Experimental colitis in young Tg2576 mice accelerates the onset of an Alzheimer's-like clinical phenotype.

Systemic inflammation and neuroinflammation affect the natural course of the sporadic form of Alzheimer's disease (AD), as supported by epidemiological and preclinical data, and several epidemiological studies indicate a higher prevalence of AD in patients with inflammatory bowel disease. In this study, we explored whether colitis induced by dextran sulfate sodium (DSS) in young, presymptomatic/preplaque mice worsens and/or anticipates age-dependent cognitive impairment in Tg2576, a widely used mouse model of AD. We demonstrated that DSS colitis induced in young Tg2576 mice anticipates the onset age of learning and memory deficit in the Morris water maze test. To explore potential mechanisms behind the acceleration of cognitive decline in Tg2576 mice by DSS colitis, we focused on gut microbiota, systemic inflammation and neuroinflammation markers. We observed a Firmicutes/Bacteroidetes ratio change in Tg2576 DSS animals comparable to that of elderly Tg2576 mice, suggesting accelerated microbiota aging in Tg2576 DSS mice, a change not observed in C57BL6 DSS mice. We also observed substantial differences between Tg2576 and WT mice in several inflammation and neuroinflammation-related parameters as early as 3 months of age, well before plaque deposition, a picture which evolved rapidly (between 3 and 5.5 months of age) in contrast to Tg2576 and WT littermates not treated with DSS. In detail, following induction of DSS colitis, WT and Tg2576 mice exhibited contrasting features in the expression level of inflammation-evoked astrocyte-associated genes in the hippocampus. No changes in microglial features occurred in the hippocampus between the experimental groups, whereas a reduced glial fibrillary acidic protein immunoreactivity was observed in Tg2576 vs. WT mice. This finding may reflect an atrophic, "loss-of-function" profile, further exacerbated by DSS where a decreased of GFAP mRNA expression level was detected. In conclusion, we suggest that as-yet unidentified peripheral mediators evoked by DSS colitis and involving the gut-brain axis emphasize an astrocyte "loss-of-function" profile present in young Tg2576 mice, leading to impaired synaptic morphological and functional integrity as a very early sign of AD.

Crocin ameliorates neuroinflammation and cognitive impairment in mice with Alzheimer's disease by activating PI3K/AKT pathway.

BACKGROUND: Crocin has a good prospect in the treatment of Alzheimer's disease (AD), but the mechanisms underlying its neuroprotective effects remain elusive. This study aimed to investigate the neuroprotective effects of Crocin and its underlying mechanisms in AD. METHODS: AD mice were set up by injecting Aß25-35 solution into the hippocampus. Then, the AD mice were injected intraperitoneally with 40 mg/kg/day of Crocin for 14 days. Following the completion of Crocin treatment, an open-field test, Y-maze test and Morris water maze test were conducted to evaluate the impact of Crocin on spatial learning and memory deficiency in mice. The effects of Crocin on hippocampal neuron injury, proinflammatory cytokine expressions (IL-1ß, IL-6, and TNF-α), and PI3K/AKT signaling-related protein expressions were measured using hematoxylin and eosin staining, Western blot, and quantitative real-time polymerase chain reaction (qRT-PCR) experiments, respectively. RESULTS: Crocin attenuated Aß25-35-induced spatial learning and memory deficiency and hippocampal neuron injury. Furthermore, the Western blot and qRT-PCR results showed that Crocin effectively suppressed inflammation and activated the PI3K/AKT pathway in Aß25-35-induced mice. CONCLUSION: Crocin restrained neuroinflammation via the activation of the PI3K/AKT pathway, thereby ameliorating the cognitive dysfunction of AD mice.

[EEG changes in patients with Alzheimer's disease]. / Izmeneniya elektroentsefalogrammy u patsientov s bolezn'yu Al'tsgeimera.

The prevalence of cognitive impairment is steadily increasing compared to previous years. According to the World Health Organization, the number of people living with dementia will increase reaching 82 million in 2030 and 152 million in 2050. The most common cause is Alzheimer's disease (AD). The pathophysiological process in AD begins several years before the onset of clinical symptoms; so identifying it at an early stage would likely improve the clinical prognosis. The article presents EEG changes in patients with AD, and discusses the possibility of using EEG as a screening method for examining patients with cognitive impairment.

[Cognitive impairment in multiple system atrophy - exclusion criteria or an integral part of the clinical picture?] / Kognitivnye narusheniya pri mul'tisistemnoi atrofii ­ kriterii isklyucheniya ili neot"emlemaya chast' klinicheskoi kartiny?

Multiple system atrophy (MSA) is a severe, orphan disease characterized by a steady increase in symptoms of parkinsonism, cerebellar disorders, and autonomic failure. In addition to autonomic failure, which is considered the defining symptom of this type of atypical parkinsonism, there are a range of other non-motor clinical manifestations, such as sleep disorders, pain syndrome, anxiety-depressive disorders, cognitive impairment (CI). CI, especially severe CI, has long been considered as a distinctive feature of MCA. Recently, there have been many clinical studies with pathomorphological or neuroimaging confirmation, indicating a high prevalence of cognitive disorders in MCA. In this article, we discuss the pathogenetic mechanisms of the development of MCA and CI in MCA, as well as the range of clinical manifestations of cognitive dysfunction.

MSC-derived exosomal miR-140-3p improves cognitive dysfunction in sepsis-associated encephalopathy by HMGB1 and S-lactoylglutathione metabolism.

MiRNAs in mesenchymal stem cells (MSCs)-derived exosome (MSCs-exo) play an important role in the treatment of sepsis. We explored the mechanism through which MSCs-exo influences cognitive impairment in sepsis-associated encephalopathy (SAE). Here, we show that miR-140-3p targeted Hmgb1. MSCs-exo plus miR-140-3p mimic (Exo) and antibiotic imipenem/cilastatin (ABX) improve survival, weight, and cognitive impairment in cecal ligation and puncture (CLP) mice. Exo and ABX inhibit high mobility group box 1 (HMGB1), IBA-1, interleukin (IL)-1ß, IL-6, iNOS, TNF-α, p65/p-p65, NLRP3, Caspase 1, and GSDMD-N levels. In addition, Exo upregulates S-lactoylglutathione levels in the hippocampus of CLP mice. Our data further demonstrates that Exo and S-lactoylglutathione increase GSH levels in LPS-induced HMC3 cells and decrease LD and GLO2 levels, inhibiting inflammatory responses and pyroptosis. These findings suggest that MSCs-exo-mediated delivery of miR-140-3p ameliorates cognitive impairment in mice with SAE by HMGB1 and S-lactoylglutathione metabolism, providing potential therapeutic targets for the clinical treatment of SAE.

Correlation of dietary inflammation index and dietary pattern with mild cognitive impairment in patients with type 2 diabetes.

OBJECTIVE: We aimed to determine the dietary patterns associated with mild cognitive impairment (MCI) in type 2 diabetes (T2DM) and the correlation of dietary inflammatory index (DII) with MCI. METHODS: The Montreal Cognitive Assessment (MoCA) was used to assess cognitive function. A semi-quantitative food frequency questionnaire was used to collect dietary data and calculate DII. Dietary patterns were determined by reduced-rank regression (RRR), grouping dietary pattern scores and DII into quartiles, with logistic regression for correlation analysis. Dose-response relationships between dietary pattern scores, DII and diabetic MCI were explored using restricted cubic splines (RCS). A mediation analysis was performed to investigate whether DII mediates the association between dietary patterns and MCI. RESULTS: In the "Mediterranean-style dietary pattern", the multivariable-adjusted odds ratio of having MCI was 0.37 (95% CI: 0.20-0.68; p for trend=0.002) in the highest versus lowest quartiles of the dietary score. In the "high-meat and low-vegetable pattern", the multivariable-adjusted odds ratio of having MCI was 6.84 (95% CI: 3.58-13.10; p for trend<0.001) in the highest versus lowest quartiles of the dietary score. In the "Western-style dietary pattern", the multivariable-adjusted odds ratio of having MCI was 2.48 (95% CI: 1.38-4.46; p for trend=0.001). The multivariable-adjusted odds ratio of having MCI was 3.99 (95% CI: 2.14-7.42; p for trend<0.001) in the highest versus lowest quartiles of DII. There is a non-linear dose-response relationship between the "high-meat and low-vegetable pattern" score and the prevalence of MCI, as well as the DII and the prevalence of MCI. The DII partially mediated the impact of the "Mediterranean-style dietary pattern" and the "high-meat and low-vegetable pattern" on MCI. CONCLUSION: In T2DM patients, greater adherence to the "Mediterranean-style dietary pattern" is associated with a lower probability of having MCI. However, excessive consumption of meat, especially red meat and processed meat, combined with a lack of vegetable intake, is associated with a higher probability of having MCI. Greater adherence to the "Western-style dietary pattern" is associated with a higher probability of having MCI. In addition, a pro-inflammatory diet is associated with a higher probability of having MCI, and DII partially mediates the impact of dietary patterns on MCI.

Irregular word reading as a marker of semantic decline in Alzheimer's disease: implications for premorbid intellectual ability measurement.

BACKGROUND: Irregular word reading has been used to estimate premorbid intelligence in Alzheimer's disease (AD) dementia. However, reading models highlight the core influence of semantic abilities on irregular word reading, which shows early decline in AD. The primary objective of this study is to ascertain whether irregular word reading serves as an indicator of cognitive and semantic decline in AD, potentially discouraging its use as a marker for premorbid intellectual abilities. METHOD: Six hundred eighty-one healthy controls (HC), 104 subjective cognitive decline, 290 early and 589 late mild cognitive impairment (EMCI, LMCI) and 348 AD participants from the Alzheimer's Disease Neuroimaging Initiative were included. Irregular word reading was assessed with the American National Adult Reading Test (AmNART). Multiple linear regressions were conducted predicting AmNART score using diagnostic category, general cognitive impairment and semantic tests. A generalized logistic mixed-effects model predicted correct reading using extracted psycholinguistic characteristics of each AmNART words. Deformation-based morphometry was used to assess the relationship between AmNART scores and voxel-wise brain volumes, as well as with the volume of a region of interest placed in the left anterior temporal lobe (ATL), a region implicated in semantic memory. RESULTS: EMCI, LMCI and AD patients made significantly more errors in reading irregular words compared to HC, and AD patients made more errors than all other groups. Across the AD continuum, as well as within each diagnostic group, irregular word reading was significantly correlated to measures of general cognitive impairment / dementia severity. Neuropsychological tests of lexicosemantics were moderately correlated to irregular word reading whilst executive functioning and episodic memory were respectively weakly and not correlated. Age of acquisition, a primarily semantic variable, had a strong effect on irregular word reading accuracy whilst none of the phonological variables significantly contributed. Neuroimaging analyses pointed to bilateral hippocampal and left ATL volume loss as the main contributors to decreased irregular word reading performances. CONCLUSIONS: While the AmNART may be appropriate to measure premorbid intellectual abilities in cognitively unimpaired individuals, our results suggest that it captures current semantic decline in MCI and AD patients and may therefore underestimate premorbid intelligence. On the other hand, irregular word reading tests might be clinically useful to detect semantic impairments in individuals on the AD continuum.

Melatonin improves maternal sleep deprivation-induced learning and memory impairment, inflammation, and synaptic dysfunction in murine male adult offspring.

INTRODUCTION: Maternal sleep deprivation (MSD), which induces inflammation and synaptic dysfunction in the hippocampus, has been associated with learning and memory impairment in offspring. Melatonin (Mel) has been shown to have anti-inflammatory, antioxidant, and neuroprotective function. However, the beneficial effect of Mel on MSD-induced cognitive impairment and its mechanisms are unknown. METHODS: In the present study, adult offspring suffered from MSD were injected with Mel (20 mg/kg) once a day during postnatal days 61-88. The cognitive function was evaluated by the Morris water maze test. Levels of proinflammatory cytokines were examined by enzyme-linked immunosorbent assay. The mRNA and protein levels of synaptic plasticity associated proteins were examined using reverse transcription-polymerase chain reaction and western blotting. RESULTS: The results showed that MSD impaired learning and memory in the offspring mice. MSD increased the levels of interleukin (IL)-1creIL-6, and tumor necrosis factor-α and decreased the expression levels of brain-derived neurotrophic factor, tyrosine kinase receptor B, postsynaptic density protein-95, and synaptophysin in the hippocampus. Furthermore, Mel attenuated cognitive impairment and restored markers of inflammation and synaptic plasticity to control levels. CONCLUSIONS: These findings indicated that Mel could ameliorate learning and memory impairment induced by MSD, and these beneficial effects were related to improvement in inflammation and synaptic dysfunction.

The relation of a cerebrospinal fluid profile associated with Alzheimer's disease with cognitive function and neuropsychiatric symptoms in sporadic cerebral amyloid angiopathy.

BACKGROUND: Patients with sporadic cerebral amyloid angiopathy (sCAA) frequently report cognitive or neuropsychiatric symptoms. The aim of this study is to investigate whether in patients with sCAA, cognitive impairment and neuropsychiatric symptoms are associated with a cerebrospinal fluid (CSF) biomarker profile associated with Alzheimer's disease (AD). METHODS: In this cross-sectional study, we included participants with sCAA and dementia- and stroke-free, age- and sex-matched controls, who underwent a lumbar puncture, brain MRI, cognitive assessments, and self-administered and informant-based-questionnaires on neuropsychiatric symptoms. CSF phosphorylated tau, total tau and Aß42 levels were used to divide sCAA patients in two groups: CAA with (CAA-AD+) or without a CSF biomarker profile associated with AD (CAA-AD-). Performance on global cognition, specific cognitive domains (episodic memory, working memory, processing speed, verbal fluency, visuoconstruction, and executive functioning), presence and severity of neuropsychiatric symptoms, were compared between groups. RESULTS: sCAA-AD+ (n=31; mean age: 72 ± 6; 42%, 61% female) and sCAA-AD- (n=23; 70 ± 5; 42% female) participants did not differ with respect to global cognition or type of affected cognitive domain(s). The number or severity of neuropsychiatric symptoms also did not differ between sCAA-AD+ and sCAA-AD- participants. These results did not change after exclusion of patients without prior ICH. CONCLUSIONS: In participants with sCAA, a CSF biomarker profile associated with AD does not impact global cognition or specific cognitive domains, or the presence of neuropsychiatric symptoms.

Circulating HMGB1 in acute ischemic stroke and its association with post-stroke cognitive impairment.

Background: Ischemic stroke frequently leads to a condition known as post-stroke cognitive impairment (PSCI). Timely recognition of individuals susceptible to developing PSCI could facilitate the implementation of personalized strategies to mitigate cognitive deterioration. High mobility group box 1 (HMGB1) is a protein released by ischemic neurons and implicated in inflammation after stroke. Circulating levels of HMGB1 could potentially serve as a prognostic indicator for the onset of cognitive impairment following ischemic stroke. Objective: To investigate the predictive value of circulating HMGB1 concentrations in the acute phase of ischemic stroke for the development of cognitive dysfunction at the 3-month follow-up. Methods: A total of 192 individuals experiencing their initial episode of acute cerebral infarction were prospectively recruited for this longitudinal investigation. Concentrations of circulating HMGB1 were quantified using an enzyme-linked immunosorbent assay (ELISA) technique within the first 24 hours following hospital admission. Patients underwent neurological evaluation including NIHSS scoring. Neuropsychological evaluation was conducted at the 3-month follow-up after the cerebrovascular event, employing the Montreal Cognitive Assessment (MoCA) as the primary tool for assessing cognitive performance. Multivariable logistic regression models were employed to investigate the relationship between circulating HMGB1 concentrations and cognitive dysfunction following stroke, which was operationalized as a MoCA score below 26, while controlling for potential confounders including demographic characteristics, stroke severity, vascular risk factors, and laboratory parameters. Results: Of 192 patients, 84 (44%) developed PSCI. Circulating HMGB1 concentrations were significantly elevated in individuals who developed cognitive dysfunction following stroke compared to those who maintained cognitive integrity (8.4 ± 1.2 ng/mL vs 4.6 ± 0.5 ng/mL, respectively; p < 0.001). The prevalence of PSCI showed a dose-dependent increase with higher HMGB1 quartiles. After controlling for potential confounders such as demographic factors (age, gender, and education), stroke severity, vascular risk factors, and laboratory parameters in a multivariable logistic regression model, circulating HMGB1 concentrations emerged as a significant independent predictor of cognitive dysfunction following stroke (regression coefficient = 0.236, p < 0.001). Conclusion: Circulating HMGB1 concentrations quantified within the first 24 hours following acute cerebral infarction are significantly and independently correlated with the likelihood of developing cognitive dysfunction at the 3-month follow-up, even after accounting for potential confounding factors. HMGB1 may be a novel biomarker to identify patients likely to develop post-stroke cognitive impairment for targeted preventive interventions.

Reversibility of Cognitive Deficits and Functional Connectivity With Transfusion in Children With Sickle Cell Disease.

BACKGROUND AND OBJECTIVES: People with sickle cell disease (SCD) are at risk of cognitive dysfunction independent of stroke. Diminished functional connectivity in select large-scale networks and white matter integrity reflect the neurologic consequences of SCD. Because chronic transfusion therapy is neuroprotective in preventing stroke and strengthening executive function abilities in people with SCD, we hypothesized that red blood cell (RBC) transfusion facilitates the acute reversal of disruptions in functional connectivity while white matter integrity remains unaffected. METHODS: Children with SCD receiving chronic transfusion therapy underwent a brain MRI measuring white matter integrity with diffusion tensor imaging and resting-state functional connectivity within 3 days before and after transfusion of RBCs. Cognitive assessments with the NIH Toolbox were acquired after transfusion and then immediately before the following transfusion cycle. RESULTS: Sixteen children with a median age of 12.5 years were included. Global assessments of functional connectivity using homotopy (p = 0.234) or modularity (p = 0.796) did not differ with transfusion. Functional connectivity within the frontoparietal network significantly strengthened after transfusion (median intranetwork Z-score 0.21 [0.17-0.30] before transfusion, 0.29 [0.20-0.36] after transfusion, p < 0.001), while there was not a significant change seen within the sensory motor, visual, auditory, default mode, dorsal attention, or cingulo-opercular networks. Corresponding to the change within the frontoparietal network, there was a significant improvement in executive function abilities after transfusion (median executive function composite score 87.7 [81.3-90.7] before transfusion, 90.3 [84.3-93.7] after transfusion, p = 0.021). Participants with stronger connectivity in the frontoparietal network before transfusion had a significantly greater improvement in the executive function composite score with transfusion (r = 0.565, 95% CI 0.020-0.851, p = 0.044). While functional connectivity and executive abilities strengthened with transfusion, there was not a significant change in white matter integrity as assessed by fractional anisotropy and mean diffusivity within 16 white matter tracts or globally with tract-based spatial statistics. DISCUSSION: Strengthening of functional connectivity with concomitant improvement in executive function abilities with transfusion suggests that functional connectivity MRI could be used as a biomarker for acutely reversible neurocognitive injury as novel therapeutics are developed for people with SCD.

Characteristics of brain lesions found using MRI imaging in patients with post-COVID with signs of cognitive decline.

OBJECTIVE: Aim: To describe and evaluate abnormalities of the brain in post-COVID patients with neurologic symptoms and cognitive deficits using MRI imaging of the brain. PATIENTS AND METHODS: Materials and Methods: We included 21 patients with a previous positive PCR testing for SARS-CoV-2 and one or more of the following symptoms: memory and cognitive decline, dizziness, anxiety, depression, chronic headaches. All patients had MRI imaging done at onset of symptoms, but after at least 1 year after positive testing for COVID-19 based on the patient's previous medical history. RESULTS: Results: All of the patients complained of lack of concentration, forgetfulness, hard to process information. 15 patients suffered from confusion, 10 from anxiety. Of the 21 patients 14 had isolated chronic headaches, 3 had isolated dizziness, 4 patients had both symptoms upon inclusion. All patients underwent MRI imaging as a part of the diagnostic workup and had varying degrees of neurodegeneration. CONCLUSION: Conclusions: Our data correlates with existing research and shows tendency for cognitive decline in post-COVID patients. This provides groundwork for further research to determine correlation between acceleration of neurodegeneration and post-COVID.

[Cognitive impairment in cerebrovascular diseases]. / Kognitivnye narusheniya pri sosudistykh zabolevaniyakh golovnogo mozga.

Cognitive impairment, which is highly prevalent, especially among older people, leads to a decrease in the quality of life of patients, impairment of daily activities, and an increased risk of dementia and mortality. Currently, much attention is paid to mild cognitive impairment. The article discusses diagnostic criteria and possible clinical variants of this syndrome. Given the high rate of progression of mild cognitive impairment to dementia, it is necessary to identify risk groups and carry out therapeutic preventive measures. Correction of potentially modifiable risk factors is considered as a promising direction of therapy. Sufficient physical and mental activity, proper diet, normalization of sleep, visual acuity and hearing are necessary. Preventing stroke and controlling vascular risk factors may reduce the risk of mild cognitive impairment progressing to dementia.

[Impairment of attention and executive functions in chronic cerebrovascular disease and Alzheimer's disease]. / Narushenie vnimaniya i upravlyayushchikh funktsii pri sosudistykh kognitivnykh narusheniyakh i bolezni Al'tsgeimera.

OBJECTIVE: To establish specific features of executive functions (EF) impairment and attention in vascular cognitive impairment (VCI) and Alzheimer's disease (AD). MATERIAL AND METHODS: Eighty people (over the age of 50) diagnosed with cerebrovascular disease (CVD) and AD, as well as 29 healthy volunteers (control group), were examined. The following neuropsychological methods were used to study the quantitative and qualitative characteristics of cognitive impairments: Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), EXIT-25, Frontal Assessment Battery (FAB), Clock Drawing Test, «12 Words¼ test, verbal associations (literal and categorical) method, Trail Making Test A and B, Symbol-Digit Modalities Test (SDMT), Stroop Test, and Benton Visual Retention Test. Mandatory inclusion criteria in the study included having a completed magnetic resonance imaging (MRI) of the brain (in T1, T2, FLAIR, DWI, SWI modes) within 1 year before enrollment in one of the groups. RESULTS: No significant differences in age, sex, and level of education were found between the groups. Groups AD and CVD were also comparable in the severity of cognitive impairment overall. Attention and working memory deficits were observed in both CVD and AD, with slightly more pronounced deficits in the AD group. Qualitative analysis of individual components of working memory revealed that both CVD and AD groups had comparable cognitive control impairment compared to the control group, while AD was characterized by a more significant decrease in intellectual flexibility compared to CVD. Sustained attention was equally impaired among patients in the CVD and AD groups, with a significant difference from the control group (p<0.05). In terms of memory, it was found that auditory-verbal memory and semantic memory were significantly more affected in AD, while visual memory was impaired in both conditions. CONCLUSION: Attention and EF impairments are not specific to the «subcortical¼ type of cognitive disorders. Already in the early stages, AD is characterized by a significant impairment of attention and EF, and such a component of EF as intellectual flexibility suffers at the onset of AD to a greater extent than in VCI. Memory impairments are not specific to AD; already at the onset of VCI, visual memory impairment comparable to AD is noted. The obtained data can be used for early neuropsychological diagnosis and differential diagnosis of dementing cerebral diseases.

[Cognitive impairment in patients with arterial hypertension]. / Kognitivnye narusheniya u patsientov s arterial'noi gipertenziei.

Arterial hypertension (AH) is a leading risk factor for cardiovascular diseases including cerebrovascular complications. Strokes and/or vascular cognitive impairment (VCI) are considered as a clinical sign of brain damage as a target organ in hypertension. To identify and assess the severity of VCI, patients with hypertension should undergo a neuropsychological assessment. Neuroimaging confirm the vascular origin of cognitive impairment. Patient management should include antihypertensive therapy along with neuroprotection. Among different neuroprotective therapy, ethylmethylhydroxypyridine succinate (mexidol) is one of medication with serious evidence of clinical efficacy.

[Comparative characteristics of neuropsychological and neurometabolic changes in patients with Alzheimer's disease and vascular cognitive impairment]. / Sravnitel'naya kharakteristika neiropsikhologicheskikh i neirometabolicheskikh pokazatelei u patsientov s bolezn'yu Al'tsgeimera i sosudistymi kognitivnymi rasstroistvami.

OBJECTIVE: To investigate the pattern and connections of neuropsychological and metabolic indices in patients with cognitive disorders of Alzheimer's and vascular (subcortical-cortical) types of different severity. MATERIAL AND METHODS: A total of 177 patients were examined, including 85 patients with Alzheimer's disease (AD) and 92 patients with vascular cognitive impairment (VCI). All patients underwent complex neuropsychological examination; 18F-FDG PET was performed in 17 patients with AD and 15 patients with VCI. RESULTS: The greatest changes in patients with AD were noted in the mnestic sphere, and the indicators significantly differed from the results of the study of patients with VCI already at the pre-dementia stage. Neurodynamic and dysregulatory disorders prevailed in patients with VCI. Patients with AD showed bilateral symmetrical reduction of metabolic activity in the cortex of parietal and temporal lobes, often in combination with marked hypometabolism in the hippocampal region. In patients with VCI, there were areas of decreased brain tissue metabolism of different localization and size, mainly in the projection of the basal ganglia and in the prefrontal and parietal cortex, as well as in the cingulate gyrus, which indirectly confirms the mechanism of disconnection of subcortical and cortical structures. In AD, impaired metabolic activity in the hippocampal region correlated with impaired temporal and spatial orientation (ρ=-0.54, p<0.05), memory impairment (ρ=-0.71, p<0.005). Hypometabolism of the parietal lobe cortex was associated with total MMSE score (ρ=-0.8, p<0.001), 10-word test (ρ=-0.89, p<0.001 and ρ=-0.82, p<0.001), visual-spatial impairment (ρ=-0.64, p<0.01), categorical association test (ρ=-0.73, p<0.005). In patients with VCI, dysregulatory disorders correlated with hypometabolism in the thalamic projection (ρ=-0.56, p<0.05), prefrontal cortex (ρ=-0.64, p<0.05) and in the cingulate gyrus (anterior regions) (ρ=-0.53, p<0.05). CONCLUSION: The results indicate the presence of differences in cognitive impairment and cerebral metabolism in patients with AD and VCI.

[Algorithms for the diagnosis and treatment of cognitive impairment and dysphagia in stroke patients]. / Algoritmy diagnostiki i lecheniya kognitivnykh narushenii i disfagii u patsientov posle insul'ta.

Stroke is a socially significant neurological disease, the second most common cause of disability and mortality. A wide range of neurological problems that occur after stroke: cognitive, motor, speech, and language disfunction, neuropsychiatric, swallowing disorders and others, complicate rehabilitation, impair social and everyday adaptation, and reduce the quality of life of patients and their caregivers. Cognitive impairment (CI) is one of the most significant and common complications of stroke. Stroke increases the risk of their development by 5-8 times. Dysphagia is also a common symptom of stroke, the cause of aspiration complications (pneumonia), and nutritional imbalance. It increases the possibility of developing CI and dementia, and contributes to an increase in mortality. Older adults with CI are at a higher risk of developing dysphagia, therefore the early symptoms of dysphagia (presbyphagia) should be diagnosed. In recent years, the connection between CI and dysphagia has been actively studied. It is extremely important to identify CI and swallowing disorders as early as possible in patients both before and at all stages after stroke; as well as to develop combined multidisciplinary protocols for the rehabilitation of patients with these disorders with pharmacological support for the process.

Association between intensity of physical activity and cognitive function in hypertensive patients: a case-control study.

Previous studies have shown that a higher intensity of physical activity (PA) is associated with a lower risk of cognitive impairment (CI), whereas hypertension is associated with higher CI. However, there are few studies on the association between PA intensity and cognitive function in hypertensive patients. This study investigated the association between PA intensity and cognitive function in hypertensive patients. A total of 2035 hypertensive patients were included in this study, including 407 hypertensive patients with CI and 1628 hypertensive patients with normal cognitive function matched 1:4 by age and sex. The International Physical Activity Questionnaire-Long Form and the Mini-mental State Examination were used to evaluate PA intensity, total metabolic equivalents, and cognitive function in patients with hypertension. Multivariate logistic regression was used to analyze the correlation between PA intensity and CI in hypertensive patients. The Spearman correlation coefficient was used to analyze the correlation between PA intensity and the total score of each component of the MMSE and the correlation between PA total metabolic equivalents and cardiac structure in hypertensive patients. After adjusting for all confounding factors, PA intensity was negatively associated with CI in hypertensive patients (OR = 0.608, 95% CI: 0.447-0.776, P < 0.001), and this association was also observed in hypertensive patients with education level of primary school and below and junior high school and above (OR = 0.732, 95% CI: 0.539-0.995, P = 0.047; OR = 0.412, 95% CI: 0.272-0.626, P < 0.001). The intensity of PA in hypertensive patients was positively correlated with orientation (r = 0.125, P < 0.001), memory (r = 0.052, P = 0.020), attention and numeracy (r = 0.151, P < 0.001), recall ability (r = 0.110, P < 0.001), and language ability (r = 0.144, P < 0.001). PA total metabolic equivalents in hypertensive patients were negatively correlated with RVEDD and LAD (r = - 0.048, P = 0.030; r = - 0.051, P = 0.020) and uncorrelated with LVEDD (r = 0.026, P = 0.233). Higher PA intensity reduced the incidence of CI in hypertensive patients. Therefore, hypertensive patients were advised to moderate their PA according to their circumstances.

Investigation of high-dose radiotherapy's effect on brain structure aggravated cognitive impairment and deteriorated patient psychological status in brain tumor treatment.

This study aims to investigate the potential impact of high-dose radiotherapy (RT) on brain structure, cognitive impairment, and the psychological status of patients undergoing brain tumor treatment. We recruited and grouped 144 RT-treated patients with brain tumors into the Low dose group (N = 72) and the High dose group (N = 72) according to the RT dose applied. Patient data were collected by using the HADS and QLQ-BN20 system for subsequent analysis and comparison. Our analysis showed no significant correlation between the RT doses and the clinicopathological characteristics. We found that a high dose of RT could aggravate cognitive impairment and deteriorate patient role functioning, indicated by a higher MMSE and worsened role functioning in the High dose group. However, the depression status, social functioning, and global health status were comparable between the High dose group and the Low dose group at Month 0 and Month 1, while being worsened in the High dose group at Month 3, indicating the potential long-term deterioration of depression status in brain tumor patients induced by high-dose RT. By comparing patient data at Month 0, Month 1, Month 3, Month 6, and Month 9 after RT, we found that during RT treatment, RT at a high dose could aggravate cognitive impairment in the short term and lead to worsened patient role functioning, and even deteriorate the overall psychological health status of patients in the long term.