Impairment Of Cognitive Function Research Articles

Modulating Ferroptosis: A Novel Approach to Promote Neural Repair in Brain Injury.

The increasing prevalence of brain injuries resulting in cognitive and motor function impairments poses a substantial global medical challenge. Nerve repair therapies offer promise for addressing brain injury-related disorders. Ferroptosis, as a cell death mechanism associated with oxidative stress and inflammation. Certain ferroptosis inhibitors, such as iron chelators and antioxidants, exhibit therapeutic potential for brain injury-related conditions. This review explores the fundamental processes and associated mechanisms that regulate neural repair by inhibiting ferroptosis, thereby alleviating brain injury and promoting neuroregeneration. Furthermore, it examines the action mechanisms and potential therapeutic applications of ferroptosis inhibitors in neural repair, aiming to provide novel insights for treating brain injuries.

Electroencephalographic markers in Major Depressive Disorder: insights from absolute, relative power, and asymmetry analyses

IntroductionMajor Depressive Disorder (MDD) leads to dysfunction and impairment in neurological structures and cognitive functions. Despite extensive research, the pathophysiological mechanisms and effects of MDD on the brain remain unclear. This study aims to assess the impact of MDD on brain activity using EEG power spectral analysis and asymmetry metrics.MethodsEEG recordings were obtained from 48 patients with MDD and 78 healthy controls. The data were segmented into 2-second windows (1024 data points) and analyzed using the Welch method, an advanced variant of the Fast Fourier Transform (FFT). A Hanning time window with 50% overlap was applied to compute the modified periodogram. Absolute and relative power, along with asymmetry values in the theta, alpha, and beta frequency bands, were calculated.ResultsPatients with MDD exhibited significantly higher absolute and relative power in the theta and beta bands and decreased power in the alpha band compared to healthy controls. Asymmetry analysis revealed significant differences between symmetric channels in the theta band (F7-F8, C3-C4, T3-T4, T5-T6), alpha band (F7-F8, C3-C4, T3-T4, T5-T6, O1-O2), and beta band (C3-C4, T3-T4, T5-T6, P3-P4).DiscussionThe findings suggest that MDD affects brain mechanisms and cognitive functions, as evidenced by altered power values in the theta and alpha bands. Additionally, asymmetry values in theta, alpha, and beta bands may serve as potential biomarkers for MDD. This study highlights that beyond the commonly used alpha asymmetry, theta and beta asymmetry can also provide valuable insights into the neurophysiological effects of MDD, aligning with previous neuroimaging studies that indicate impairments in memory, attention, and neuroanatomical connectivity in MDD.

Antidopaminergic medications in Huntington's disease

Huntington's disease (HD) is a progressive neurodegenerative disorder marked by motor, cognitive, and behavioral impairments. Antidopaminergic medications (ADMs), such as VMAT2 inhibitors and antipsychotics, are commonly used to manage HD motor disturbances and behavioral disorders. For patients and caregivers, ADMs are an important tool for managing symptoms that negatively affect daily life. However, the impact of ADM use in HD is not firmly understood due to a lack of robust, systematic studies that assessed their overall effect on HD disease. A mounting body of evidence suggests these medications may be associated with worse clinical measures of cognitive function and functional impairment. While regulatory guidelines highlight adverse effects like sedation, cognitive dysfunction, and extrapyramidal symptoms, it is unclear whether ADMs directly impact disease progression or if the side effects mimic or exacerbate measures of HD symptoms in clinical trials. Given ADM effects on the central nervous system and biological uncertainty within HD outcomes, clinical trial designs should recognize the impact of ADMs on key outcomes, as measured by acceptable scales including Total Functional Capacity, Stoop Word Reading, Symbol Digit Modality Test, and the composite Unified Huntington's Disease Rating Scale. The development of novel HD interventions requires consideration of concomitant ADM use that may influence measures of disease presentation. In this review, we highlight the role of ADMs in HD management, their symptomatic benefits and potential risks, especially with high dose associated side effects, interactions with CYP2D6 inhibitors, and the individualized need for careful dose monitoring for clinical care and trial design.

Assessing the Impact of Physical Activity on Dementia Progression Using Clustering and the MRI-Based Kullback–Leibler Divergence

Dementia, including Alzheimer’s disease, is a neurodegenerative illness characterized by the progressive impairment of cognitive functions, posing a significant global health threat. Physical exercise is widely recognized for its preventive role, providing benefits for both the body composition and brain health. This study aimed to explore the relationship between physical exercise, the body composition, and the progression of dementia. The analysis used clinical and neuroradiology data from 42 patients enrolled in the Alzheimer’s Disease Neuroimaging Initiative (ADNI). Our study mainly focused on crucial parameters such as the body mass index (BMI), skeletal muscle index (SMI), and MRI biomarkers, including the hippocampal volume and white matter integrity. We grouped the participants according to the similarities of their body compositions through clustering techniques. Then, atrophy-related changes in the brain structures were computed using the Kullback–Leibler divergence. Our findings suggest that a higher BMI and greater muscle mass may slow down brain atrophy, suggesting a protective effect on the brain. Based on these results, preserving muscle mass and metabolic health through resistance and aerobic exercise appears crucial in reducing the risk of dementia. Body composition interventions may slow neurodegenerative changes and promote brain health. This is an essential piece of information about prevention strategies, especially for individuals at risk of dementia who may benefit from following structured physical activity strategies.

Maternal diet and vulnerability to cognitive impairment in adulthood: possible link with Alzheimer's disease?

Aging is the main risk factor for developing cognitive impairments and associated neurodegenerative diseases. However environmental factors, including nutritional health, are likely to promote or reduce cognitive impairments and neurodegenerative pathologies. An intricate relationship exists between maternal nutrition; and adult eating behavior, metabolic phenotype and cognitive abilities. The objective of the present review was to collect available data suggesting a link between maternal overnutrition and latter impairment of cognitive functions in the progeny, and to related this relationship with Alzheimer's disease (AD). Indeed, cognitive impairments are major behavioral signs of AD. We first reviewed studies showing an association between unbalanced maternal diet and cognitive impairments in the progeny in humans and rodent models. Then we looked for cellular and molecular hallmarks which could constitute a breeding ground for AD in those models. With this end, we focused on synaptic dysfunction, altered neurogenesis, neuroinflammation and oxidative stress, and pathological protein aggregation. Finally, we proposed an indirect mechanism linking maternal unbalanced diet and progeny's vulnerability to cognitive impairments and neurodegeneration through promoting metabolic diseases. We also discussed the involvement of progeny's gut microbiota in the maternal diet-induced vulnerability to metabolic and neurodegenerative diseases. Further investigations are needed to fully decipher how maternal diet programs the fetus and infant brain. Addressing this knowledge gap would pave the way to precise nutrition and personalized medicine to better handle cognitive impairments in adulthood.

Confined spaces in space: Cerebral implications of chronic elevations of inspired carbon dioxide and implications for long-duration space travel.

Cerebrovascular regulation is critically dependent upon the arterial partial pressure of carbon dioxide ( ), owing to its effect on cerebral blood flow, tissue , tissue proton concentration, cerebral metabolism and cognitive and neuronal function. In normal environments and in the absence of pathology, at least over acute time frames, hypercapnia is usually managed readily via the respiratory chemoreflex arcs and/or acid-base buffering capacity, such that there is minimal impact on cerebrovascular and neurological function. However, in non-normal environments, such as enclosed spaces, or with pathology, extended exposures to elevations in can be detrimental to cerebral health. Given the direct effect of protons on cellular function, even if pH is normalized, it is feasible that higher proton concentrations could still produce detrimental effects. Although it seems that humans can work safely in mildly hypercapnic environments for extended periods, chronic respiratory acidosis can cause bone demineralization, renal calcification, perinatal developmental abnormalities, systemic inflammation and impairments in cognitive function and visuomotor skills and can produce cerebral acidosis, potentially inducing sustained alterations in cerebral function. With the advancement of new initiatives in spaceflight, including proposed long-duration missions to Mars, the study of the effects of chronic inspired CO2 on human health is relevant. In this review, we draw on evidence from preclinical, physiological and clinical research in humans to summarize the cerebral ramifications of prolonged and chronic exposures to elevated partial pressures of inspired CO2 and respiratory acidosis.

Novel donepezil-tacrine hybrid (TAHB3) induces neurodifferentiation, neuroprotective effects, and activates the PI3K/AKT pathway on PC12 cells

Background Alzheimer's disease (AD) is a neurodegenerative disease characterized by the impairment of cognitive functions and neuronal loss. AD has no cure; current treatments like acetylcholinesterase inhibitors (AChEI) alleviate symptoms but do not halt disease progression. Objective We aimed to evaluate the effects and mechanisms of two novel AChEI hybrid compounds (TAHB3 and TA8Amino), regarding cytotoxicity, neuroprotection and neurodifferentiation in PC12 cells. Methods The effects of TAHB3 and TA8Amino on neurodifferentiation were analyzed on PC12 cells which were treated with AChEI compounds for seven days, following morphological, and quantitative analyses to calculate the differentiation percentages, neurite length, and protein expression. Regarding cytotoxicity and neuroprotection assays, PC12 cells were differentiated into mature neurons, then treated with TAHB3 or TA8Amino, following a posttreatment with H2O2 (an inducer of oxidative damage); the analyses were performed using the XTT assay and flow cytometry. Results The hybrid compound TAHB3 induced differentiation of PC12 cells, but TA8Amino did not cause the same effect. Both compounds did not show cytotoxic effects to PC12 cells and did not change the cell cycle progression, nor induce cell death. Only TAHB3 showed neuroprotective potential against induced-oxidative damage, and TAHB3 increased the levels of p-AKT, suggesting its action through the activation of the PI3K/AKT pathway. Conclusions Our results showed that TAHB3 can induce neurodifferentiation, besides a neuroprotective activity, indicating the potential of AChEI hybrid compounds as novel candidates to be explored for the establishment of novel therapeutic strategies for patients with AD.

Correlation between motor symptoms, cognitive function, and optical coherence tomography findings in Parkinson's disease.

This study aimed to evaluate the total macular thickness as well as the thickness of the inner and outer retinal layers in patients with Parkinson's disease. It also aimed to verify the correlation of these parameters with motor symptoms and cognitive function. A total of 46 eyes of 23 patients with Parkinson's disease and 40 eyes of 20 healthy controls were included in the study. The patients' cognitive, functional, and nonmotor symptoms were evaluated using the Katz Index of Independence and Pfeffer's Activities of Daily Living, Mini-Mental State Examination, Frontal Assessment Battery, Schwab and England Staging Scales, and Movement Disorders Society Nonmotor Symptoms Scale. The macular thickness measurements obtained via total, inner, and outer optical coherence tomography were recorded. Furthermore, the correlation of the parameters of optical coherence tomography with cognitive, functional, and nonmotor symptoms was assessed. The scores of the Katz Index of Independence and Pfeffer's Activities of Daily Living as well as the Movement Disorders Society Nonmotor Symptoms Scale were significantly lower in patients with Parkinson's disease than in healthy controls. Moreover, the former had greater total macular thickness. The temporal and inferior outer sectors were significantly greater for the ganglion cell complex thickness in patients. A significant correlation was observed between the total macular thickness and the Movement Disorder Society-Unified Parkinson's Disease Rating Scale, Parte III (MDS-UPDRS-III) values. Contrarily, there was a negative correlation between the outer macular thickness and the MDS-UPDRS-III values. Meanwhile, the total macular thickness and ganglion cell complex thickness were significantly correlated with the scores of the Mini-Mental State Examination, Schwab and England Staging Scale, Frontal Assessment Battery, and Katz Index of Independence and Pfeffer's Activities of Daily Living. In addition, the Schwab and England scale was correlated with the outer macular thickness. The total and inner macular thicknesses at the temporal and inferior outer sectors were greater in patients with Parkinson's disease than in the control group. These findings indicate that macular thickness may be greater in those with Parkinson's disease, particularly when associated with mild motor symptoms. In addition, the parameters of the total, inner, and outer optical coherence tomography were significantly associated with motor and nonmotor symptoms as well as cognitive function impairment.

Clinical manifestations and neuroanatomical correlates of reversible impairment of cognitive functions in patients with normotensive hydrocephalus: Case Report

From a neuropsychological perspective, normotensive hydrocephalus NPH is characterized by cognitive impairment associated with the compression exerted by ventricular dilatation on the cingulate cortex and fronto-striatal circuits. The Rey-Osterrieth Complex Figure Test (ROCFT) is a neuropsychological assessment measure widely used by clinicians and researchers because of the wide variety of cognitive information it allows to estimate. We present the case of young male patient with refractory structural epilepsy secondary to a childhood brain injury resulting from a metastasis of a renal tumor. Referred to Neuropsychology for behavioral changes and cognitive impairment; presenting atypical performance in the copying phase of the ROCFT. Failures in visual integration and coding of the ROCFT copy show that, in cases of NPH, brain structures such as the cerebellum and posterior cingulum can also be compromised by the compression exerted by the cerebral hemispheres as they move due to ventricular dilatation. Failures in integration, planning, rotation and displacement of ROCFT elements have been reported in patients with secondary psychotic conditions and posterior cingulate tumors. Failures in visual integration associated with NPH may be related to the involvement of more postero-caudal brain structures such as the cerebellum and posterior cingulum or to secondary psychosis.

Regulation of presynaptic homeostatic plasticity by glial signalling in Alzheimer's disease.

Alzheimer's disease (AD), the most common form of dementia among the elderly, affects numerous individuals worldwide. Despite advances in understanding the molecular underpinnings of AD pathology, effective treatments to prevent or cure the disease remain elusive. AD is characterized not only by pathological hallmarks such as amyloid plaques and neurofibrillary tangles but also by impairments in synaptic physiology, circuit activity and cognitive function. Synaptic homeostatic plasticity plays a vital role in maintaining the stability of synaptic and neural functions amid genetic and environmental disturbances. A key component of this regulation is presynaptic homeostatic potentiation, where increased presynaptic neurotransmitter release compensates for reduced postsynaptic glutamate receptor functionality, thereby stabilizing neuronal excitability. The role of presynaptic homeostatic plasticity in synapse stabilization in AD, however, remains unclear. Moreover, recent advances in transcriptomics have illuminated the complex roles of glial cells in regulating synaptic function in ageing brains and in the progression of neurodegenerative diseases. Yet, the impact of AD-related abnormalities in glial signalling on synaptic homeostatic plasticity has not been fully delineated. This review discusses recent findings on how glial dysregulation in AD affects presynaptic homeostatic plasticity. There is increasing evidence that disrupted glial signalling, particularly through aberrant histone acetylation and transcriptomic changes in glia, compromises this plasticity in AD. Notably, the sphingosine signalling pathway has been identified as being protective in stabilizing synaptic physiology through epigenetic and homeostatic mechanisms, presenting potential therapeutic targets for treating neurodegenerative disorders.

A microbead-enhanced electrochemical platform for β-amyloid peptide (1–42) detection

Alzheimer’s disease is the most prevalent form of dementia and is primarily characterized by the accumulation of β-amyloid and phosphorylated tau proteins in the brain, along with the degeneration of nerve cells, which leads to impairment of various cognitive functions. A significant biomarker of Alzheimer’s disease is the decreased level of soluble β-amyloid peptide (1–42) (Aβ1-42) in cerebrospinal fluid (CSF), as pathology progresses when CSF-Aβ1-42 levels drop below 192 pg mL−1. In this study, we developed an amperometric immunosensor based on magnetic beads as the platform for constructing the immunosensor. Monoclonal antibodies are immobilized on the MBs, enabling selective detection of Aβ1-42. The detection antibody is conjugated with the enzyme horseradish peroxidase, which, in the presence of H2O2 and hydroquinone, catalyzes the decomposition of H2O2 and the oxidation of hydroquinone to p-quinone, generating an electric current measured at a potential of −200 mV (vs. the Ag pseudo-reference electrode) using screen-printed carbon electrodes. The amperometric sandwich-type immunosensor demonstrates a linear response in the concentration range of 10 to 10,000 pg mL−1, with a detection limit of 7.4 pg mL−1, exhibiting excellent selectivity against the assessed interferents. These findings suggest the potential application of this immunosensor in the early diagnosis of Alzheimer’s disease, offering a sensitive and specific tool for clinical analysis. Despite its high performance, further studies are required to validate its robustness and applicability in complex clinical samples.

Altered neural recruitment during single and dual tasks in athletes with repeat concussion.

Sports-related concussions (SRCs) pose significant challenges to college-aged athletes, eliciting both immediate symptoms and subacute cognitive and motor function impairment. While most symptoms and impairments resolve within weeks, athletes with repeat SRCs may experience heightened risk for prolonged recovery trajectories, future musculoskeletal injuries, and long-term neurocognitive deficits. This study aimed to investigate the impact of repeat SRCs on dual task performance and associated neural recruitment using functional near-infrared spectroscopy (fNIRS). A total of 37 college-aged athletes (ages 18-24) participated in this cross-sectional observational study, 20 with a history of two or more SRCs, and 17 controls that had never sustained an SRC. Participants completed the Neuroimaging-Compatible Dual Task Screen (NC-DTS) while neural recruitment in the frontoparietal attention network and the primary motor and sensory cortices was measured using fNIRS. Athletes with repeat SRCs exhibited comparable single task and dual task performance to control athletes. Neuroimaging results indicated altered neural recruitment patterns in athletes with repeat SRCs during both single and dual tasks. Specifically, athletes with repeat SRCs demonstrated increased prefrontal cortex (PFC) activation during single motor tasks compared to controls (p < 0.001, d = 0.47). Conversely, during dual tasks, these same athletes exhibited reduced PFC activation (p < 0.001, d = 0.29) compared to their single task activation. These findings emphasize that while athletes with repeat SRCs demonstrate typical single and dual task performance, persistent alterations in neural recruitment patterns suggest ongoing neurophysiological changes, possibly indicating compensatory neural strategies and inefficient neural resource allocation, even beyond symptom resolution and medical clearance.

CRISES PSICOGÉNICAS NÃO EPILETIFORMES E PERTURBAÇÃO BORDERLINE DA PERSONALIDADE NUMA JOVEM ADOLESCENTE

Psychogenic Non-epileptic Seizures (PNES) are paroxysmal and involuntary episodes of sudden/temporary behavioral changes, with impairment of motor, autonomic, cognitive and emotional functions. Of the patients diagnosed, some resolve quickly, but in the majority of cases, the symptoms persist for months or years. The persistence of PNES may be associated with another underlying pathology, mainly a Personality Disorder, particularly borderline. The present clinical case report to a 16-year-old female adolescent, referred at the age of 13 to the Child and Adolescent Psychiatry Service (CAPS) after multiple visits to the emergency department due to persistent symptoms of anxiety, sadness, ongoing suicidal ideation, self-injurious behavior and recurrent episodes of falling from her own height. As an intervention, it is worth mentioning follow-up in multiple specialty consultations, without any alterations being detected. The young girl attended CAPS appointments, individual psychotherapy, psychopharmacological and family interventions and multiple hospitalizations in mental health facilities.In carrying out the differential diagnosis, the following diagnostic hypotheses were considered: Functional Neurological Symptom Disorder, Major Depressive Disorder and Borderline Personality Disorder (BPD). As in this case, literature confirms that in many patients with PNES, with severe disability and persistence for months or years, show co-occurrence with BPD. This comorbidity predicts a worse prognosis for PNES. This clinical case illustrates the complexity of the condition, particularly the refractoriness of the functional neurological symptoms and the ineffective response to the multiple interventions. In the future, it would be important to invest in research into other types of therapeutic approaches for these patients.

Enriched environment rescues bisphenol A induced anxiety-like behavior and cognitive impairment by modulating synaptic plasticity

Bisphenol A (BPA) is an exogenous endocrine disruptor in the environmental context, garnering attention for its harmful effects on the nervous system function and behavior. Research indicates that being exposed to BPA may result in anxiety-like behavior and impairment in cognitive function. Enriched environment (EE) is beneficial to improve cognitive behavior, but whether EE can improve BPA-induced behavioral impairment is still unclear. This research explored the possible pathways through which EE alleviates anxiety-like behavior and cognitive impairment in mice exposed to BPA. Except for the control mice, all mice received BPA treatment. After BPA treatment, some mice were housed normally, some housed with EE, and some were given NMDA and AMPA receptor agonists. Our research revealed that exposure to BPA results in anxiety-like behavior in open field and elevated-plus maze experiments. Additionally, spatial and learning memory cognitive impairments were observed in Y-maze and water maze tests. Furthermore, exposure to BPA led to a decrease in both the density and maturity of dendritic spines, as well as a reduction in neurite length and branch numbers. PSD-95, GluA1, and NR2A expression were down-regulated, and excitatory synaptic transmission was decreased. However, EE treatment increased dendrite spine density and maturity, up-regulated PSD-95, GluA1and NR2A expression, enhanced excitatory synaptic transmission, and relieved anxiety-like behavior and cognitive impairment in BPA mice. Furthermore, administering NMDA or AMPA receptor agonists to BPA mice led to an increase in dendritic spine density and maturity, a rise in mEPSC amplitude, as well as a restoration of anxiety-like behavior and cognitive deficits induced by BPA. The findings of this study provide proof that EE has a neuroprotective effect in reducing anxiety-related behavior and cognitive decline caused by BPA.

Temporal changes of neurobehavior in rats following varied blast magnitudes and screening of serum biomarkers in early stage of brain injury

Blast neurotrauma has been linked to impairments in higher-order cognitive functions, including memory, attention, and mood. Current literature is limited to a single overpressure exposure or repeated exposures at the same level of overpressure. In this study, a rodent model of primary blast neurotrauma was employed to determine the pressure at which acute and chronic neurological alterations occurred. Three pressure magnitudes (low, moderate and high) were used to evaluate injury thresholds. A biology shock tube (BST) was used to simulate shock waves with overpressures of 60 kPa, 90 kPa and 120 kPa respectively. Neurological behavior of the rats was assessed by the Multi-Conditioning System (MCS) at 1 d, 7 d, 28 d and 90 d after shock wave exposure. Serum dopamine (DA), 5-hydroxytryptamine (5-HT), brain-derived neurotrophic factor (BDNF) and gamma-aminobutyric acid (GABA) were measured at the same time points. The proteomic analysis was conducted to identify potentially vulnerable cellular and molecule targets of serum in the immediate post-exposure period. Results revealed that: (1) Anxiety-like behavior increased significantly at 1 d post-exposure in the medium and high overpressure (90 kPa, 120 kPa) groups, returned to baseline at 7 days, and anxiety-like behavior in the high overpressure groups re-emerged at 28 d and 90 d. (2) High overpressure (120 kPa) impaired learning and memory in the immediate post-exposure period. (3) The serum DA levels decreased significantly at 1 d post-exposure in the medium and high overpressure groups; The 5-HT levels decreased significantly at 1 d and 90 d in the high overpressure groups; The BDNF levels decreased significantly at 90 d in the high overpressure groups. (4) Proteomic analysis identified 38, 306, and 57 differentially expressed proteins in serum following low, medium and high overpressure exposures, respectively. Two co-expressed proteins were validated. Functional analysis revealed significant enrichment of 1121, 2096, and 1121 Gene Ontology (GO) items and 33, 47, and 26 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, indicating extensive molecular responses to overpressure in the early phase. These findings suggest that exposure, even at moderate levels, can induce persistent neurobehavioral and molecular alterations, highlighting the need for further research into the long-term consequences of blast neurotrauma.

The Underestimated Role of Iron in Frontotemporal Dementia: A Narrative Review.

The term frontotemporal dementia (FTD) comprises a group of neurodegenerative disorders characterized by the progressive degeneration of the frontal and temporal lobes of the brain with language impairment and changes in cognitive, behavioral and executive functions, and in some cases motor manifestations. A high proportion of FTD cases are due to genetic mutations and inherited in an autosomal-dominant manner with variable penetrance depending on the implicated gene. Iron is a crucial microelement that is involved in several cellular essential functions in the whole body and plays additional specialized roles in the central nervous system (CNS) mainly through its redox-cycling properties. Such a feature may be harmful under aerobic conditions, since it may lead to the generation of highly reactive hydroxyl radicals. Dysfunctions of iron homeostasis in the CNS are indeed involved in several neurodegenerative disorders, although it is still challenging to determine whether the dyshomeostasis of this essential but harmful metal is a direct cause of neurodegeneration, a contributor factor or simply a consequence of other neurodegenerative mechanisms. Unlike many other neurodegenerative disorders, evidence of the dysfunction in brain iron homeostasis in FTD is still scarce; nonetheless, the recent literature intriguingly suggests its possible involvement. The present review aims to summarize what is currently known about the contribution of iron dyshomeostasis in FTD based on clinical, imaging, histological, biochemical and molecular studies, further suggesting new perspectives and offering new insights for future investigations on this underexplored field of research.

Assessment of cognitive function in patients with metabolic dysfunction-associated steatotic liver disease

Background. Since the relationship between the initial stage of steatotic liver disease and dementia and cognitive function (CF) remains undetermined, there is a need to study such a combination. The aim is to evaluate CF in patients with metabolic dysfunction-associated steatotic liver disease (MASLD). Materials and methods. Thirty-nine outpatients with chronic forms of coronary heart disease were examined: 26 made up the main group with concomitant MASLD and 13 patients were included in the control group with an intact liver. In all of them, CF was evaluated using the Mini-Mental State Examination (MMSE). Results. The CF according to the MMSE was lower in patients with MASLD than among those with an intact liver (25.27 vs 28.22; p &lt; 0.01). Mild cognitive disorders were diagnosed in 7.69 %, moderate — in 65.38 %, and severe — in 26.93 % of patients with MASLD. In total, the frequency of deterioration of CF (MMSE ≤ 27) among patients with an intact liver was 33.33 %, while it was significantly higher (92.31 %) in patients with concomitant MASLD (p &lt; 0.05). Conclusions. CF can be an important criterion of the state of health and its changes, determines the course of the disease, allows assessing the activity of the endogenous intoxication syndrome and the state of the cardiovascular system. Impairment of cognitive functions occurs already at the stage of liver steatosis, which should be taken into account in the clinic.

Exploring Neuroprotection against Radiation-Induced Brain Injury: A Review of Key Compounds.

Brain radiation is a crucial tool in neuro-oncology for enhancing local tumor control, but it can lead to mild-to-profound and progressive impairments in cognitive function. Radiation-induced brain injury is a significant adverse effect of radiotherapy for cranioencephalic tumors, primarily caused by indirect cellular damage through the formation of free radicals. This results in late neurotoxicity manifesting as cognitive impairment due to free radical production. The aim of this review is to highlight the role of different substances, such as drugs used in the clinical setting and antioxidants such as ascorbate, in reducing the neurotoxicity associated with radiation-induced brain injury. Currently, there is mainly preclinical and clinical evidence supporting the benefit of these interventions, representing a cost-effective and straightforward neuroprotective strategy.

Short chain fatty acids mediates complement C1q pathway alleviation of perioperative neurocognitive disorders.

Perioperative neurocognitive disorders (PND) is one of the most common postoperative complications, which can lead to a harmful impact on self-dependence, longer hospital stays, increased medical costs, morbidity, and mortality amongst older adults. Microglia can modulate synapse elimination involved in the complement component protein 1q (C1q) pathway to induce cognitive dysfunction, which is significantly improved by short chain fatty acids (SCFAs) treatment. Here we investigate the effects of SCFAs treatment on PND via mediating C1q complement pathway. High-throughput sequencing of 16S rDNA from fecal samples of male SD rats was applied to assess the changes in gut microbiota. Fecal microbiota transplantation (FMT) was performed to investigate whether gut microbiota from PND rats could alter cognitive impairment. The blood from the rat tail vein was collected to measure the SCFAs concentrations. Hippocampal and brain tissue samples were obtained to perform Western blots, Golgi and immunofluorescence staining. Primary microglia treated with SCFAs or Histone deacetylase inhibitor were cultured to measure microglial activation states and the expression of acetylated histone. The 16S rDNA sequencing results showed that PND rats had the significant changes in the species diversity of the gut microbiota and the metabolite of specifc species. Gut microbiota from PND rats could alter spatial learning and memory, and meanwhile, the changed SCFAs concentrations in plasma were involved. The synapse elimination in PND rats was strikingly reversed by SCFAs treatment involved in modulation complement C1q via suppressing neuroinflammation. This suggests that a link between gut microbiota dysbiosis and cognitive function impairment is involved in synapse elimination via mediating complement C1q pathway. SCFAs treatment can alleviate PND, the mechanisms of which may be associated with regulating complement C1q pathway.

Comparison of single-point insulin sensitivity estimator (SPISE) index and cognitive performance in vitamin B12-deficient young adults: An analytical cross-sectional study.

Vitamin B12 is an essential micronutrient, aids in synthesis of neurotransmitters, and vital for cognitive function. In the current younger population with more of electronic gadgets and scientific world seems to slow down critical thinking and impairs the trick of comprehensive subjective learning. Vitamin B12 deficiency has been linked to insulin-resistant state and future cardiovascular risk. This study compared single-point insulin sensitivity estimator (SPISE) index, cognitive performance, and CVS risk in vitamin B12-adequate and -deficient young adults. Study participants were 60 young female participants, 18 to 35 years with the inclusion criteria of BMI more than 22.9 and waist circumference >85 cm. Anthropometric variables were measured. Lipid profile analytes were analyzed in an integrated Beckman Coulter AU series autoanalyzer. Based on SPISE index categorized as insulin resistant Group A <5.82 and non-insulin resistant Group B ≥5.82. Cognitive function was assessed based on Mini-Mental State Examination screening tool. Analytical cross-sectional study. Individuals with low vitamin B12 levels had a low SPISE index of less than 5.82 and low HDL-C levels, which indicates abnormal lipidemia and reduced insulin sensitivity. Mini-Mental State Examination was low in B12-deficient. B12 revealed positive correlation with MMSE, SPISE Index, and HDLc, whereas negative correlation with TGL and TGL/HDLc ratio. Individuals with low vitamin B12 levels express low SPISE index, and low performance on MMSE confirms risk of impairment of cognitive function and cardiovascular risk.