Manifestations Of Cognitive Impairment Research Articles

Identification of brain aging subtypes in multiple brain regions from cognitively normal individuals

AbstractBackgroundAlthough late‐onset Alzheimer’s disease (LOAD) occurs in older individuals (age 65 or older), multiple lines of evidence suggests that the dysregulation of brain functions initiates decades earlier. Through examining multiple large‐scale human brain transcriptomic data, we demonstrated that cognitively normal brain aging from donors in their 40s‐60s can group into several subtypes based on their hippocampal transcriptomes. One subtype represents healthy brain aging and some evidence suggests these donors may remain cognitively normal in much older ages, while some brain aging subtypes showed gene expression changes highly similar to those observed in AD, supporting molecular changes linked to AD have occurred much earlier than the manifestation of cognitive impairment. However, whether the brain aging subtype is a common phenomenon across multiple brain regions or very specific to the hippocampus remains unknown.MethodWe compiled and studied transcriptomic data in another commonly studied human brain region (prefrontal cortex) from donors who were cognitively normal. We performed hierarchical clustering in these samples to infer subtypes, differential gene expression analysis was done between samples from different subtypes. We annotated and compared these DEGs with other AD gene expression signatures.ResultWe discovered that aging subtypes could also be observed in the prefrontal cortical region. Similarly to the hippocampus, the differentially expressed genes among aging subtypes also highly overlapped with AD gene signatures. By comparing aging subtypes defined from hippocampal vs. cortical transcriptomes from the same individuals, we found that an AD similar hippocampal sample does not necessarily correspond to AD similar cortical sample in the same donor, suggesting the brain regional complexity of the disease.ConclusionOur analysis of the transcriptomic data from multiple brain regions from cognitively normal individual supports that gene regulation changes related to AD occurs decades earlier than the manifestation of clinical phenotype. Understanding the molecular changes in these early changes in multiple brain regions could be critical to gain new insights into the mechanisms of AD initiation.

Myricetin improves pathological changes in 3×Tg-AD mice by regulating the mitochondria-NLRP3 inflammasome-microglia channel by targeting P38 MAPK signaling pathway

BackgroundAlzheimer's disease (AD) represents the common neurodegenerative disease featured by the manifestations of cognitive impairment and memory loss. AD could be alleviated with medication and improving quality of life. Clinical treatment of AD is mainly aimed at improving the cognitive function of patients. Donepezil, memantine and galantamine are commonly used drug. But they could only relieve AD, not cure it. Therefore, new treatment strategies focusing on AD pathogenesis are of great significance and value. Myricetin (Myr) is a natural flavonoid extracted from Myrica rubra. And it shows different bioactivities, such as anti-inflammation, antioxidation as well as central nervous system (CNS) activities. Nonetheless, its associated mechanism in treating AD remains unknown. PurposeHere we focused on investigating Myr's effect on treating AD and exploring if its protection on the nervous system activity was associated with specifically inhibiting P38 MAPK signaling pathway while regulating mitochondria-NLRP3 inflammasome-microglia. Study design and methodsThis work utilized triple transgenic mice (3 × Tg-AD) as AD models and Aβ25–35 was used to induce BV2 cells to build an in vitro AD model. Behavioristics, pathology and related inflammatory factors were examined. Molecular mechanisms are investigated by western-blot, immunofluorescence staining, CETSA, molecular docking, network pharmacology. ResultsAccording to our findings, Myr could remarkably improve memory loss, spatial learning ability, Aβ plaque deposition, neuronal and synaptic damage in 3 × Tg-AD mice through specifically inhibiting P38 MAPK pathway activation while restraining microglial hyperactivation. Furthermore, Myr promoted the transformation of microglial phenotype, restored the mitochondrial fission-fusion balance, facilitated mitochondrial biogenesis, and restrained NLRP3 inflammasome activation and neuroinflammation. For the in-vitro experiments, P38 agonist dehydrocorydaline (DHC) was utilized to confirm the key regulatory role of P38 MAPK signaling pathway on the mitochondria-NLRP3 inflammasome-microglia channel. ConclusionsOur results revealed the therapeutic efficacy of Myr in experimental AD, and implied that the associated mechanism is possibly associated with inhibiting tmitochondrial dysfunction, activating NLRP3 inflammasome, and neuroinflammation which was mediated by P38 MAPK pathway. Myr is the drug candidate in AD therapy via targeting P38 MAPK pathway.

Radiation-induced neuroinflammation monitoring by the level of peripheral blood monocytes with high expression of translocator protein

Purpose Currently there are no effective diagnostic methods for the control of neuroinflammation before manifestation of cognitive impairment after head irradiation. The translocator protein (TSPO) is highly expressed in glial cells upon brain damage, therefore we compared the changes in the number of cells with high TSPO expression in the brain and peripheral blood during radiation-induced neuroinflammation. Materials and methods Hippocampal cytokines mRNA expression and the content of cells with high TSPO expression in the brain and peripheral blood monocytes were analyzed up to eight months after mice head γ-irradiation at a dose of 2 Gy or 8Gy. Results Mice irradiation at a dose of 8 Gy causes neuroinflammation, accompanied by an increase of M1 microglia and TSPOhigh cells in the brain, elevated gene expression of pro-inflammatory and decreased of anti-inflammatory cytokines along with an increased number of microglia and astrocytes in the hippocampus. The content of TSPOhigh cells in the brain correlates with the level TSPOhigh monocytes in three days, one month and two months after exposure. Conclusions An increase in the level of the monocytes with high expression of TSPO may be considered as a marker for an early diagnostics of post-radiation brain damage leading to cognitive impairment.

The Increase of Theta Power and Decrease of Alpha/Theta Ratio as a Manifestation of Cognitive Impairment in Parkinson's Disease.

In this study, we aim to assess and examine cognitive functions in Parkinson's Disease patients using EEG recordings, with a central focus on characteristics associated with a cognitive decline. Based on neuropsychological evaluation using Mini-Mental State Examination, Montreal Cognitive Assessment, and Addenbrooke's Cognitive Examination-III, 98 participants were divided into three cognitive groups. All the particpants of the study underwent EEG recordings with spectral analysis. The results revealed an increase in the absolute theta power in patients with Parkinson's disease dementia (PD-D) compared to cognitively normal status (PD-CogN, p=0.00997) and a decrease in global relative beta power in PD-D compared to PD-CogN (p=0.0413). An increase in theta relative power in the left temporal region (p=0.0262), left occipital region (p=0.0109), and right occipital region (p=0.0221) were observed in PD-D compared to PD-N. The global alpha/theta ratio and global power spectral ratio significantly decreased in PD-D compared to PD-N (p = 0.001). In conclusion, the increase in relative theta power and the decrease in relative beta power are characteristic changes in EEG recordings in PD patients with cognitive impairment. Identifying these changes can be a useful biomarker and a complementary tool in the neuropsychological diagnosis of cognitive impairment in Parkinson's Disease.

POLYPHARMACY IN ADULTS WITH CHRONIC DISEASE – CHARACTERISTICS AND ASSOCIATION WITH COGNITIVE DISORDERS

Polypharmacy in the elderly with multimorbidity in particular results in drug interactions and manifestation of cognitive impairments and functional deficits. To analyze the characteristics of polypharmacy, predictors affecting its variability and its impact on possible cognitive impairment in adults over 60 years of age with a diagnosed chronic disease at risk for dementia. A national prospective multicenter study started in 2022 in 46 outpatient clinics of family medicine specialists in primary care. Participants older than 60 years of age with a confirmed minimum of one chronic disease and at risk for dementia were included. A general and clinical information questionnaire and 3 standardized questionnaires were used – Mini-cog test, IADL test and Geriatric Depression Scale (GDS). Eight hundred fifty-eight participants were analyzed, with female predominance (57.69%). Sex and age as independent predictors significantly affected the variability of polypharmacy consistently 0.7% vs. 0.5%. Elevated cholesterol [OR=1.449 (1.09 – 1.92) 99% CI] and obesity [OR=1.695 (1.30 – 3.30) 99% CI] were associated with female sex. Four hundred ninety-seven participants (57.92%) received ≤2 groups of medications for treatment of chronic diseases. There was no significant association between the obtained Mini-cog test scores and the number of medication groups participants received (p=0.12). The higher GDS score was significantly associated with polypharmacy (p=0.03). A non-significant negative correlation was found between the IADL score and the number of medication groups used for therapy of chronic diseases (p=0.38).

How is semantic memory affected in Mild Cognitive Impairment?

AbstractBackgroundMild cognitive impairment (MCI) is a condition considered by many as a transitional stage between healthy aging and Alzheimer’s disease. Although its diagnosis is typically based on the assessment of episodic memory, evidences show that impairment in semantic memory would be one of the first manifestations of cognitive impairment. This study aims to investigate how semantic memory is affected in MCI. Precisely, we will explore if core memory of common knowledge is impaired in MCI, and if the performance in semantic memory task vary with the modality of presentation of the stimuli (verbal vs visual).MethodA group of healthy people aged between 60 and 90 years old (mean: 77.4 N = 43), and a age‐matched group meeting the criteria for MCI (N = 32), who have lived in Quebec (Canada) for at least 30 years, completed two neuropsychological tests evaluating the semantic memory of famous people, which have been proven to be the most sensible way to detect even subtle variation in semantic memory.ResultResults indicate that performance in both tests is impaired in the MCI group, compared to the healthy elderly group. This means that the MCI group have more difficulty to name famous people (t (69) = 5,173, p < 0.01), as well as answer basic questions on them (ex: their profession, nationality, etc.), when presented from their picture (t (69) = 4.849, p < 0.01) or their name (t (65) = 3.488, p < 0.01), compared to healthy people of the same age. There was no difference between their performances when the stimuli was presented in the visual or verbal modality (t (30) = 0.928, p > 0.05).ConclusionThis study demonstrates that semantic memory of famous people is impaired in MCI, and that impairment affects the capacity to name famous people as well as remembering facts about them. In addition, there are no difference if the stimuli are presented visually or verbally. This suggests that the impairment in semantic memory in MCI is due to a degradation of the memory, and is not modulated by other cognitive functions or modality.

Possible manifestations of cognitive impairment in children suffering from pancreatic dysfunction

The article investigates possible manifestations of cognitive impairment in children suffering from pancreatic dysfunction. The authors point out that improving blood glucose control in patients with type I diabetes mellitus is an important factor in reducing cognitive impairment, especially in children. At the present stage, the treatment of cognitive dysfunction has become an interdisciplinary multidisciplinary complex treatment, which in the future will not only improve the quality of life of patients, but also minimize the above-mentioned dysfunction as such.

Blood-based epigenome-wide analyses of cognitive abilities

BackgroundBlood-based markers of cognitive functioning might provide an accessible way to track neurodegeneration years prior to clinical manifestation of cognitive impairment and dementia.ResultsUsing blood-based epigenome-wide analyses of general cognitive function, we show that individual differences in DNA methylation (DNAm) explain 35.0% of the variance in general cognitive function (g). A DNAm predictor explains ~4% of the variance, independently of a polygenic score, in two external cohorts. It also associates with circulating levels of neurology- and inflammation-related proteins, global brain imaging metrics, and regional cortical volumes.ConclusionsAs sample sizes increase, the ability to assess cognitive function from DNAm data may be informative in settings where cognitive testing is unreliable or unavailable.

The study of epidemiology of dementia and Alzgeimer’s disease in Ukraine

Against the background of systematic aging of the population and increase in life expectancy the problems of the spread of all forms of dementia, including Alzheimer’s disease, are becoming increasingly important. Аim. To study epidemiology of dementia and Alzheimer’s disease in Ukraine. Materials and methods. Data from the Center for Mental Health and Monitoring of Drugs and Alcohol of the Ministry of Health of Ukraine for 2015-2019 were studied. In the research, in addition to general theoretical methods, methods of epidemiological studies were also used. Results and discussion. It has been found that since 2018 in Ukraine, the incidence rates of all mental disorders (4.0 %) increased, including organic lesions with symptomatic manifestations of cognitive impairment (2.0 %), all forms of dementia (6.0 %), vascular dementia and Alzheimer’s disease (9.0 % each). The structure of dementia is dominated by vascular forms of dementia (62.59 %), while Alzheimer’s disease has been characterized since 2015 by a systematic increase in the proportion (%) from 7.0 % to 12.0 %. The average prevalence of dementia in Ukraine is 99.72, and Alzheimer’s disease is 5.34 per 100 thousand population. A significant fluctuation in the prevalence of dementia and Alzheimer’s disease in different regions of the country has been proven. Thus, in the regions of the country, these indicators differed by 6 or more times. The highest prevalence rates of dementia were observed in 7 regions (Vinnytsia, Donetsk, Zaporizhia, Zhytomyr, Kharkiv, Cherkasy and Chernihiv regions) and Kyiv, and for Alzheimer’s disease – in 3 regions (Zaporizhia, Kherson, Chernihiv) and Kyiv. Conclusions. It is necessary to introduce an effective system for recording and monitoring cases of all forms of dementia, including Alzheimer’s disease. This will form the basis for the development of models for the rational distribution of healthcare resources for the effective treatment and social rehabilitation of these groups of patients in Ukraine.

Manifestation of cognitive impairments after a prior coronavirus infection COVID-19 in a patient with ApoE ε4 genotype

Nowadays, the novel coronavirus infection (COVID-19) pandemic is one of the most important global health problems. There is increasing evidence that COVID-19 affects central and peripheral nervous system as well. The paper presents a clinical case of a 47 old patient with the ApoE ε4 haplotype and family history of Alzheimer’s disease who developed cognitive impairment after acute COVID-19. Before the infection the patient has no cognitive complaints and preserved everyday activity. After novel coronavirus infection, which was observed in mild form, the patient had started to complain on constant excessive forgetfulness. Neuropsychological assessment confirmed the presence of pre-mild cognitive impairment of predominantly single domain amnestic type. However, brain MRI showed only subtle periventricular white matter changes usually attributed to small vessel disease. Memory complaints were observed for 3 months of follow up despite intensive cognitive training, optimization of lifestyle and therapy with choline alphoscerate. Probable links between coronavirus infectious and cognitive impairment manifestation are discussed. There is data that ApoE ε4 haplotype is associated with increase of microglia mediated neuro-inflammation and it can be significant for accelerating of progression of neurodegenerative diseases after COVID-19. Further follow up of the patient is necessary for determination of nosological diagnosis explaining manifested predominantly amnestic type pre-mild cognitive impairment.

Diagnosis of cognitive dysfunction in the military with mental and behavioral disorders due to alcohol use associated with depression

Cognitive impairment, which in most cases are not considered by the doctor, and thus remain outside the scope of medical care, are characteristic for almost all patients with mental illness. Ignoring the manifestations of cognitive impairment is primarily due to the fact that the range of cognitive abilities has individual characteristics for each person and therefore their definition does not have clear criteria for evaluation. The article presents the traditional methods of psychodiagnostics studies for identifying cognitive disorders, depressive states, individual typological features in the military with mental and behavioral disorders due to alcohol consumption to improve the quality of diagnosis and further medical support for patients in this category. Typical symptoms in this group of patients were: sleep disturbances; low mood; unexpected attacks of anger, indignation, unreasonable fear; anxiety; irritability, autonomic disorders, depression. According to the informed consent, we used several standardized neuropsychological tests, which had high characteristics of validation and reliability, to study the individual psychological differences of patients, according to the literature [1,2]. Emotional disturbances were assessed before and after treatment using the Mini Mental State Examination (MMSE) scale [10], which determined short-term and long-term memory in patients; auditory functions were studied according to the method of A.Luria; to conduct a clock drawing test, the subject was asked to draw a clock, the results of which indicated that the patient had clinically significant cognitive impairment; G. Eisenko's questionnaire was used to identify the main individual personality traits; Spielberger-Hanin questionnaire was used to assess the manifestations of reactive and personal anxiety [7]; the level of depression was determined by the Tsung scale. To objectively assess the pain response, dynamic recording of pupil diameter (pupillometry) was used to determine the human autonomic response [13] and a visual analog scale (VAS). According to the results of the study, it was found that in patients of both groups - 86 people (main and control) revealed up to 50% borderline cognitive impairment, which can be considered a reliable prognostic informative sign of the mental state of patients. Low anxiety on the Spielberger-Hanin scale has been reported in patients with depressive symptoms. All other screening diagnostic scales revealed borderline cognitive impairment in all patients. Thus, it has been proven that borderline cognitive impairment in patients with mental and behavioral disorders due to alcohol use interacts with depression, which significantly affects cognitive abilities. To eliminate cognitive impairment (CI), patients of both groups were offered a comprehensive traditional treatment with the additional use of the metabolic drug cytoflavin. Literature sources [8] confirm the expediency of using a complex metabolic neuroprotective drug, the action of which is directed at the synthesis of energy complexes through various receptor, enzymatic and mediator systems. According to the authors [8], cytoflavin can be attributed to metabolic drugs, which acts as an inducer of major metabolic pathways in cells, promotes the utilization of free oxygen and prevents ischemic changes in organs and tissues by reducing the level of peroxide processes. Complex therapy of treatment of borderline cognitive states with a course of cytoflavin is pathogenetically justified, which provided in our study an improvement in the psychological state of soldiers of both groups. Purpose: to study the dynamics of the validity and effectiveness of methods for assessing the cognitive status of patients with mental and behavioral disorders due to alcohol use associated with depression and carrying out a correction of cognitive dysfunction by additional administration of cytoflavin. Conclusion: Based on a battery of diagnostic tests, accurate and adequately comparable indicators were obtained, which allowed to establish an objective picture of cognitive impairment, their correlation with depression, which significantly affected the outcome of treatment. Correction of cognitive dysfunction was performed by additional administration of cytoflavin 2 tablets 2 times a day PO for half an hour before meals.

Features of functional state restoration among military personnel after traumatic brain injury combined with acubarotrauma

Aim – to study the restoration features of postconcussion symptoms and cognitive disorders based on the dynamics of the psychophysiological characteristics of combatants who received brain concussion and acubarotrauma in the acute period.Materials and methods. The study involved 43 members of the armed forces (average total time of stay in a combat zone 15.5 ± 2.0 months) with an average age of 32.0 ± 1.3 years who received a mild traumatic brain injury (concussion) during 2019 and treated at the military mobile hospital (66.7 % of them had acubarotrauma). The manifestations of postconcussion symptoms were evaluated and analyzed using a modified questionnaire by K.Ciceron and the Hospital Anxiety and Depression Scale (HADS).Results. The prevalence of acubarotrauma characteristics has been determined among the wounded servicemen – participants of ATO (JFO) who had been hospitalized with a concussion to the military mobile hospital, and their structural changes after treatment, characterized by a significant improvement in all the studied data – dysfunction of the auditory analyzer, as well as cognitive and affective disorders, anxiety, depression, somatic, sensory disturbances inherent to individuals with a concussion have been assessed. A direct effect of the deployment time in combat zone on such characteristics after treatment of both studied groups as anxiety manifestations (P < 0.01), somatic manifestations (P < 0.001), sensory disturbances (P < 0.01) has been noted. A discriminant model allows to reliably (P < 0.001) determine patterns of informative characteristics of functional state in patients with concussion and those who additionally had acubarotrauma on admission to the hospital.Conclusions. Pathological comorbidity (concussion combined with acubarotrauma) contributes to the predominance of sensory and cognitive impairment manifestations after trauma, was accompanied by a significantly better recovery dynamics of somatic manifestations, sensory impairment and affective reactions due to the approximation of these characteristics to normative values compared with patients that had only a concussion. It has been established that the presence of comorbid pathology before its treatment had a significant effect on sensory and cognitive impairment, dysfunction of the auditory analyzer both prior to and after the treatment and, conversely, anxiety manifestations prior to and after the treatment somatic manifestations and affective reactions after treatment were negatively correlated with the factor of acubarotrauma. The features of the deployment time in the combat zone influence on the post-concussion symptoms manifestations have been revealed. The most informative characteristics allowing to differentiate patients with concussion and those who had acubarotrauma (anxious feeling, neuro-emotional stress, taste or smell changes, vision problems) have been highlighted.

T58. EFFECTIVENESS OF ORALLY ADMINISTERED CO-ENZYME Q10 FOR SCHIZOPHRENIA: COGNITIVE, FUNCTIONAL AND BIOCHEMICAL OUTCOMES FROM A DOUBLE BLIND, RANDOMISED, PLACEBO CONTROLLED TRIAL

BackgroundCoenzyme Q10 (CoQ10) is an endogenous compound that is essential for energy production within the mitochondria and also functions as a potent anti-oxidant, inhibiting oxidative stress and damage. Often deficits in CoQ10 are associated with fatigue, and cognitive and psychological impairment. In light of its many functions, CoQ10 supplementation to minimise decline and improve symptoms has been investigated in multiple disorders including neurological and neuropsychiatric disorders, with results indicating positive effects on fatigue, cognitive impairment and affective difficulties for disorders such as bipolar disorder and chronic fatigue syndrome. There is also evidence of mitochondrial dysfunction in schizophrenia. In light of this evidence, the current study aimed to investigate the potential effect of CoQ10 supplementation on 1) cognitive function and 2) psychological and physical health in schizophrenia and schizoaffective disorder.MethodsA double blind, randomised, placebo controlled study was conducted to assess the effects of CoQ10 supplementation (300mg/day) on cognitive, psychological and physical variables in 70 patients with schizophrenia and schizoaffective disorder. The effects of CoQ10 supplementation were compared to placebo at 3 and 6 months. Plasma CoQ10 was measured at all time points, along with measures of mitochondrial function (via plasma lactate concentration). Sensitivity analysis followed an intention to treat approach that used multiple imputations to account for missing values.ResultsOverall there was no effect of CoQ10 supplementation on cognitive outcome measures. This is despite observing an increase in plasma CoQ10 concentration in the CoQ10 group compared to the placebo. CoQ10 supplementation also had no effect on mitochondrial function, energy, psychological symptoms, quality of life, functional status, physical activity or blood pressure at either time point.DiscussionThere is considerable evidence that mitochondrial dysfunction is present in patients with schizophrenia and schizoaffective disorder, and this dysfunction is implicated in the manifestation of cognitive impairment and clinical symptoms. CoQ10 can be taken as a nutritional supplement with minimal side effects to target mitochondrial dysfunction via promoting ATP generation and increasing antioxidant capacity. However, we found no effect of CoQ10 supplementation on any variable under investigation. It is possible that CoQ10 might act as a protective agent against exacerbated oxidative stress in these patients, and future studies might be warranted to examine this possibility. However, the current data is conclusive that CoQ10 supplementation does not ameliorate existing deficits in schizophrenia. These findings are translatable to clinical and community settings.

COGNITIVE IMPAIRMENT IS VERY COMMON AMONG PATIENTS WITH HEART FAILURE REGARDLESS OF EJECTION FRACTION

Cognitive impairment (CI) is a common co-morbiditiy associated with increased readmission rate and mortality in patients with heart failure (HF). However, the prevalence, characteristics and manifestations of CI may be different among patients with HF classified by left ventricular ejection fraction

Chemotherapy-related cognitive impairment: mechanisms, clinical features and research perspectives.

The term chemotherapy-related cognitive impairment (CRCI), or cognitive dysfunction, or chemo fog, or chemo brain, is referred to a decline in a variety of neuropsychological tasks after chemotherapy, or following other anticancer treatments such as radiation therapy or surgery, in patients with non-central nervous system cancers. Furthermore, several pieces of evidence suggest that clinical manifestations of cognitive impairment may occur in cancer patients, prior to chemotherapy or in those not treated with cancer therapies. In these circumstances, it should be more appropriate to use the term cancer-related cognitive dysfunction. Because there is no consensus about its definition and diagnostic criteria, no specific test for CRCI diagnose exists. Whatever the cause, this manifestation of central nervous system toxicity is of increasing concern as the survival rates for cancer have improved steadily and, in turn, cognitive dysfunction can negatively impact the patients and cancer survivors' quality of life. The aim of this work is to offer an overview of the topic and recommendations for future research.

Influence of Standardized Extract Ginkgo biloba EGb761® Towards Quality of Life Indicators in Patients with Diabetes Mellitus Type 2

Cognitive impairment in patients with type 2 diabetes mellitus (DM-2) currently attracts a lot of attention due to their impact on quality of life and the effectiveness of treatment. The aim of research is to find the most effective medication which influences the cognitive functions positively. The research included 120 patients with average age of 61.22 ± 8.6 and average DM-2 duration of 10.84 ± 8.2 years. Mini Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA test), Trail Making Test (TMT), Parts A and B, Hospital Anxiety and Depression Scale (HADS), and The Short Form-36 (SF-36) were used. It was revealed that patients with DM type 2 had cognitive dysfunction generally presented by mild cognitive impairment. Patients with DM-2 have an early manifestation of cognitive impairment. After the initial estimation of indicators, all the patients were taking standardized extract Ginkgo biloba (EGb 761®) in the dose 240 mg a day for 6 months. Estimation of all the indicators after 3 and 6 months of treatment showed significant cognitive improvement. By matching the available experimental and clinical data, we can conclude that in the setting of DM-2 EGb 761®, by producing a positive effect towards various factors which results from insulin resistance of the brain, improves functions of the brain, which manifests in improvement of main QoL indicators in DM-2.

Cognitive characteristics in Chinese non-demented PD patients based on gender difference

BackgroundCognitive impairment is one of the non-motor symptoms in Parkinson’s disease (PD). In the present study, we aim to examine the cognitive function of non-demented Parkinson’s disease patients and compare the results between male and female patients as well as control groups in search of any gender effect.MethodsSixty PD Patients (30 males and 30 females) from the Movement Disorders Clinic at Huashan Hospital Affiliated to Fudan University were recruited to participate in the study. One hundred age and gender matched control subjects without neurological or psychiatric disorders were voluntarily recruited. The participants were administered measures of cognition in five domains including memory, language, spatial processing abilities, attention and executive function.ResultsPD patients attained significantly lower scores in the visual spatial function, language and attention/executive function compared with the control group. Anti-parkinsonian treated patients performed worse in Rey-copy score, Clock Drawing Test (CDT) and Verbal Fluency-City than untreated ones. In regard to gender differences, though no general cognitive differences were found in Mini-mental State Examination (MMSE), men surpassed women on Boston naming test (BNT) while women were superior on Auditory Verbal Learning Test-long (AVLT) delayed cued recall test.ConclusionsCognitive impairments were common in PD patients even in the absence of dementia. PD patients with anti-parkinsonian medication had worse cognitive impairment than untreated patients. Genders may have different manifestations of cognitive impairment in PD patients.

Adapting the concepts of brain and cognitive reserve to post-stroke cognitive deficits: Implications for understanding neglect

Advanced lesion mapping and connectivity analyses are currently the main tools used to understand the mechanisms underlying post-stroke cognitive deficits. However, the factors contributing to pre-stroke architecture of cognitive networks are often ignored, even though they reportedly play a decisive role in the manifestation of cognitive impairment in neurodegeneration. The present review on post-stroke cognitive deficits therefore adopts the concept of brain and cognitive reserve, which was originally developed to account for the individual differences in the course of aging and neurodegenerative diseases. By focusing on spatial neglect, a typical network disorder, it is discussed how individual susceptibility to stroke lesion might explain the reported discrepancies in lesion anatomy, non-spatial deficits and recovery courses. A detailed analysis of the literature reveals that premorbid brain (age, brain atrophy, previous strokes, leukoaraiosis, genetic factors, etc.) and cognitive reserve (IQ, life experience, education, occupation, premorbid cognitive impairment, etc.) greatly impact the brain's capacity for compensation. Furthermore, the interaction between pre-stroke brain/cognitive reserve and the degree of stroke-induced system impairment (e.g., hypoperfusion, lesion load) determines both the extent of neglect symptoms variability and the course of recovery. Premorbid brain/cognitive reserves should thus be considered to: (i) understand the mechanisms of post-stroke cognitive disorders and sufficiently explain their inter-individual variability; (ii) provide a prognosis for cognitive recovery and hence post-stroke dependency; (iii) identify individual targets for cognitive rehabilitation: in the case of reduced brain/cognitive reserve, neglect might occur even with a confined lesion, and non-spatial training of general attentional capacity should represent the main therapeutic target also for treatment of neglect; this might be true also for non-cognitive domains, e.g., motor deficit. This alternative view of how neglect and other cognitive deficits occur and recover promotes discussion about plasticity and recovery to a general rather than a single stroke-based domain, providing more efficiency in recovery research.

The cognitive neuropsychological phenotype of carriers of the FMR1 premutation.

The fragile X-associated tremor/ataxia syndrome (FXTAS) is a late-onset neurodegenerative disorder affecting a subset of carriers of the FMR1 (fragile X mental retardation 1) premutation. Penetrance and expression appear to be significantly higher in males than females. Although the most obvious aspect of the phenotype is the movement disorder that gives FXTAS its name, the disorder is also accompanied by progressive cognitive impairment. In this review, we address the cognitive neuropsychological and neurophysiological phenotype for males and females with FXTAS, and for male and female unaffected carriers. Despite differences in penetrance and expression, the cognitive features of the disorder appear similar for both genders, with impairment of executive functioning, working memory, and information processing the most prominent. Deficits in these functional systems may be largely responsible for impairment on other measures, including tests of general intelligence and declarative learning. FXTAS is to a large extent a white matter disease, and the cognitive phenotypes observed are consistent with what some have described as white matter dementia, in contrast to the impaired cortical functioning more characteristic of Alzheimer’s disease and related disorders. Although some degree of impaired executive functioning appears to be ubiquitous among persons with FXTAS, the data suggest that only a subset of unaffected carriers of the premutation - both female and male - demonstrate such deficits, which typically are mild. The best-studied phenotype is that of males with FXTAS. The manifestations of cognitive impairment among asymptomatic male carriers, and among women with and without FXTAS, are less well understood, but have come under increased scrutiny.

Psychiatric symptoms in patients with Shiga toxin-producing E. coli O104:H4 induced haemolytic-uraemic syndrome.

BackgroundIn May 2011 an outbreak of Shiga toxin-producing enterohaemorrhagic E. coli (STEC) O104:H4 in Northern Germany led to a high number of in-patients, suffering from post-enteritis haemolytic-uraemic syndrome (HUS) and often severe affection of the central nervous system. To our knowledge so far only neurological manifestations have been described systematically in literature.AimTo examine psychiatric symptoms over time and search for specific symptom clusters in affected patients.Methods31 in-patients suffering from E. coli O104:H4 associated HUS, were examined and followed up a week during the acute hospital stay. Psychopathology was assessed by clinical interview based on the AMDP Scale, the Brief Symptom Inventory and the Clinical Global Impressions Scale.ResultsAt baseline mental disorder due to known physiological condition (ICD-10 F06.8) was present in 58% of the examined patients. Patients suffered from various manifestations of cognitive impairment (n = 27) and hallucinations (n = 4). Disturbances of affect (n = 28) included severe panic attacks (n = 9). Psychiatric disorder was significantly associated with higher age (p<0.0001), higher levels of C-reactive protein (p<0.05), and positive family history of heart disease (p<0.05). Even within the acute hospital stay with a median follow up of 7 days, symptoms improved markedly over time (p <0.0001).ConclusionsAside from severe neurological symptoms the pathology in E.coli O104:H4 associated HUS frequently includes particular psychiatric disturbances. Long term follow up has to clarify whether or not these symptoms subside.