Impaired Brain Function Research Articles

Moringa oleifera Leaf Extract Improves Cognitive Function in Rat Offspring Born to Protein-Deficient Mothers

Background: Malnutrition during pregnancy and the first 1000 days of life can impair brain function and hippocampus development. Research has shown that protein deficiency (PD) in pregnant and lactating mothers can lead to neurocognitive issues from early life into adulthood. Moringa oleifera has been used as a dietary supplement for malnutrition; however, its neuroprotective effects on offspring with PD are unclear. Aims: This study aimed to investigate the effects of ethanol leaf extract of Moringa oleifera (EEMO) on rat offspring born to mothers who experienced protein deficiency during pregnancy and lactation. Methods: Female Sprague Dawley rats were given low (9% protein) or normal protein diets (18% protein) during pregnancy and lactation. Afterward, EEMO was administered to the offspring starting from the end of lactation for 5 weeks. Results: Offspring from mothers with protein deficiency showed low birth weight, slow weight gain, low BMI, low albumin levels, and anemia compared to those born with mothers fed with a standard protein diet. However, pups treated with EEMO showed higher cognitive improvement and a decrease in the ratio of abnormal to normal cells in the cornu ammoni (CA) CA1, CA2, CA3, and CA4 regions of the hippocampus. Conclusion: The present study suggests that EEMO supplementation could improve conditions of protein deficiency and cognitive function, making it a cost-effective dietary supplement for addressing these issues.

Shear force-ROS sequential responsive drug delivery system for improving cerebral thrombosis microcirculation and neurological function.

The ischemic strokes seriously threaten human health with high incidence and disability rates. Cerebral embolism and impaired brain function are the two major clinical features of this disease. Therefore, rapid restoration of cerebral blood supply and synchronous improvement of impaired neurological function is the key to treating strokes. Herein, based on the microenvironment of cerebral thrombosis and pathological characteristics of damaged neurons, we constructed a shear force and reactive oxygen species (ROS) dual-responsive system (UK@Fuc/CDPC-PTPCS) for sequential targeted delivery of thrombolytic agent urokinase (UK) and neuroprotective drug cytosolic choline (CDPC). Results proved that after intravenous administration, UK@Fuc/CDPC-PTPCS can quickly locate to cerebral thrombosis site via the active recognition capability of fucoidan (Fuc) to P-selectin overexpressed on activated platelets. Subsequently, the sharply increased blood shear force separated the core-shell structure by breaking the host-guest interaction of β-cyclodextrin (β-CD), so the UK loaded in the shell was first released to rapid thrombolysis and then restored cerebral blood supply. Afterward, the stroke homing peptide (SHp) modified CDPC-PTPCS core actively recognized ischemic damaged neuronal cells. Then high intracellular ROS triggered CDPC release at specific sites to exert neuroprotective effects. This study offered a new therapeutic strategy for ischemic stroke.

Potential molecular mechanisms of tobacco smoke exposure in Alzheimer's disease.

Smoking is detrimental to health, with tobacco use being a critical factor in the development of various neurodegenerative diseases, including Alzheimer's disease (AD), which progressively impairs brain function and poses a significant threat to public health. This study aims to examine the potential genetic alterations induced by smoking that are associated with AD and to investigate the underlying regulatory mechanisms. The research will provide theoretical foundations for targeted prevention and treatment strategies for AD. This study analyzed datasets from the Gene Expression Omnibus (GEO) and the Comparative Toxicogenomics Database (CTD) to identify genes affected by tobacco smoke exposure and those altered in patients with AD relative to normal controls. We conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses using OmicShare tools to screen for key pathways. Key genes were identified by constructing protein-protein interaction networks (PPI) in the STRING database with the aid of CytoHubba. Additionally, the binding activity of the proteins encoded by these key genes to nicotine, the main component of tobacco, was analyzed using molecular docking techniques. Finally, the analytical results were verified using Quantitative Real-Time Polymerase Chain Reaction. The CTD identified 12,164 CE-related genes affected by tobacco smoke exposure. A comparison of these datasets yielded 94 common genes that were both influenced by tobacco and differentially expressed across all brain regions. The GO and KEGG pathway enrichment analyses showed that these common differentially expressed genes (DEGs) were predominantly enriched in the Wnt/β-catenin and PI3K-AKT signaling pathways. The DEGs' PPI network, constructed using the STRING database, highlighted key genes such as HSP90AB1, SOS2, MAGI1, and YWHAZ. Molecular docking studies demonstrated that nicotine binds effectively to the protein structures of these key genes, primarily through amino acid residues such as Ser and Glu. Experimental validation showed that HSP90AB1 and YWHAZ exhibited notable expression discrepancies under varying concentrations of cigarette smoke extract (CSE) treatments, particularly demonstrating a pronounced down-regulation trend at elevated concentrations. The study indicates that tobacco may impact the function of transmembrane transporter proteins and contribute to the development of AD by affecting key genes such as HSP90AB1 and YWHAZ, as well as signaling pathways like PI3K-AKT.

Developing predictive nomogram models using quantitative electroencephalography for brain function in type a aortic dissection: a prospective observational study.

Type A aortic dissection (TAAD) remains a significant challenge in cardiac surgery, presenting high risks of adverse outcomes such as permanent neurological dysfunction and mortality despite advances in medical technology and surgical techniques. This study investigates the use of quantitative electroencephalography (QEEG) to monitor and predict neurological outcomes during the perioperative period in TAAD patients. This prospective observational study was conducted at the hospital, involving patients undergoing TAAD surgery from February 2022 to January 2023. QEEG parameters, including the dynamic amplitude-integrated electroencephalography (aEEG) grade, which assesses changes in brain function over time, alongside aEEG and relative band power (RBP), were monitored and analyzed to assess brain function preoperatively, intraoperatively, and within 2hours postoperatively. A predictive nomogram model was developed using these QEEG metrics along with other clinical variables to forecast neurological outcomes. In this study, we analyzed the factors contributing to adverse outcomes (AO) and transient neurological dysfunction (TND) following TAAD surgery. For AO, multivariable analysis identified pre-mental status (odds ratio [OR]=4.652, 95% confidence interval [CI]=2.316-10.074, P < 0.001), cardiopulmonary bypass time (OR=1.014, 95% CI=1.006-1.023, P =0.001), and dynamic aEEG grade (OR=9.926, 95% CI=4.493-25.268, P < 0.001) as independent risk factors. The AO model showed high discriminative ability with an area under the curve of 0.888 (95% CI=0.818-0.960) and good calibration (Brier score=0.0728). For TND, significant preoperative differences included dynamic aEEG grade (P < 0.001) and Log(Post-RBP Alpha%) (6.00 vs. 4.00, P < 0.001). Multivariable analysis identified cardiopulmonary bypass time (OR=1.014, 95% CI=1.006-1.023, P =0.001), Post-RBP Alpha% (OR=0.263, 95% CI=0.121-0.532, P < 0.001), and dynamic aEEG grade (OR=12.444, 95% CI=5.337-30.814, P < 0.001) as independent risk factors. The TND model had an area under the curve of 0.893 (95% CI=0.844-0.941) and good calibration (Brier score=0.125). These findings highlight the role of QEEG in predicting postoperative neurological dysfunction in TAAD patients. Through perioperative QEEG monitoring of TAAD patients, combined with clinical indicators such as cardiopulmonary bypass time and preoperative mental status, we developed clinical predictive models for AO and TND after surgery. These models allow for early detection of postoperative brain function impairment, as assessed by QEEG parameters monitored intraoperatively and during the first 2hours after surgery, a period chosen based on clinical definitions of delayed awakening and supported by the findings of this study. This study provides evidence supporting postoperative brain function monitoring in TAAD patients, with potential clinical implications for improved outcomes.

The maternal X chromosome affects cognition and brain ageing in female mice.

Female mammalian cells have two X chromosomes, one of maternal origin and one of paternal origin. During development, one X chromosome randomly becomes inactivated1-4. This renders either the maternal X (Xm) chromosome or the paternal X (Xp) chromosome inactive, causing X mosaicism that varies between female individuals, with some showing considerable or complete skew of the X chromosome that remains active5-7. Parent-of-X origin can modify epigenetics through DNA methylation8,9 and possibly gene expression; thus, mosaicism could buffer dysregulated processes in ageing and disease. However, whether X skew or its mosaicism alters functions in female individuals is largely unknown. Here we tested whether skew towards an active Xm chromosome influences the brain and body-and then delineated unique features of Xm neurons and Xp neurons. An active Xm chromosome impaired cognition in female mice throughout the lifespan and led to worsened cognition with age. Cognitive deficits were accompanied by Xm-mediated acceleration of biological or epigenetic ageing of the hippocampus, a key centre for learning and memory, in female mice. Several genes were imprinted on the Xm chromosome of hippocampal neurons, suggesting silenced cognitive loci. CRISPR-mediated activation of Xm-imprinted genes improved cognition in ageing female mice. Thus, the Xm chromosome impaired cognition, accelerated brain ageing and silenced genes that contribute to cognition in ageing. Understanding how Xm impairs brain function could lead to an improved understanding of heterogeneity in cognitive health in female individuals and to X-chromosome-derived pathways that protect against cognitive deficits and brain ageing.

Kemampuan Bahasa Tulis pada Individu dengan Alzheimer: Kajian Neurolinguistik

Impaired brain function in individual with Alzheimer’s progressively affects to the cognitive and motor functions required to perform written language skills. This study aims to identify and describe the written skill in individual with Alzheimer’s through a case study approach. Data was obtained from a 56 years old elderly whose initials is KA and lives in PPSLU Potroyudan Jepara. Data collection techniques were carried out through documentation, observation, and interviews. Then, KA’s handwriting analysed using writing disorders theory through Neurolinguistic studies. The results showed that there are four forms of disturbance in KA’s written language, those are irregular writing, word omission in long sentences, letter omission, and letter replacement. The findings showed that Allzheimer which causes dysfunction in several parts of the brain also resulted in agraphia and a decrease in the syntactic complexity of writing.

AI-based models to predict decompensation on traumatic brain injury patients.

Traumatic Brain Injury (TBI) is a form of brain injury caused by external forces, resulting in temporary or permanent impairment of brain function. Despite advancements in healthcare, TBI mortality rates can reach 30%-40% in severe cases. This study aims to assist clinical decision-making and enhance patient care for TBI-related complications by employing Artificial Intelligence (AI) methods and data-driven approaches to predict decompensation. This study uses learning models based on sequential data from Electronic Health Records (EHR). Decompensation prediction was performed based on 24-h in-mortality prediction at each hour of the patient's stay in the Intensive Care Unit (ICU). A cohort of 2261 TBI patients was selected from the MIMIC-III dataset based on age and ICD-9 disease codes. Logistic Regressor (LR), Long-short term memory (LSTM), and Transformers architectures were used. Two sets of features were also explored combined with missing data strategies by imputing the normal value, data imbalance techniques with class weights, and oversampling. The best performance results were obtained using LSTMs with the original features with no unbalancing techniques and with the added features and class weight technique, with AUROC scores of 0.918 and 0.929, respectively. For this study, using EHR time series data with LSTM proved viable in predicting patient decompensation, providing a helpful indicator of the need for clinical interventions.

ВЛИЯНИЕ ГУСТОГО ЭКСТРАКТА CALLICARPA NUDIFLORA НА НЕКОТОРЫЕ БИОХИМИЧЕСКИЕ ПОКАЗАТЕЛИ ПРИ ЭКСПЕРИМЕНТАЛЬНОЙ ЧЕРЕПНО-МОЗГОВОЙ ТРАВМЕ

In the modern world, neurotrauma has become one of the main problems in the field of medicine. Such injuries can be caused by various factors, including accidents, falls, violence, sports injuries, etc. The consequences of neurotrauma can be different, including impaired brain function, Alzheimer's disease, dementia, mood disorders and other negative consequences, so the search for new methods of treating neurotrauma is an urgent task for medicine. It is known that the consequence of traumatic brain injury (TBI) is short- and long-term cognitive deficit, usually manifested in impaired attention, learning, memory and higher integrative functions. Callicarpa nudiflora Hook. &amp; Arn is a plant species used in traditional Asian medicine to treat various diseases, including diseases of the nervous system. According to its chemical composition, Callicarpa nudiflora Hook. &amp; Arn contains flavonoids, phenylpropanoids, macro- and microelements: potassium, iron, copper, sodium, calcium, etc. The object of this study is the extract of Callicarpa nudiflora Hook. &amp; Arn (Callicarpa nudiflora). Quantitative determination of the total content of reducing substances in the analyzed extract in terms of gallic acid was analyzed spectrophotometrically by the reaction of the interaction of the studied extract with the Folin-Ciocalteu reagent. However, the neuroprotective effect of this plant under experimental neurotrauma has not been sufficiently studied. The study found that the extract of Callicarpa nudiflora under experimental craniocerebral trauma leads to new opportunities for assessing the psycho-emotional status. The study will expand our current knowledge of the pharmacological properties of Callicarpa nudiflora Hook. &amp; Arn and provide a deeper understanding of what molecular mechanisms may be involved in its neuroprotective effects.

Role of Computed Tomography in the Diagnosis, Treatment and Prognosis of Patients with Traumatic Head Injury

Background: Traumatic brain injury is defined as damage to the brain caused by external mechanical forces such as: A. Sudden acceleration or deceleration, pressure wave or projectile penetration, resulting in temporary or permanent impairment of brain function. B. In a rapidly developing country like Bangladesh, urbanization and industrialization have led to an increase in road traffic, which is the main cause of head injuries due to road accidents. Objectives: To evaluate the prognostic importance of CT on the outcome of head injury patients. Observation of the sequential anatomical course of pathological processes in the brain response to head injury and correlation with Glasgow Coma Scale. Methods: This is a hospital study carried out in patients of head injury referred to the BSM Medical University Hospital from July 2022 to August 2023. Total 120 patients were included; incidence of head injuries was more in males than females. The study included patients with head and craniofacial trauma who underwent CT scans. Patients were examined with a dual-slice CT, Siemens Somatom Emotion Duo. A P value of less than 0.05 was considered statistically significant. Results: Total 120 patients were included; incidence of head injuries was more in males than females. Headache was the commonest presentation. Contusions were the most common intraparenchymal injury found in 58, followed by EDH in 52 patients, followed by SDH and SAH which accounted for 52 and 32 respectively. Intraparenchymal hematoma was found in 24 of patients and DAI in 16, intraventricular hemorrhage in 10 patients. Conclusion: Parenchymal contusions, Subdural and extra dural hematoma were equally encountered findings in our study while subarachnoid haemorrhage was seen less frequently while intraventricula rhaemorrhage was rare.

Mechanisms and Potential Benefits of Neuroprotective Agents in Neurological Health.

The brain contains many interconnected and complex cellular and molecular mechanisms. Injury to the brain causes permanent dysfunctions in these mechanisms. So, it continues to be an area where surgical intervention cannot be performed except for the removal of tumors and the repair of some aneurysms. Some agents that can cross the blood-brain barrier and reach neurons show neuroprotective effects in the brain due to their anti-apoptotic, anti-inflammatory and antioxidant properties. In particular, some agents act by reducing or modulating the accumulation of protein aggregates in neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, Huntington's disease, Amyotrophic lateral sclerosis, and prion disease) caused by protein accumulation. Substrate accumulation causes increased oxidative stress and stimulates the brain's immune cells, microglia, and astrocytes, to secrete proinflammatory cytokines. Long-term or chronic neuroinflammatory response triggers apoptosis. Brain damage is observed with neuronal apoptosis and brain functions are impaired. This situation negatively affects processes such as motor movements, memory, perception, and learning. Neuroprotective agents prevent apoptosis by modulating molecules that play a role in apoptosis. In addition, they can improve impaired brain functions by supporting neuroplasticity and neurogenesis. Due to the important roles that these agents play in central nervous system damage or neurodegenerative diseases, it is important to elucidate many mechanisms. This review provides an overview of the mechanisms of flavonoids, which constitute a large part of the agents with neuroprotective effects, as well as vitamins, neurotransmitters, hormones, amino acids, and their derivatives. It is thought that understanding these mechanisms will enable the development of new therapeutic agents and different treatment strategies.

Potential therapeutic effect of teneligliptin on unpredictable chronic mild stress-induced depression in mice: targeting the role of AMP-activated protein kinase signaling pathway

Background Depression is a widespread and complex mental disorder that is challenging to treat. The unpredictable chronic mild stress (UCMS) model, based on stress diathesis, is used to study depression because antidepressants often reverse its effects, providing predictive validity. However, the mechanisms behind UCMS are not fully understood. AMP-activated protein kinase (AMPK) is essential for regulating neuronal energy metabolism, and disruptions in its activation can impair brain function and synaptic integrity. Teneligliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor with anti-inflammatory, antioxidant, autophagy-modulating, and antiapoptotic properties, has not been studied for its potential to activate AMPK by inhibiting DPP-4, stimulating glucagon-like peptide-1, and decreasing the mammalian target of rapamycin pathway, which may enhance neuroprotection and neurogenesis. This study is the first to show teneligliptin’s potential therapeutic effect on UCMS-induced depression in mice by targeting the AMPK signaling pathway. Objective The current study was performed to assess the behavioral, oxidative stress biomarkers, neurotransmitter assay, and histopathology of the brain in UCMS-induced depression in mice. Materials and methods Mice were divided into five groups: group I (normal control, received saline), group II (UCMS model with 1 week of stress), group III (UCMS+fluoxetine 10 mg/kg daily for 4 weeks), and groups IV and V (UCMS+teneligliptin 30 mg/kg and 60 mg/kg, respectively, for 4 weeks). Body weight, forced swim test, tail suspension, locomotor activity, oxidative biomarkers (malondialdehyde, reduced glutathione, superoxide dismutase, nitrite levels), neurotransmitters (dopamine, serotonin), and brain histopathology were assessed to evaluate antidepressant activity. Results and conclusion Mice treated with teneligliptin (30 and 60 mg/kg) in the UCMS model showed significant weight loss compared with the disease group. They also exhibited reduced immobility in forced swim and tail suspension tests and increased locomotor activity. Significant changes were noted in oxidative stress biomarkers and neurotransmitters (dopamine, serotonin), with improved histopathological conditions. In conclusion, teneligliptin improved behavioral and antidepressant effects by reducing oxidative stress and increasing dopamine and serotonin levels. As a DPP-4 inhibitor, it may activate AMPK in the brain, lower DPP-4 enzyme levels, and enhance glucagon-like peptide-1-R and mammalian target of rapamycin, potentially promoting neurogenesis and neuroprotection, thus being beneficial for depression treatment.

Diffusion‐Based Causality‐Preserving Neural Network for Dementia Recognition

ABSTRACTAnalyzing large‐scale functional brain networks for brain disorders often relies on undirected correlations in activation signals between brain regions. While focusing on co‐occurring activations, this approach overlooks the potential for directionality inherent in brain connectivity. Established research indicates the causal nature of brain networks, suggesting that activation patterns co‐occur and potentially influence one another. To this end, we propose a novel dffusion vector auto‐regressive (Diff‐VAR) method, enabling the assessment of whole‐brain effective connectivity (EC) as a directed and weighted network by integrating the search objectives into the deep neural network model as learnable parameters. The EC learned by our method identifies widespread differences in flow of influence within the brain network for individuals with impaired brain function compared to those with normal brain function. Moreover, we introduce an adaptive smoothing mechanism to enhance the stability and reliability of inferred EC. We evaluated the results of our proposed method on the Alzheimer's Disease Neuroimaging Initiative (ADNI) database. The model's performance is compared with existing correlation‐based and causality‐based methods. The results revealed that the brain networks constructed by our method achieve high classification accuracy and exhibit features consistent with physiological mechanisms. The code is available at https://github.com/SaqibMamoon/Diff‐VAR.

Fully Automated and AI-Assisted Optical Fiber Sensing System for Multiplexed and Continuous Brain Monitoring.

Continuous and comprehensive brain monitoring is crucial for timely identification of changes or deterioration in brain function, enabling prompt intervention and personalized treatments. However, existing brain monitoring systems struggle to offer continuous and accurate monitoring of multiple brain biomarkers simultaneously. This study introduces a multiplexed optical fiber sensing system for continuous and simultaneous monitoring of six cerebrospinal fluid (CSF) biomarkers using tip-functionalized optical fibers and computational algorithms. Optimized machine learning models are developed and integrated for real-time spectra analysis, allowing for precise and continuous readout of biomarker concentrations. The developed machine learning-assisted fiber optic sensing system exhibits high sensitivity (0.04, 0.38, 0.67, 2.62, 0.0064, 0.33 I/I0 change per units of temperature, dissolved oxygen, glucose, pH, Na+, Ca2+, respectively), reversibility, and selectivity toward target biomarkers with a total diameter less than 2.5 mm. By monitoring brain metabolic and ionic dynamics, this system accurately identified brain physiology deterioration and recovery using ex vivo traumatic brain injury models. Additionally, the system successfully tracked biomarker fluctuations in clinical CSF samples with high accuracy (R2 > 0.93), demonstrating excellent sensitivity and selectivity in reflecting disease progression in real time. These findings underscore the enormous potential of automated and multiplexed optical fiber sensing systems for intraoperative and postoperative monitoring of brain physiologies.

Cholesterol Metabolism in Neurodegenerative Diseases.

Significance: Cholesterol plays a crucial role in the brain, where it is highly concentrated and tightly regulated to support normal brain functions. It serves as a vital component of cell membranes, ensuring their integrity, and acts as a key regulator of various brain processes. Dysregulation of cholesterol metabolism in the brain has been linked to impaired brain function and the onset of neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease, and Huntington's disease. Recent Advances: A significant advancement has been the identification of astrocyte-derived apoliprotein E as a key regulator of de novo cholesterol biosynthesis in neurons, providing insights into how extracellular signals influence neuronal cholesterol levels. In addition, the development of antibody-based therapies, particularly for AD, presents promising opportunities for therapeutic interventions. Critical Issues: Despite significant research, the association between cholesterol and neurodegenerative diseases remains inconclusive. It is crucial to distinguish between plasma cholesterol and brain cholesterol, as these pools are relatively independent. This differentiation should be considered when evaluating statin-based treatment approaches. Furthermore, assessing not only the total cholesterol content in the brain but also its distribution among different types of brain cells is essential. Future Direction: Establishing a causal link between changes in brain/plasma cholesterol levels and the onset of brain dysfunction/neurodegenerative diseases remains a key objective. In addition, conducting cell-specific analyses of cholesterol homeostasis in various types of brain cells under pathological conditions will enhance our understanding of cholesterol metabolism in neurodegenerative diseases. Manipulating cholesterol levels to restore homeostasis may represent a novel approach for alleviating neurological symptoms. Antioxid. Redox Signal. 41, 1051-1072.

Roles of the gut microbiota in human neurodevelopment and adult brain disorders.

Growing evidence demonstrates the connection between gut microbiota, neurodevelopment, and adult brain function. Microbial colonization occurs before the maturation of neural systems and its association with brain development. The early microbiome interactions with the gut-brain axis evolved to stimulate cognitive activities. Gut dysbiosis can lead to impaired brain development, growth, and function. Docosahexaenoic acid (DHA) is critically required for brain structure and function, modulates gut microbiota, and impacts brain activity. This review explores how gut microbiota influences early brain development and adult functions, encompassing the modulation of neurotransmitter activity, neuroinflammation, and blood-brain barrier integrity. In addition, it highlights processes of how the gut microbiome affects fetal neurodevelopment and discusses adult brain disorders.

Periodontitis associated with brain function impairment in middle-aged and elderly individuals with normal cognition.

The present study aimed to investigate changes in intranetwork functional connectivity (FC) and internetwork FC in middle-aged and elderly individuals with normal cognition (NC) and varying degrees of periodontitis to determine the effects of periodontitis on brain function. Periodontal findings and resting-state functional magnetic resonance imaging data were acquired from 51 subjects with NC. Independent component analysis and correlation analysis were used for the statistical analysis of the data. Differences in intranetwork FC were observed among groups in the anterior default-mode network (aDMN), dorsal attention network and dorsal sensorimotor network (dSMN). Compared with the nonperiodontitis (NP) group or the mild-periodontitis group, the analysis of internetwork FC showed increased FC between the auditory network and the ventral attention network (VAN), between the aDMN and the salience network (SN), and between the SN and the VAN and decreased FC between the posterior default-mode network and the right frontoparietal network in the moderate-to-severe periodontitis group. Additionally, internetwork FC between the dSMN and the VAN was also increased in the moderate-to-severe periodontitis group compared to the NP group. The altered intra- and internetwork FC were significantly correlated with the periodontal clinical index. Our results confirmed that periodontitis was associated with both intra- and internetwork FC changes even in NC. The present study indicates that periodontitis might be a potential risk factor for brain damage and provides a theoretical clue and a new treatment target for the early prevention of Alzheimer disease. Recent research has proposed that periodontitis is a potential risk factor for Alzheimer disease (AD). However, the relationship between periodontitis and the brain function of middle-aged and elderly individuals with normal cognition (NC) remains unclear. Analyzing the effect of periodontitis on brain function in the NC stage can provide clues to AD development and help achieve early prevention of dementia. The present study aimed to investigate changes in brain functional connectivity (FC) in NC with different severity of periodontitis to determine the effects of periodontitis on brain function. Both changed intranetwork FC and internetwork FC were found in the moderate-to-severe periodontitis group, and periodontitis was associated with brain network function impairment in NC. The present study indicates that periodontitis might be a potential risk factor for brain damage even in NC stage, and provides a theoretical clue and a new treatment target for the early prevention of AD.

The Impact of Social Media Addiction on Teenagers

Abstract: Electronic devices and social media platform usage has become so prevalent that it become almost indispensable for people to stay in contact and usage in daily life. Even though social media provides numbers of benefits, the overuse of social media can lead to problems such as social media addiction. In this research, the cause, impact, and solutions of social media addiction will be discussed. Due to the high susceptivity of teenagers to social media addiction, this research aims to figure out possible ways to interfere with teenagers addiction and discuss possible treatments for it. This research used document analysis as the method. This research found social media addiction is caused by triggers, reward systems, and emotional needs; the impact of social media addiction is impaired brain functions, mental health issues, and overall well-being, including the cycle of depression and addiction, and the high rates of suicidal thoughts. This research also poses solutions, including setting limits to social media usage, adopting coping strategies, seeking therapy, and incorporating physical exercise.

The fate of neuronal synapse homeostasis in aging, infection, and inflammation.

Neuroplasticity is the brain's ability to reorganize and modify its neuronal connections in response to environmental stimuli, experiences, learning, and disease processes. This encompasses a variety of mechanisms, including changes in synaptic strength and connectivity, the formation of new synapses, alterations in neuronal structure and function, and the generation of new neurons. Proper functioning of synapses, which facilitate neuron-to-neuron communication, is crucial for brain activity. Neuronal synapse homeostasis, which involves regulating and maintaining synaptic strength and function in the central nervous system (CNS), is vital for this process. Disruptions in synaptic balance, due to factors like inflammation, aging, or infection, can lead to impaired brain function. This review highlights the main aspects and mechanisms underlying synaptic homeostasis, particularly in the context of aging, infection, and inflammation.

Utility of Electroencephalograms for Enhancing Clinical Care and Rehabilitation of Children with Acquired Brain Injury.

The objective of this literature review was to present evidence from recent studies and applications focused on employing electroencephalogram (EEG) monitoring and methodological approaches during the rehabilitation of children with acquired brain injuries and their related effects. We describe acquired brain injury (ABI) as one of the most common reasons for cognitive and motor disabilities in children that significantly impact their safety, independence, and overall quality of life. These disabilities manifest as dysfunctions in cognition, gait, balance, upper-limb coordination, and hand dexterity. Rehabilitation treatment aims to restore and optimize these impaired functions to help children regain autonomy and enhance their quality of life. Recent advancements in monitoring technologies such as EEG measurements are increasingly playing a role in clinical diagnosis and management. A significant advantage of incorporating EEG technology in pediatric rehabilitation is its ability to provide continuous and objective quantitative monitoring of a child's neurological status. This allows for the real-time assessment of improvement or deterioration in brain function, including, but not limited to, a significant impact on motor function. EEG monitoring enables healthcare providers to tailor and adjust interventions-both pharmacological and rehabilitative-based on the child's current neurological status.

Clinical association of habitual breakfast skipping with cognitive decline and neurodegeneration among older adults

ObjectiveUnhealthy lifestyles have a considerable impact on the incidence of dementia. Skipping breakfast disturbs energy homeostasis and impairs brain function. In this study, we investigated the association between breakfast skipping and cognitive performance among community-dwelling adults. MethodsWe recruited 859 community-dwelling adults aged ≥60 years from January 1 to December 31, 2021. Participants’ sociodemographic information and breakfast skipping habits were self-reported. Participants were followed up for 36 months and cognitive function was assessed using the Mini-Mental State Examination (MMSE) with an interval of 18 months. Trajectories of cognitive change were compared between individuals with and without breakfast skipping. To reduce the risk of bias owing to unmatched sample sizes between the groups, we conducted 1:1 propensity score matching (PSM) based on age, sex, education level, and ApoE genotype. ResultsAt baseline and 18-month follow-up, no difference was found in MMSE scores between participants with and without breakfast skipping. However, those who habitually skipped breakfast had significantly lower MMSE scores than those who did not at 36-month follow-up. Individuals with habitual breakfast skipping had a steeper rate of cognitive decline than those without habitual breakfast skipping during follow-up. Breakfast skipping was a risk factor for longitudinal cognitive decline, defined as a decrease in MMSE scores of ≥3, adjusted for age, sex, education, body mass index, ApoE ε4 carrier status, hypertension, diabetes, and hyperlipidemia. At the last follow-up, participants who habitually skipped breakfast had significantly higher levels of ptau181 and NfL than those who did not. In the PSM cohort, similar findings were obtained regarding cognitive trajectories and plasma biomarkers. ConclusionBreakfast skipping was linked to an increased risk of long-term cognitive decline and neurodegeneration among older adults. The link between unhealthy dietary habits and cognitive decline may be attributed to a deficiency in neurorestoration resulting from inadequate energy consumption.