown conflicting results. Most previous studies only assessed complaints in the memory domain. We investigate the association of SCCs across cognitive domains with development of mild cognitive impairment (PD-MCI) and dementia (PDD) in PD and to assess agreement between SCCs and objective cognitive impairments in this population. This is a retrospective analysis of a prospective cohort study. Participants were enrolled at six North-American movement disorders centers. They underwent neuropsychological and non-cognitive clinical evaluations, including the modified Neurobehavioral Inventory to elicit SCC (rated by each patient and independently by their close contact (CC)). Associations between SCCs and development of future cognitive impairment were assessed. Agreement between SCCs and objective impairment within the same domain was also calculated. Of 138 included PD patients, 42% fulfilled criteria for PD-MCI. None of the NBI items predicted development of cognitive impairment after one and two years in PD with normal cognition. In PD-MCI patients, SCCs related to attention predicted dementia at year one. CC ratings of SCCs related to memory and language problems predicted PDD in PD-MCI patients. According to CC reported patients' complaints, there was a significant agreement between SCCs and objective cognitive test scores on attention. Eliciting SCCs including cognitive domains other than memory is crucial for a complete evaluation, including both patient and CC report. Memory, language, and especially attention SCCs in PD-MCI may predict progression to dementia.

Age at onset in multiple sclerosis as a possible predictor for cognitive impairment in children and adolescents

Pediatric-onset multiple sclerosis (MS) can lead to cognitive impairment (CI). In general, in early-onset MS, there are disturbances in cognitive processes, such as information processing speed, attention, and controlling functions. Also, unlike adults with MS, children show a failure in various spheres of speech activity. The age of onset in MS, its duration and recurrence rate can affect not only the accumulation of a stable neurological deficit, but also the state of the cognitive sphere.Objective: to study of the features of CI in children and adolescents with MS; to assess the relationship of CI to clinical characteristics, such as age at onset in the disease and its duration.Patients and methods. The study involved 45 pediatric and adolescent patients with an established diagnosis of MS, who underwent a general neuropsychological examination of the cognitive sphere (Luria’s tests) with transfer to a point system; in addition, psychometric techniques were used to assess attention, controlling functions, memory, verbal fluency, and various types of thinking. Clinical characteristics, such as age at onset in MS and its duration at the time of the examination, were also taken into account.Results and discussion. The leading factors that combine certain symptom complexes of CI in children and adolescents with MS were established. These factors include attention, controlling functions, auditory-verbal and visuospatial memories, various spheres of speech activity. Early-onset MS (at age of 5–8 years) was ascertained to have a greater impact on the formation of speech and controlling functions than adolescence- onset (at age of 13–16-years).Conclusion. The risk of cognitive deficit and subsequent disability was found to be highest in early-onset MS.

Disrupted functional network connectivity predicts cognitive impairment after acute mild traumatic brain injury.

AimsThis study aimed to detect alterations of brain functional connectivity (FC) in acute mild traumatic brain injury (mTBI) and to estimate the extent to which these FC differences predicted the characteristics of posttraumatic cognitive impairment.MethodsResting‐state fMRI data were acquired from acute mTBI patients (n = 50) and healthy controls (HCs) (n = 43). Resting‐state networks (RSNs) were established based on independent component analysis (ICA), and functional network connectivity (FNC) analysis was performed. Subsequently, we analyzed the correlations between FNC abnormalities and cognitive impairment outcomes.ResultsAltered FC within the salience network (SN), sensorimotor network (SMN), default mode network (DMN), executive control network (ECN), visual network (VN), and cerebellum network (CN) was found in the mTBI group relative to the HC group. Moreover, different patterns of altered network interactions were found between the mTBI patients and HCs, including the SN‐CN, VN‐SMN, and ECN‐DMN connections. Correlations between functional disconnection and cognitive impairment measurements in acute mTBI patients were also found.ConclusionThis study indicated that widespread FNC impairment and altered integration existed in mTBI patients at acute stage, suggesting that FNC disruption as a biomarker may be applied for the early diagnosis and prediction of cognitive impairment in mTBI.

Predictors of cognitive impairment in treatment-resistant depression

BackgroundCognitive impairment is a well-recognized symptom of major depressive disorder; however, contributing factors are not fully characterized. The present study examined the neurocognitive profiles and predictors of cognitive impairment in patients with treatment-resistant depression (TRD). MethodsModerate to severely depressed TRD patients were compared to matched healthy volunteers (HV) in verbal learning and recall and executive functions. Based on cognitive scores, cluster analysis was performed to identify subsets within the TRD sample. Predictors of cognitive impairment were also investigated. ResultsTRD patients showed worse performance in tests assessing verbal memory, executive attentional shifting, and inhibitory control. The cluster analysis revealed two groups: a cognitively impaired (CI) group that showed a generalized deficit across cognitive domains, and a relatively cognitively intact group that performed better than CI in all domains except attentional shifting. A logistic binomial regression of the two groups revealed three significant contributing risk factors for CI: 1) older age, 2) lower premorbid IQ, and 3) benzodiazepine use. Cognitive impairment and benzodiazepine use were associated with worse functioning. ConclusionsSignificant cognitive impairment is present in TRD and is associated with worse functioning. Age, lower premorbid IQ, and benzodiazepine use increased the likelihood of generalized cognitive impairment in TRD patients. The detrimental effect of benzodiazepine on cognitive impairment is independent of anxiety symptoms. Further research is needed to characterize the timeline of cognitive impairment in depression.

Elevated serum alkaline phosphatase as a predictor of cognitive impairment in patients with acute ischaemic stroke: A retrospective cohort study

BackgroundIn the present study, we assessed the relationship between serum alkaline phosphatase (ALP) levels and cognitive function changes in acute ischaemic stroke patients. MethodsWe retrospectively collected the demographic data and clinical information from the medical records of patients after the onset of ischaemic stroke. We used the Chinese version of the Mini-Mental State Examination to assess cognitive function. Mixed linear and logistic regression models adjusted for several factors were used to explore the relationship between ALP and cognitive impairment. ResultsA total of 1019 patients were included in the analysis, including 523 poststroke patients with cognitive impairment (PSCI) and 496 patients with non-PSCI. The incidence of poststroke cognitive impairment was 51.3 %. The serum ALP level in the PSCI group was significantly higher than that in the non-PSCI group (86.5 ± 18.9 U/L vs 68.6 ± 15.5 U/L, P < 0.001). The mixed linear model fully adjusted for all variables indicated that the ALP level was positively associated with cognitive impairment (based on the Mini-mental State Examination score) decline, with changes from -0.54 to -0.16 per unit increase in ALP. The logistic regression revealed that the odds of cognitive impairment increased by 42 % when the ALP concentration increased by one U/L (odds ratio (OR) = 1.42, 95 %CI: 1.17−3.09, P = 0.012). The spline regression model further confirmed the dose-response relationships between ALP levels and three-month cognitive impairment (P for nonlinear trend = 0.012). ConclusionThe present study revealed that relatively high serum ALP levels at baseline might be an independent risk factor for cognitive impairment in patients with acute ischaemic stroke.

Predictable hematological markers associated with cognitive decline in valid rodent models of cognitive impairment

Endogenous (hyperglycemia) and exogenous (therapeutic, prophylactic, street drugs) factors can considerably contribute to cognitive impairment (CI). Currently, there are few invasive and/or noninvasive markers that correlate with CI and those that do exist require expensive or invasive techniques to predict and accurately measure the cognitive decline. Therefore, we sought to determine hematological markers as predictors of CI in two different chemically induced valid rodent models of CI (streptozotocin induced hyperglycemic model and chemotherapy [doxorubicin/cyclophosphamide] treated rodent model). Hematological markers were analyzed in the above rodent models of CI CI and compared to their respective control groups. There was a significant increase in creatinine kinase, lactate dehydrogenase and aspartate aminotransferase (AST) in the chemotherapy group. Blood urea nitrogen (BUN), alkaline phosphatase (ALP), bilirubin, creatinine and glucose levels were significantly increased in the streptozotocin group. Interestingly, triglycerides were significantly elevated in both the streptozotocin and chemotherapy groups. Previous studies with human subjects have shown a potential link between the increase in triglyceride levels and CI. Likewise, our data indicate a notable correlation with an increase in triglycerides to cognitive impairment in the rodent models. This suggests elevated levels of triglycerides could prove to be a potential noninvasive hematological marker for the increased risk of CI. Further studies are warranted to determine the causal relationship between elevated triglyceride levels and CI.

Retinal thickness as a potential biomarker of neurodegeneration and a predictor of early cognitive impairment in patients with multiple sclerosis

ABSTRACT Objectives The purpose of this research is to predict the cognitive impairment and to determine its correlation with retinal thickness, mainly (RFNL and GCIPL) in cases of multiple sclerosis. Methods 60 multiple sclerosis patients and 30 age and sex-matched healthy controls were included in this study. Cognitive functions were evaluated in all study participants by the Montreal Cognitive Assessment (MoCA). OCT imaging was done to determine the thickness. The correlation between the cognitive domains of MoCA and the thickness of the retinal nerve fiber layers was analyzed by Spearman correlation. ROC curve was constructed to determine the cut-off points for retinal thickness, and a binary logistic regression was performed to determine the independent predictive capacity of established cut-off points. Results Impaired cognition was found in 26 MS patients (43.3%). Cognitively impaired patients were significantly older (P < 0.05), had significantly longer disease duration (P < 0.05), had higher average EDSS scores (4.3 ± 1.22 vs 3.1 ± 1.45, P < 0.001), and occurred more in progressive types of MS (P < 0.001). A significant positive correlation was found between cognitive function and RNFL thickness and GCIPL (P < 0.001). The retinal thickness (RNFL and GCIPL) cut-off points established for the prediction of cognitive impairment in MS patients were 79 μm and 76 μm, respectively. Conclusion The clear correlation between cognitive impairment and atrophy of inner retinal layers (RNFL and GCIPL) proposes that OCT is valuable in evaluating the neurodegeneration and prediction of early cognitive impairment in MS. ABBREVIATIONS EDSS: Expanded Disability Status Scale; HCs: Healthy controls; GCIPL: Ganglion cell–inner plexiform layer; ILM: Internal limiting membrane; INL: Inner nuclear layer; MoCA: Montreal Cognitive Assessment; MS: Multiple sclerosis; PPMS: Primary progressive multiple sclerosis; RNFL: Retinal nerve fiber layer; RRMS: Relapsing-remitting multiple sclerosis; SD: Standard deviations; SPMS: Secondary progressive multiple sclerosis; SPSS: Statistical Package for the Social Sciences.

Predictors of cognitive impairment in Parkinson's disease: a systematic review and meta-analysis of prospective cohort studies.

Cognitive impairment is a debilitating manifestation in Parkinson's disease (PD). We sought to investigate predictors of PD-CI (PD with cognitive impairment). We systematically searched PubMed and Cochrane Library for prospective cohort studies and pooled estimates via random-effects models. Primary analyses for all types of cognitive impairments and subgroup analyses by separate outcomes were conducted. A total of 28,009 studies were identified, of which 57 studies with 31 factors were included in the meta-analysis. In the primary analysis, 13 factors were associated with PD-CI, comprising advanced age [relative risk (RR) = 1.07, 95% confidence interval (CI) = 1.03-1.12], age at onset (RR = 4.43, 95% CI = 1.87-10.54), postural-instability-gait disorder (RR = 3.76, 95% CI = 1.36-10.40), higher Hoehn and Yahr stage (RR = 1.83, 95% CI = 1.35-2.47), higher UPDRS III score (RR = 1.04, 95% CI = 1.01-1.08), rapid eye movement sleep behavior disorder (RR = 3.72, 95% CI = 1.20-11.54), hallucinations (RR = 3.09, 95% CI = 1.61-5.93), orthostatic hypotension (RR = 2.98, 95% CI = 1.41-6.28), anxiety (RR = 2.59, 95% CI = 1.18-5.68), APOE ε2 (RR = 6.47, 95% CI = 1.29-32.53), APOE ε4 (RR = 3.04, 95% CI = 1.88-4.91), electroencephalogram theta power > median (RR = 2.93, 95% CI = 1.61-5.33), and alpha power < median (RR = 1.77, 95% CI = 1.07-2.92). In the subgroup analysis, MAPT H1/H1 genotype increased the risk of dementia in PD. Sixty-four studies were included in the systematic review, of which 12 factors were additionally correlated with PD-CI using single studies. Advanced age, genetic variation in APOE and MAPT, gait disturbance, motor assessments, non-motor symptoms, and electroencephalogram may be promising predictors for PD-CI.