Impairment In Multiple Cognitive Domains Research Articles

The risk of Alzheimer's disease and cognitive impairment characteristics in eight mental disorders: A UK Biobank observational study and Mendelian randomization analysis.

The cognitive impairment patterns and the association with Alzheimer's disease (AD) in mental disorders remain poorly understood. We analyzed data from 486,297 UK Biobank participants, categorizing them by mental disorder history to identify the risk of AD and the cognitive impairment characteristics. Causation was further assessed using Mendelian randomization (MR). AD risk was higher in individuals with bipolar disorder (BD; hazard ratio [HR]=2.37, P<0.01) and major depressive disorder (MDD; HR=1.63, P<0.001). MR confirmed a causal link between BD and AD (ORIVW=1.098), as well as obsessive-compulsive disorder (OCD) and AD (ORIVW=1.050). Cognitive impairments varied, with BD and schizophrenia showing widespread deficits, and OCD affecting complex task performance. Observational study and MR provide consistent evidence that mental disorders are independent risk factors for AD. Mental disorders exhibit distinct cognitive impairment prior to dementia, indicating the potential different mechanisms in AD pathogenesis. Early detection of these impairments in mental disorders is crucial for AD prevention. This is the most comprehensive study that investigates the risk and causal relationships between a history of mental disorders and the development of Alzheimer's disease (AD), alongside exploring the cognitive impairment characteristics associated with different mental disorders. Individuals with bipolar disorder (BD) exhibited the highest risk of developing AD (hazard ratio [HR]=2.37, P<0.01), followed by those with major depressive disorder (MDD; HR=1.63, P<0.001). Individuals with schizophrenia (SCZ) showed a borderline higher risk of AD (HR=2.36, P=0.056). Two-sample Mendelian randomization (MR) confirmed a causal association between BD and AD (ORIVW=1.098, P<0.05), as well as AD family history (proxy-AD, ORIVW=1.098, P<0.001), and kept significant after false discovery rate correction. MR also identified a nominal significant causal relationship between the obsessive-compulsive disorder (OCD) spectrum and AD (ORIVW=1.050, P<0.05). Individuals with SCZ, BD, and MDD exhibited impairments in multiple cognitive domains with distinct patterns, whereas those with OCD showed only slight declines in complex tasks.

Atypical clinical variants of Alzheimer's disease: are they really atypical?

Alzheimer's disease (AD) is a neuropathological disorder defined by the deposition of the proteins, tau and β-amyloid. Alzheimer's disease is commonly thought of as a disease of the elderly that is associated with episodic memory loss. However, the very first patient described with AD was in her 50's with impairments in multiple cognitive domains. It is now clear that AD can present with multiple different non-amnestic clinical variants which have been labeled as atypical variants of AD. Instead of these variants of AD being considered "atypical," I propose that they provide an excellent disease model of AD and reflect the true clinical heterogeneity of AD. The atypical variants of AD usually have a relatively young age at onset, and they show striking cortical tau deposition on molecular PET imaging which relates strongly with patterns of neurodegeneration and clinical outcomes. In contrast, elderly patients with AD show less tau deposition on PET, and neuroimaging and clinical outcomes are confounded by other age-related pathologies, including TDP-43 and vascular pathology. There is also considerable clinical and anatomical heterogeneity across atypical and young-onset amnestic variants of AD which reflects the fact that AD is a disease that causes impairments in multiple cognitive domains. Future studies should focus on careful characterization of cognitive impairment in AD and consider the full clinical spectrum of AD, including atypical AD, in the design of research studies investigating disease mechanisms in AD and clinical treatment trials, particularly with therapeutics targeting tau.

Mild Behavioral Impairment in Parkinson's Disease: An Updated Review on the Clinical, Genetic, Neuroanatomical, and Pathophysiological Aspects.

Neuropsychiatric symptoms (NPS), including depression, anxiety, apathy, visual hallucinations, and impulse control disorders, are very common during the course of Parkinson's disease (PD), occurring even at the prodromal and premotor stages. Mild behavioral impairment (MBI) represents a recently described neurobehavioral syndrome, characterized by the emergence of persistent and impactful NPS in later life, reflecting arisk of dementia. Accumulating evidence suggests that MBI is highly prevalent in non-demented patients with PD, also being associated with an advanced disease stage, more severe motor deficits, as well as global and multiple-domain cognitive impairment. Neuroimaging studies have revealed that MBI in patients with PD may be related todistinct patterns of brain atrophy, altered neuronal connectivity, and distribution of dopamine transporter (DAT) depletion, shedding more light on its pathophysiological background. Genetic studies in PD patients have also shown that specific single-nucleotide polymorphisms (SNPs) may be associated with MBI, paving the way for future research in this field. In this review, we summarize and critically discuss the emerging evidence on the frequency, associated clinical and genetic factors, as well as neuroanatomical and neurophysiological correlates of MBI in PD, aiming to elucidate the underlying pathophysiology and its potential role as an early "marker" of cognitive decline, particularly in this population. In addition, we aim to identify research gaps, and propose novel relative areas of interest that could aid in our better understanding of the relationship of this newly defined diagnostic entity with PD.

Abnormal grey matter structural changes in patients with end-stage kidney disease and mild cognitive impairment: correlations with clinical features

End-stage kidney disease and mild cognitive impairment (ESKD-MCI) affect the quality of life and long-term treatment outcomes of patients affected by these diseases. Clarifying the morphological changes from brain injuries in ESKD-MCI and their relationship with clinical features is helpful for the early identification and intervention of MCI before it progresses to irreversible dementia. This study gathered data from 23 patients with ESKD-MCI, 24 patients with ESKD and non-cognitive impairment (NCI), and 27 health controls (HCs). Structural magnetic resonance studies, cognitive assessments, and general clinical data were collected from all participants. Voxel-based morphometry analysis was performed to compare grey matter (GM) volume differences between the groups. The patients’ GM maps and clinical features were subjected to univariate regression to check for possible correlations. Patients with ESKD-MCI displayed significantly more impairments in multiple cognitive domains, including global cognition, visuospatial and executive function, and memory, compared to patients with ESKD-NCI. Using a more liberal threshold (P < 0.001, uncorrected), we found that compared to patients with ESKD-NCI, patients with ESKD-MCI exhibited clusters of regions with lower GM volumes, including the right hippocampus (HIP), parahippocampal gyrus (PHG), Rolandic operculum, and supramarginal gyrus. The volumes of the right HIP and PHG were negatively correlated with serum calcium levels. ESKD-MCI was associated with a subtle volume reduction of GM in several brain areas known to be involved in memory, language, and auditory information processing. We speculate that these slight morphometric impairments may be associated with disturbed calcium metabolism.

Global assessment, cognitive profile, and characteristics of mild cognitive impairment in Parkinson's disease.

Cognitive deficits are evident throughout the course of Parkinson's disease (PD), with 24% of patients experiencing subtle cognitive disturbances at the time of diagnosis, and with up to 80% of patients developing PD dementia (PDD) at advanced stages of the disease PD patients with mild cognitive impairment (MCI), an at-risk phenotype of PDD, present with heterogeneous clinical characteristics that complicate the management of PD. This study aims to examine the characteristics of PD-MCI by using the Movement Disorder Society (MDS) diagnostic criteria and evaluate the validity of global cognitive scales in identifying PD-MCI. Seventy-nine (79) PD patients completed neuropsychological assessments and a comprehensive cognitive battery. PD-MCI was classified according to the level 2 MDS task force criteria. Mini-Mental State Examination (sMMSE), Montreal Cognitive Assessment (MoCA) and Parkinson's Disease Cognitive Rating Scale (PDCRS) were examined against a level 2 dichotomised PD-MCI diagnosis. Characteristics of PD-MCI were evaluated using logistic regression analysis. Twenty-seven patients met criteria for PD-MCI (34%). The MoCA and PDCRS demonstrated high validity to screen for PD-MCI. Impairments in multiple cognitive domains were observed in 77.8% of PD-MCI patients. There were significantly more males in the PD-MCI group compared to PD patients without MCI (p<0.01). PD patients with MCI exhibited impairments in the attention/working memory, executive function and memory domains. Heterogeneous cognitive characteristics in PD warrant further investigation into specific cognitive subtypes to advance understanding and effective evaluation of PD-MCI.

Patterns of Impaired Neurocognitive Performance on the Global Neuropsychological Assessment, and Their Brain Structural Correlates in Recent-onset and Chronic Schizophrenia.

Schizophrenia is associated with impairment in multiple cognitive domains. There is a paucity of research on the effect of prolonged illness duration (≥ 15 years) on cognitive performance along multiple domains. In this pilot study, we used the Global Neuropsychological Assessment (GNA), a brief cognitive battery, to explore the patterns of cognitive impairment in recent-onset (≤ 2 years) compared to chronic schizophrenia (≥ 15 years), and correlate cognitive performance with brain morphometry in patients and healthy adults. We assessed cognitive performance in patients with recent-onset (n = 17, illness duration ≤ 2 years) and chronic schizophrenia (n = 14, duration ≥ 15 years), and healthy adults (n = 16) using the GNA and examined correlations between cognitive scores and gray matter volumes computed from T1-weighted magnetic resonance imaging images. We observed cognitive deficits affecting multiple domains in the schizophrenia samples. Selectively greater impairment of perceptual comparison speed was found in adults with chronic schizophrenia (p = 0.009, η2partial = 0.25). In the full sample (n = 47), perceptual comparison speed correlated significantly with gray matter volumes in the anterior and medial temporal lobes (TFCE, FWE p < 0.01). Along with generalized deficit across multiple cognitive domains, selectively greater impairment of perceptual comparison speed appears to characterize chronic schizophrenia. This pattern might indicate an accelerated or premature cognitive aging. Anterior-medial temporal gray matter volumes especially of the left hemisphere might underlie the impairment noted in this domain in schizophrenia.

Cognitive impairment in chronic migraine compared to pseudotumor cerebri.

We aimed to define the prevalence of objective cognitive impairment in a group of chronic migraineurs, and to define how migraineurs with cognitive impairment differed from those without impairment, and in doing so to compare cognitive impairment in chronic migraine to another chronic headache-related disorder already associated with cognitive impairment (i.e. pseudotumor cerebri syndrome). Cognitive impairment in migraine, especially chronic migraine, has been too little studied. Only a few studies have been done, demonstrating that cognitive impairment exists in chronic migraineurs. It is not known how this compares to other headache-related conditions. We administered a cognitive battery consisting of the National Adult Reading Test, Mini-Mental Status Examination, Digit Span, Boston Naming Test, Rey Auditory Verbal Learning Test, Trail Making Test, Controlled Oral Word Association, and Category Fluency. Cognitive impairment was defined as mild single-domain with one test score, and mild multi- -domain with two scores more than two standard deviations below the mean for age-, gender-, and education-adjusted norms. The data from this study was compared to our previously published population of patients with pseudotumor cerebri syndrome. One hundred prospectively recruited patients with chronic migraine were enrolled. Fifty-seven patients had normal cognitive profiles. Forty-three patients demonstrated mild cognitive impairment, and more than half (n = 24) showed impairment in multiple cognitive domains. Migraineurs with multi-domain impairment had higher pain intensity, shorter duration of disease, were taking narcotics, had more impaired vision-related mental health scores, and worse social health scores. We found an association between objective cognitive impairment and subjective perception of impairment only when controlling for pain. We found no associations with depression and topiramate use. The mean composite cognitive Z score was no different in chronic migraineurs and patients with pseudotumor cerebri. Most chronic migraineurs have normal cognitive profiles, but a large proportion of them do experience mild cognitive impairment, especially in multiple domains. The impairment seen in migraine is similar to that in pseudotumor cerebri syndrome, which has already been associated with mild cognitive impairment. Cognitively impaired migraineurs are different from non-impaired/less impaired migraineurs in several ways, which may be an important factor in influencing their migraine treatment.

Nomogram to Predict Cognitive Impairment in Patients with Asymptomatic Middle Cerebral Artery Stenosis.

This study aims to investigate the characteristics and influencing factors of cognitive impairment in patients with asymptomatic middle cerebral artery stenosis (aMCAS) and to construct a nomogram to predict the risk of cognitive impairment in patients with aMCAS. We collected 54 patients with aMCAS and 35 healthy controls to investigate the impaired cognitive domains and pathogenesis in patients with aMCAS. All patients underwent a cranial MRI, CT perfusion, transcranial Doppler ultrasound, blood tests, and a comprehensive neuropsychological evaluation. According to the MoCA score, patients were divided into cognitively normal and cognitively impaired groups. To construct the nomogram, we conducted univariate and multivariate logistic regression analyses to identify factors that affect cognitive function. And the performance of nomogram was evaluated by ROC curves, calibration curves, decision curve analysis (DCA), and clinical impact curve (CIC). In 54 patients with aMCAS, 24 patients presented with cognitive normal, and 30 patients presented with cognitive impairment. The results of multivariate logistic regression suggested that perfusion decompensation, middle cerebral artery mean flow velocity, and LDL-cholesterol levels were independent influencing factors of cognitive impairment. In the following step, a nomogram was constructed. The AUC of the nomogram is 0.862. Calibrating curves show good agreement between nomogram predictions and actual observations, while DCA and CIC show great clinical usefulness. Patients with aMCAS have cognitive impairment in multiple cognitive domains, and impaired executive function was observed during the perfusion compensation period. Furthermore, a nomogram was constructed and validated to predict the risk of cognitive impairment in patients with aMCAS, which can help clinicians to identify at an early stage and improve the management of patients.

BDNF VAL66MET MODERATES THE EFFECTS OF HYPERTENSION ON EXECUTIVE FUNCTIONING IN OLDER ADULTS DIAGNOSED WITH AMCI

Abstract Brain-derived neurotrophic factor (BDNF) has a demonstrated role in promoting memory functions and neuronal survival. A common variant in the BDNF gene, the Val66Met polymorphism, has been found to reduce BDNF expression and increase vulnerability to neurocognitive impairments and age-related cognitive declines. Research suggests that BDNF Val66Met may be associated with hypertension, a well-established risk factor for health and brain functioning across the lifespan. While BDNF is most studied for its effect on learning and memory, its role in moderating other cognitive domains is not as well understood, especially those most affected by hypertension. Furthermore, no study to date has investigated these relationships exclusively with older adults and those at increased risk for cognitive decline. Therefore, the aim of this study was to investigate the effect of BDNF Val66Met and hypertension on the executive function ability of older adults (mean age 71.3±9.2 years) diagnosed with amnestic Mild Cognitive Impairment (aMCI) (N = 108). Results showed that BDNF Val66Met moderated the relationship between hypertension and executive functioning, such that hypertensive carriers of the BDNF Met allele performed significantly worse compared to Val-Val homozygotes, and independent to the effects of aging. These results indicate that genetic and vascular risk interactions can predispose older adults with aMCI to impairments in multiple cognitive domains, and potentially increase susceptibility to further declines or conversion to dementia. These findings have implications for future research on dementia disease pathology, and highlight the importance of strategies that target fixed and modifiable risk factors to promote cognitive resilience.

Executive Dysfunction, Social Cognition Impairment, and Gray Matter Pathology in Myotonic Dystrophy Type 2: A Pilot Study.

In contrast to myotonic dystrophy type 1, the cognitive and radiologic profile of myotonic dystrophy type 2 (DM2) is relatively poorly characterized. To conduct a pilot study to systematically evaluate cognitive and radiologic features in a cohort of Greek individuals with DM2. Eleven genetically confirmed individuals with DM2 and 26 age- and education-matched healthy controls were administered the Edinburgh Cognitive and Behavioural Amyotrophic Lateral Sclerosis Screen (ECAS) to screen for impairment in multiple cognitive domains. MRI data were evaluated by morphometric analyses to identify disease-specific gray and white matter alterations. The following statistical thresholds were used for cognitive comparisons: PFDR < 0.05 and Bayes factor (BF 10 ) >10. The DM2 group exhibited cognitive impairment (ECAS Total score; PFDR = 0.001; BF 10 = 108.887), which was dominated by executive impairment ( PFDR = 0.003; BF 10 = 25.330). A trend toward verbal fluency impairment was also identified. No significant impairments in memory, language, or visuospatial function were captured. The analysis of subscores revealed severe impairments in social cognition and alternation. Voxel-based morphometry identified widespread frontal, occipital, and subcortical gray matter atrophy, including the left superior medial frontal gyrus, right medial orbitofrontal gyrus, right operculum, right precuneus, bilateral fusiform gyri, and bilateral thalami. DM2 may be associated with multifocal cortical and thalamic atrophy, which is likely to underpin the range of cognitive manifestations mostly characterized by executive impairment and specifically by impaired social cognition.

Plasma β-amyloid, tau, neurodegeneration biomarkers and inflammatory factors of probable Alzheimer's disease dementia in Chinese individuals.

BackgroundPlasma-derived β-amyloid, tau, and neurodegeneration (ATN) biomarkers can accurately diagnose Alzheimer’s disease (AD) and predict its progression. Few studies have investigated the relationship between plasma biomarkers and changes in plasma inflammatory markers in clinically diagnosed AD.MethodsSeventy-four participants were recruited, including 30 mild-to-moderate AD dementia patients and 44 normal controls (NC). All participants underwent neuropsychological testing and blood sampling for biomarker testing. AD was clinically diagnosed according to the National Institute on Aging-Alzheimer’s Association (NIA-AA) core criteria and required age-mismatched hippocampal atrophy. We performed Single Molecule Array (Simoa), an ultra-sensitive enzyme-linked immunosorbent assay (ELISA), to examine plasma ATN markers, including β-amyloid (Aβ) 40, Aβ42, p-tau181, total (t)-tau, neurofilament protein light chain (NfL), and inflammatory factors (TNF-α, IL-1β, IL-6, and IL-8).ResultsThe level of the plasma Aβ42/Aβ40 ratio was significantly declined and the levels of the plasma p-tau181, NfL and TNF-α were significantly higher in the AD group than the NC group, but there was no significant difference in the levels of plasma t-tau, IL-1β, IL-6, and IL-8 between the AD and NC groups. The levels of plasma p-tau181, NfL, Aβ42/Aβ40 ratio, and TNF-α were all associated with impairments in multiple cognitive domains. Among them, the plasma Aβ42/Aβ40 ratio, and the p-tau181 and TNF-α levels were associated with impairments in global cognition, memory, and visuospatial abilities, but not with executive function, only plasma NfL level was associated with executive function. Plasma NfL showed higher diagnostic performance in AD than in NC individuals (AUC = 0.833). A combined diagnostic prediction model of plasma Aβ42/Aβ40 ratio, p-tau 181, and NfL had the highest value than each factor alone (AUC = 0.902),with a sensitivity and specificity of 0.867 and 0.886, respectively.ConclusionThe levels of plasma ATN biomarkers (Aβ42/Aβ40 ratio, p-tua181, and NfL) were significantly changed in clinically diagnosed AD patients and they all associated with different domains of cognitive impairment. Plasma ATN biomarkers better differentiate mild-to-moderate AD dementia from NC when they are incorporated into diagnostic models together rather than individually. Plasma ATN biomarkers have the potential to be a screening tool for AD. However, the expression of inflammatory factors in AD patients requires further research.

Automated Early Detection of Alzheimer's Disease by Capturing Impairments in Multiple Cognitive Domains with Multiple Drawing Tasks.

Background:Automatic analysis of the drawing process using a digital tablet and pen has been applied to successfully detect Alzheimer’s disease (AD) and mild cognitive impairment (MCI). However, most studies focused on analyzing individual drawing tasks separately, and the question of how a combination of drawing tasks could improve the detection performance thus remains unexplored.Objective:We aimed to investigate whether analysis of the drawing process in multiple drawing tasks could capture different, complementary aspects of cognitive impairments, with a view toward combining multiple tasks to effectively improve the detection capability.Methods:We collected drawing data from 144 community-dwelling older adults (27 AD, 65 MCI, and 52 cognitively normal, or CN) who performed five drawing tasks. We then extracted motion- and pause-related drawing features for each task and investigated the associations of the features with the participants’ diagnostic statuses and cognitive measures.Results:The drawing features showed gradual changes from CN to MCI and then to AD, and the changes in the features for each task were statistically associated with cognitive impairments in different domains. For classification into the three diagnostic categories, a machine learning model using the features from all five tasks achieved a classification accuracy of 75.2%, an improvement by 7.8% over that of the best single-task model.Conclusion:Our results demonstrate that a common set of drawing features from multiple drawing tasks can capture different, complementary aspects of cognitive impairments, which may lead to a scalable way to improve the automated, reliable detection of AD and MCI.

Abnormal Functional Connectivity of Thalamic Subdivisions in Alzheimer’s Disease: A Functional Magnetic Resonance Imaging Study

Alzheimer’s disease (AD) is characterized by global cognitive impairment in multiple cognitive domains. Thalamic dysfunction during AD progression has been reported. However, there are limited studies regarding dysfunction in the functional connectivity (FC) of thalamic subdivisions and the relationship between such dysfunction and clinical assessments. This study examined dysfunction in the FC of thalamic subdivisions and determined the relationship between such dysfunction and clinical assessments. Forty-eight patients with AD and 47 matched healthy controls were recruited and assessed with scales for multiple cognitive domains. Group-wise comparisons of FC with thalamic subdivisions as seed points were conducted to identify abnormal cerebral regions. Moreover, correlation analysis was conducted to evaluate the relationship between abnormal FC and cognitive performance. Decreased FC of the intralaminar and medial nuclei with the left precuneus was observed in patients but not in heathy controls. The abnormal FC of the medial nuclei with the left precuneus was correlated with the Mini Mental State Examination score in the patient group. Using the FC values showing between-group differences, the linear support vector machine classifier achieved quite good in accuracy, sensitivity, specificity and area under the curve. Dysfunction in the FC of the intralaminar and medial thalamus with the precuneus may comprise a potential neural substrate for cognitive impairment during AD progression, which in turn may provide new treatment targets.

Cerebral Glutamate Regulation and Receptor Changes in Perioperative Neuroinflammation and Cognitive Dysfunction.

Glutamate is the major excitatory neurotransmitter in the central nervous system and is intricately linked to learning and memory. Its activity depends on the expression of AMPA and NMDA receptors and excitatory amino transporters on neurons and glial cells. Glutamate transporters prevent the excess accumulation of glutamate in synapses, which can lead to aberrant synaptic signaling, excitotoxicity, or cell death. Neuroinflammation can occur acutely after surgical trauma and contributes to the development of perioperative neurocognitive disorders, which are characterized by impairment in multiple cognitive domains. In this review, we aim to examine how glutamate handling and glutamatergic function are affected by neuroinflammation and their contribution to cognitive impairment. We will first summarize the current data regarding glutamate in neurotransmission, its receptors, and their regulation and trafficking. We will then examine the impact of inflammation on glutamate handling and neurotransmission, focusing on changes in glial cells and the effect of cytokines. Finally, we will discuss these changes in the context of perioperative neuroinflammation and the implications they have for perioperative neurocognitive disorders.

Extended Interval Dosing Natalizumab and impact on neuropsychological deficits in Relapsing-Remitting Multiple Sclerosis.

Background: Cognitive impairment and neuropsychiatric symptoms are frequently reported in Relapsing-Remitting Multiple Sclerosis (RRMS). Natalizumab (NTZ) is usually administered on a 4-weekly Standard Interval Dosing (SID) schedule. However, Extended Interval Dosing (EID) at 6–8 weekly intervals has been proven non-inferior regarding relapse risk, with a lower risk of Progressive Multifocal Leukoencephalopathy (PML). The impact of EID NTZ on neuropsychological deficits in RRMS has not been studied. Objective: To determine if EID NTZ demonstrates an improvement in neuropsychological parameters in RRMS patients. Method: We performed a retrospective, observational analysis of 34 RRMS patients treated between August 2015–2017. Patients underwent baseline neuropsychological testing before commencing EID NTZ. A second evaluation was performed, on average 28 months after commencing treatment. Results: Z scores at the initial assessment showed baseline cognitive impairment in multiple domains. 14/20 Z-scores showed an improvement post-NTZ and 5/14 reached statistical significance; namely Trails A (visual attention/processing speed), Line-orientation (visual-spatial), Picture-naming (word finding), Digital-Span (attention, executive function and memory) and Story-recall (memory). The Hospital Anxiety and Depression Scale (HADS) data remained unchanged. Correlation matrix showed no association between HADS scores, the time between assessments and the changes in Z scores. Conclusion: This data suggests the efficacy of EID NTZ in improving cognitive impairment in RRMS. A prospective observational study is warranted.

Application of the Chinese Version of the Montreal Cognitive Assessment-Basic for Assessing Mild Cognitive Impairment in Parkinson's Disease.

Mild cognitive impairment (MCI) is a common and pivotal non-motor symptom in Parkinson’s disease (PD). It is necessary to use the appropriate tools to characterize the cognitive profiles and identify the subjects at risk of MCI in clinical practice. A cohort of 207 non-demented patients with PD and 52 age- and gender-matched cognitively normal controls (NCs) underwent the Chinese Version of Montreal Cognitive Assessment-Basic (MoCA-BC) evaluation. Patients with PD also received detailed motor and non-motor evaluation by serial scales. Cognitive profiles were investigated in patients with PD-MCI, relative to patients with normal cognition (PD-NC) and cognitively NCs. In addition, differences in demography, major motor and non-motor symptoms were compared between patients with PD-MCI and PD-NC. There were 70 patients with PD-MCI, occupying 33.8% of the total patients. Patients with PD-MCI had impairment in multiple cognitive domains, especially in executive function, memory and visuospatial function on MoCA-BC, relative to cognitively NCs or PD-NC. Compared with PD-NC patients, PD-MCI patients were older (p = 0.002) and had a later onset age (p = 0.007) and higher score of the Unified Parkinson’s Disease Rating Scale (UPDRS) part III (p = 0.001). The positive rate of clinical possible rapid eye movement sleep behavior disorder (cpRBD) in the PD-MCI group was significantly increased relative to the PD-NC group (p = 0.003). Multivariate logistic analysis showed that older age (OR = 1.06; p = 0.012), higher score of UPDRS-III (OR = 1.03; p = 0.018) and the presence of cpRBD (OR = 2.10; p = 0.037) were independently associated factors of MCI in patients with PD. In conclusion, executive function, memory and visuospatial function are the main impaired cognitive profiles in PD-MCI via MoCA-BC. Aging, motor severity and RBD may be independently related factors of MCI in PD.

Multi-domain cognitive impairments at school age in very preterm-born children compared to term-born peers

BackgroundPreterm infants are at risk for functional impairments in motor, cognitive, and behavioral development that may persist into childhood. The aim of this study was to determine the co-occurrence of cognitive impairments in multiple cognitive domains at school age in very preterm born children compared to term-born children.MethodsComparative study including 60 very preterm-born children (gestational age ≤ 32 weeks) and 120 term-born controls. At school age, we assessed intelligence with the WISC-III, and visuomotor integration with the NEPSY-II, verbal memory with the AVLT, attention with the TEA-ch, and executive functioning with the BRIEF. We investigated co-occurrence of various abnormal (<5th percentile) and suspect-abnormal (<15th percentile, including both suspect and abnormal) cognitive functions.ResultsAt mean age 8.8 years, 15% of preterm children had abnormal outcomes in multiple cognitive functions (≥2), versus 3% of the controls (odds ratio, OR 4.65, 95%-confidence interval, CI 1.33–16.35). For multiple suspect-abnormal cognitive outcomes, rates were 55% versus 25% (OR 3.02, 95%-CI 1.49–6.12). We found no pattern of co-occurrence of cognitive impairments among preterm children that deviated from term-born controls. However, low performance IQ was more frequently accompanied by additional cognitive impairments in preterms than in controls (OR 5.43, 95%-CI 1.75–16.81).ConclusionsA majority of preterm children showed co-occurrence of impairments in multiple cognitive domains, but with no specific pattern of impairments. The occurrence of multi-domain cognitive impairments is higher in preterms but this seems to reflect a general increase, not one with a pattern specific for preterm-born children.

Western Diet Consumption During Development: Setting the Stage for Neurocognitive Dysfunction.

The dietary pattern in industrialized countries has changed substantially over the past century due to technological advances in agriculture, food processing, storage, marketing, and distribution practices. The availability of highly palatable, calorically dense foods that are shelf-stable has facilitated a food environment where overconsumption of foods that have a high percentage of calories derived from fat (particularly saturated fat) and sugar is extremely common in modern Westernized societies. In addition to being a predictor of obesity and metabolic dysfunction, consumption of a Western diet (WD) is related to poorer cognitive performance across the lifespan. In particular, WD consumption during critical early life stages of development has negative consequences on various cognitive abilities later in adulthood. This review highlights rodent model research identifying dietary, metabolic, and neurobiological mechanisms linking consumption of a WD during early life periods of development (gestation, lactation, juvenile and adolescence) with behavioral impairments in multiple cognitive domains, including anxiety-like behavior, learning and memory function, reward-motivated behavior, and social behavior. The literature supports a model in which early life WD consumption leads to long-lasting neurocognitive impairments that are largely dissociable from WD effects on obesity and metabolic dysfunction.

Older adults with epilepsy: memory complaints and objective neuropsychological performance.

People with epilepsy frequently complain of poor memory. To assess the occurrence of memory complaints in older adults with epilepsy (OAE) and whether it is associated with clinical variables, objective cognitive performance, and quality of life (QoL). The Memory Complaint Questionnaire (MAC-Q) was related to objective cognitive performance, the Neurological Disorders Depression Inventory for Epilepsy (NDDI-E), the Quality of Life in Epilepsy Inventory (QOLIE-31), and the clinical characteristics of 83 OAE. OAE showed worse cognitive performance and higher MAC-Q scores when compared to a similar control group (n=40). Impairment in multiple cognitive domains occurred in 34 (41%) OAE and was associated with older age and lower educational level. Memory complaints (MAC-Q≥25) were reported by 45 (54.2%) OAE and associated with older age, lower educational level, onset at ≥60 years, higher NDDI-E scores, lower QOLIE-31 scores, and impairment in multiple cognitive domains. OAE presented worse cognitive performance and greater memory complaints. Episode onset at ≥60 years of age was associated with complaints, but not with objective cognitive deficit. We found an association between subjective and objective cognitive performance, with aspects of epilepsy and worse QoL scores.

Cognitive profiles in adult-onset neuronal intranuclear inclusion disease: a case series from the memory clinic.

This study aimed to analyze the characteristics of cognitive impairment in adult-onset neuronal intranuclear inclusion disease (NIID). Seven patients with adult-onset NIID were collected consecutively from the memory clinic of Xuanwu hospital from February to December 2019. These cases were diagnosed with skin biopsy triggered by DWI high-intensity signals in corticomedullary junction on brain MRI. We used a battery of neuropsychological scales to detect the patient's performance in each cognitive domain, and made a detailed analysis on the characteristics of cognitive impairment. All seven cases had cognitive impairment, and four of them had met the criteria for dementia. The scores of Montreal Cognitive Assessment and Frontal Assessment Battery were abnormal in all patients. The executive dysfunction was confirmed by the abnormal scores of Trail Making Test (5/7, 71%) and Clock Drawing Test (4/7, 57%). Bad performance in Auditory Verbal Learning Test (6/7, 86%) demonstrated that the memory was also a very commonly impaired cognitive domain. The low score on the animal fluency (4/7, 57%), Boston Naming Test (3/7, 43%), and Pentagon and Cube Copying Test (4/7, 57%) indicated that the language and visuospatial skills were also impaired. Fazekas scores were significantly correlated to the global cognition, executive and language functions (r = 0.788-0.906, P < 0.05). There is obvious impairment in multiple cognitive domains in adult-onset NIID, and both the executive dysfunction and memory deficit are very common. Leukoencephalopathy may be the main course of cognitive impairment in adult-onset NIID.