Brain Cell Damage Research Articles

Advances in the Application of CRISPR-Cas9 in Stem Cell Therapy

Stem cell research has advanced rapidly, offering promising treatments for refractory diseases due to their unique capabilities for self-renewal and pluripotent differentiation. Stem cells play pivotal roles in treating genetic disorders, neurodegenerative diseases (NDDs), cardiovascular conditions, and cancer. In genetic diseases, combining stem cells with gene-editing tools like CRISPR-Cas9 enables precise correction of pathogenic genes, while healthy stem cells repair tissue by replacing diseased cells. For NDDs, iPSCs can differentiate into dopaminergic neurons to replace damaged brain cells and enhance neural regeneration. In cardiovascular diseases, they promote myocardial and vascular repair. In cancer, stem cells boost anti-tumor immunity and deliver drugs directly to tumor sites, improving treatment efficacy. Despite these breakthroughs, challenges persist. High-quality stem cell production is limited, and controlling differentiation to prevent tumorigenesis remains critical. Allogeneic transplants risk immune rejection, and using embryonic stem cells raises ethical concerns. Regulatory frameworks and clinical standards are needed to ensure safety and efficacy, alongside addressing ethical and patient rights issues. With continued innovation, stem cell therapy is going to revolutionize medicine, offering novel methods for complex diseases and improving global health

Eucalyptol Attenuates Cerebral Ischemia/Reperfusion Injury in Mice

Background One of the leading causes of acute brain injury is cerebral ischemia/reperfusion (I/R) injury. It is an ailment that occurs when the brain does not receive enough oxygen-rich blood supply, which damages brain cells. Oxidative stress is recognized as a significant mechanism that causes I/R injury and is a critical focal point for therapy. Apoptosis and inflammation are all pathogenic processes underpinning I/R damage. Eucalyptol (EU), a plant-derived substance, protects neuronal damage. We postulate that EU inhibits apoptosis and oxidative stress after focal cerebral I/R damage in mice. Purpose Thus, the present work sought to examine the neurological protective benefits of EU in mice models of cerebral ischemia/reperfusion (CI/R) injury. Methods The measurement of neurological function, infarct volume, and the amount of water in the brain were evaluated subsequently. The brain tissue was examined to assess the activities of oxidative stress, inflammatory cytokines, and matrix metalloproteinases (MMP) levels, and histopathology was determined. Using enzyme-linked immunosorbent assay (ELISA), apoptotic marker expression was used to measure the levels of B-cell lymphoma 2 (Bcl-2), caspase-3, and Bcl-2 associated X-protein (Bax) proteins that exist as indicators of apoptosis. Results EU treatment malondialdehyde (MDA) levels decreased while glutathione (GSH), superoxide dismutase (SOD), A-TOC, and catalase (CAT) activity increased. Following EU therapy dramatically reduced cerebral dysfunction, which was supported by reduced histological damage in I/R injury. Furthermore, with lower levels of MMP-2 and 9, EU treatment could be a novel approach for preventing CI/R injury. EU-treated mice had a notable reduction in cleaved Bax, caspase-3, and increased Bcl-2 protein activities. EU therapy shields the brain against CI/R injury by inhibiting cell death. Conclusion According to the present study’s findings, EU is a promising neuroprotective agent that can be used to treat CI/R injury in mice. By focusing on these aspects, nurses can provide comprehensive care to patients involved in studies on the effects of EU on CI/R injury, promoting better outcomes through careful monitoring, supportive interventions, and education.

Hypoxic irreversible brain cells damage, associated risk factors and antihypoxants

It is reported that in the final stage of many diseases the immediate cause of biological death in humans and warm-blooded animals is hypoxic irreversible damage to brain cells. This explains the fact that to prevent biological death in all critical conditions without exception, inhalation with breathing gases containing oxygen has long been successfully used. This is also why oxygenation of the blood is considered one of the main conditions for preserving human life in all critical situations and forms the basis of emergency medical care in the intensive care unit. However, inhalation of oxygen gas and increasing blood oxygen saturation should be carried out as early as possible, and more precisely — before the onset of the stage of hypoxic irreversible damage in brain cells. The fact is that after the onset of irreversible da­mage brain cells die even in the presence of oxygen. In this connection, the mechanisms of adaptation of the organism to oxygen deficiency play a great role for longer preservation of brain cells viability and human life in conditions of hypoxemia. In order to increase resistance to hypoxemia, antihypoxants are traditionally used. But they can preserve the viability of brain cells not always, but only if they are introduced into the body before the onset of hypoxic irreversible damage to brain cells and in the case of unused reserves of adaptation to hypoxemia in the body. Risk factors of hypoxic irreversible damage of brain cells are indicated, among which excessively long duration of hypoxemia and hyperthermia are emphasized. It is shown that the most important circumstance for the development of hypoxic irreversible damage of brain cells is not so much the degree of hypoxemia as the degree of hypoxia of brain tissue and its duration, which exceeds the period of human resistance to hypoxia. It has been shown that human resistance to hypoxia can be assessed using the Stange test. It has been reported that fever and local cerebral hyperthermia decrease, and hibernation and local cerebral hypothermia increase, the resistance of brain cells to hypoxia. In this regard, recommendations not only to eliminate fever and local inflammatory processes in the head, but also recommendations to reduce brain temperature are highly appropriate to improve resistance to hypoxia. It is pointed out that among the methods of local therapeutic hypothermia, targeted temperature management is the most advanced. In addition, it is reported that in recent years a new group of promising antihypoxants — alkaline solutions of hydrogen peroxide — has been created. It is shown that hydrogen peroxide is able to decompose very quickly into water and oxygen gas under the action of catalase, which is found in all tissues. The peculiarities of using alkaline solutions of hydrogen peroxide as antihypoxants we all have to study in the future.

Neurotranscriptomic and behavioral effects of ISRIB, and its therapeutic effects in the traumatic brain injury model in zebrafish

Traumatic brain injury (TBI) is a global medical concern and has a lasting impact on brain activity with high risks of mortality. Current treatments are inadequate for repairing damaged brain cells or correcting cognitive and behavioral disabilities in TBI patients. Mounting evidence links TBI to the activation of the Integrated Stress Response (ISR) signaling in the brain. A novel small molecule, ISRIB, is an effective inhibitor of the ISR pathway, offering potential advantages for brain health. Here, we investigated how ISRIB affects brain transcriptome and behavior in zebrafish TBI model evoked by telencephalic brain injury. Overall, while TBI diminished memory and social behavior in zebrafish, administering ISRIB post-injury markedly reduced these behavioral deficits, and modulated brain gene expression, rescuing TBI-activated pathways related to inflammation and brain cell development. Collectively, this supports the role of brain ISR in TBI, and suggests potential utility of ISRIB for the treatment of TBI-related states.

Explainable and Interpretable Model for the Early Detection of Brain Stroke Using Optimized Boosting Algorithms.

Background/Objectives: Stroke stands as a prominent global health issue, causing con-siderable mortality and debilitation. It arises when cerebral blood flow is compromised, leading to irreversible brain cell damage or death. Leveraging the power of machine learning, this paper presents a systematic approach to predict stroke patient survival based on a comprehensive set of factors. These factors include demographic attributes, medical history, lifestyle elements, and physiological metrics. Method: An effective random sampling method is proposed to handle the highly biased data of stroke. The stroke pre-diction using optimized boosting machine learning algorithms is supported with explainable AI using LIME and SHAP. This enables the models to discern intricate data patterns and establish correlations between selected features and patient survival. Results: The performance of three boosting algorithms is studied for stroke prediction, which include Gradient Boosting (GB), AdaBoost (ADB), and XGBoost (XGB) with XGB achieved the best outcome overall with a training accuracy of 96.97% and testing accuracy of 92.13%. Conclusions: Through this approach, the study seeks to uncover actionable insights to guide healthcare practitioners in devising personalized treatment strategies for stroke patients.

Candidate Molecular Biomarkers of Traumatic Brain Injury: A Systematic Review.

Traumatic brain injury (TBI) is one of the leading causes of mortality and disability among young and middle-aged individuals. Adequate and timely diagnosis of primary brain injuries, as well as the prompt prevention and treatment of secondary injury mechanisms, significantly determine the potential for reducing mortality and severe disabling consequences. Therefore, it is crucial to have objective markers that indicate the severity of the injury. A number of molecular factors-proteins and metabolites-detected in the blood immediately after trauma and associated with the development and severity of TBI can serve in this role. TBI is a heterogeneous condition with respect to its etiology, clinical form, and genesis, being accompanied by brain cell damage and disruption of blood-brain barrier permeability. Two oppositely directed flows of substances and signals are observed: one is the flow of metabolites, proteins, and nucleic acids from damaged brain cells into the bloodstream through the damaged blood-brain barrier; the other is the infiltration of immune cells (neutrophils and macrophages) and serological proteins. Both flows aggravate brain tissue damage after TBI. Therefore, it is extremely important to study the key signaling events that regulate these flows and repair the damaged tissues, as well as to enhance the effectiveness of treatments for patients after TBI.

Pemberdayaan Siswa-Siswi SMA Negeri 3 Kota Sibolga tentang Pelatihan Sederhana Bantuan Hidup Dasar (BHD) dalam Upaya Memberikan Pertolongan Pertama

Community service by the D-III Nursing Study Program in Central Tapanuli, Medan Ministry of Health Polytechnic, was carried out in the form of material presentations and demonstrations to students of SMA Negeri 3 Sibolga about Basic Life Support as first aid. Basic Life Support (BHD) is a series of first aid that is carried out to help anyone who experiences respiratory or cardiac arrest. One solution for first aid is to educate the public about Basic Life Support so that the possibility of brain cell damage will be smaller and give the victim enough time to be taken to the hospital on time. The target of service activities is 100 students of SMA Negeri 3 Sibolga. The aim of this Community Service is to realize community service as one of the Tri Darma activities of Higher Education, increasing the knowledge and skills of students in providing basic life support as emergency first aid. The methods used are counseling, training and question and answer/discussion and evaluation. After the counseling and demonstration of Basic Life Support was carried out, the results showed that the majority of respondents had sufficient knowledge at 58%, 35% had good knowledge and 7% had less knowledge. Competency evaluation is carried out by giving participants the opportunity to demonstrate directly the implementation of BHD using a phantom. The results obtained were that 63% had capable category skills and 37% had less capable skills, meaning that students still received assistance.

Role of S100 and YKL40 on Intraventricular Cerebral Hemorrhages in the Preterm Infant and the Neuroprotective Role of miR-138-siRNAs-HIF-1a and miR-21-siRNAs-HVCN1 in Neonatal Mice with Nerve Injury.

Epilepsy and intraventricular-cerebral hemorrhage is a common complication irreversible in preterm infants. Inflammation leads to an increase in intracellular calcium, acidosis, and oxygen usage, and finally, may damage brain cells. Increases in HIF-1a and HVCN1 can reduce the complications of oxygen consumption and acidosis in infants with intraventricular hemorrhage (IVH). On the other hand, decreases in S100B can shield nerve cells from apoptosis and epilepsy by reducing brain damage. In this research, we investigated how miR-138-siRNAs-HIF-1a and miR-21- siRNAs-HVCN1 affect apoptosis in hypoxic mice. On the first and third days after delivery, the YKL40, HIF-1a, HVCN1, and S100b genes were compared between two groups of preterm infants with and without maternal inflammation. Afterward, the miRNAs were transfected into cell lines to monitor variations in YKL40, HIF-1a, HVCN1, and S100b gene expression and nerve cell apoptosis. We changed the expression of S100b, HVCN1, and HIF-1a genes by using specific siRNAs injected into mice. Using real-time PCR, Western blotting, flow cytometry (FCM), and immunofluorescence, and changes in gene expression were evaluated (IHC). HVCN1 gene expression showed a strong negative correlation with epilepsy in both groups of infants (P< 0.001). Significant correlations between epilepsy and the expression levels of the S100b, YKL40, and HIF-1a genes were found (P<0.001). According to FCM, after transfecting miRNA-431 and miRNA-34a into cell lines, the apoptosis index (A.I.) were 41.6 3.3 and 34.5 5.2%, respectively, while the A.I. were 9.6 2.7 and 7.1 4.2% after transfecting miRNA-21 and miRNA-138. MiR-138-siRNAs-HIF-1a and miR-21-siRNAs-HVCN1 were simultaneously injected into hypoxic mice, and IHC double-labeling revealed that this reduced apoptosis and seizures compared to the hypoxic group. Our findings demonstrate that miR-138-siRNAs-HIF-1a and miR-21-siRNAs- HVCN1 injections prevent cerebral ischemia-induced brain damage in hypoxia mice by increasing HVCN1 and HIF-1a and decreasing S100b, which in turn lessens apoptosis and epilepsy in hypoxic mice.

Investigating recovery after a spontaneous intracerebral haemorrhage in zebrafish larvae.

Intracerebral haemorrhage is a debilitating stroke sub-type with high morbidity and mortality rates. For survivors, rehabilitation is a long process, and with no available therapeutics to limit the immediate pathophysiology of the haemorrhage, recovery is dependent on individual neuroplasticity. We have previously shown that zebrafish larvae can be used to model spontaneous brain haemorrhage. Zebrafish exhibit innate recovery mechanisms and are often used as a model system for investigation into regeneration after injury, including injury to the nervous system. Here, we investigate the spontaneous and immediate recovery in zebrafish larvae following an intracerebral haemorrhage at 2 days post-fertilisation, during pre-protected stages and over the first 3 weeks of life. We have shown that following the onset of bleed at ∼2 days post-fertilisation zebrafish are capable of clearing the haematoma through the ventricles. Brain cell damage associated with intracerebral haemorrhage is resolved within 48 h, and this recovery is associated with survival rates equal to wildtype and non-haemorrhaged sibling control animals. Larvae express more nestin-positive neural progenitor cells 24 h after injury when the most damage is observed, and through mass spectrometry analysis, we have determined that these cells are highly proliferative and may specially differentiate into oligodendrocytes. This study provides an insight into the haematoma resolution processes in a live, intact organism, and may suggest potential therapeutic approaches to support the recovery of intracerebral haemorrhage patients.

Danggui-Shaoyao-San (DSS) ameliorating cognitive impairment in ischemia–reperfusion vascular dementia mice through miR-124 regulating PI3K/Akt signaling pathway

Vascular dementia (VD) is a disease characterized by cognitive impairment and memory loss due to brain cell damage caused by cerebral vascular ischemia. Danggui-Shaoyao-San (DSS) has been used clinically to treat diseases for centuries. The VD model was established by bilateral common carotid artery (BCCA) repeated ischemia–reperfusion (I/R) and caudal bleeding. Target prediction of DSS and miR-124 in PI3K/Akt signaling pathway by network pharmacology. The effect of DSS on cognitive dysfunction were evaluated through methods such as behavioral experiments, cerebral blood flow monitoring, HE and Nissl staining, western blot, and q-PCR. Prediction result showed that both DSS and miR-124 could target Akt1. DSS treatment significantly reduced hippocampal cell damage, improved learning and memory ability. Mechanically, DSS treatment up-regulated the expression levels of PI3K and Akt protein, and its gene. Bcl-2/Bax index is up-regulated and cell apoptosis reduced. LC3II/LC3I index decreased and autophagy of brain cells increased. Moreover, DSS down-regulated the expression level of miR-124. And inhibition of miR-124 up-regulate the expression of PI3K, Akt. These results suggested that DSS can reduce the content of miR-124 in the hippocampus of VD mice, thus regulating the PI3K/Akt signaling pathway and improving the learning and memory ability of VD mice.

Impact of environmental concentrations of fipronil on DNA integrity and brain structure of Bombus atratus bumblebees

Fipronil (FP) is an insecticide used in the treatment and control of pests, but it also adversely affects bees. Currently, there is no data on the genotoxic effects of FP in the brain of bumblebees. Thus, through the comet assay and routine morphological analysis, we analyzed the morphological effects and potential genotoxicity of environmentally relevant concentrations of FP on the brain of Bombus atratus. Bumblebees were exposed at concentrations of 2.5 μg/g and 3.5 μg/g for 96 hours. After the exposure, the brains were removed for morphological and morphometric analysis, and the comet assay procedure - used to detect DNA damage in individual cells using electrophoresis. Our data showed that both concentrations (2.5 μg/g and 3.5 μg/g) caused DNA damage in brain cells. These results corroborate the morphological data. We observed signs of synapse loss in the calyx structure, intercellular spaces between compact inner and non-compact inner cells, and cell swelling. This study provides unprecedented evidence of the effects of FP on DNA and cellular structures in the brain of B. atratus and reinforces the need to elucidate its toxic effects on other species to allow future risk assessments and conservation projects.

Exposure to hyperbaric O2 levels leads to blood-brain barrier breakdown in rodents

IntroductionHyperbaric oxygen has been used as a medical treatment tool in hyperbaric chambers and is an integral part of professional and combat divers’ activity. In extreme cases, exposure to hyperbaric oxygen can develop central nervous system oxygen toxicity (CNS-OT), which leads to seizures and eventually death. CNS-OT is caused by neuronal hyperactivity due to high oxygen levels, potentially damaging brain cells including the blood-brain barrier (BBB). However, the effect of hyperbaric oxygen levels on the healthy BBB has not been characterized directly yet.MethodsSix or three different groups of ~ eight rats or mice, respectively, were exposed to increasing levels of partial pressure of oxygen (0.21 to 5 ATA) in a hyperbaric chamber, followed by MRI scanning with gadolinium. Statistical significance (adjusted p-value ≤ 0.05) was assessed using linear regression and ordinary one-way (rats) or two-way (mice) ANOVA with correction of multiple comparison tests. In rats, the effect of 100% oxygen at 5 ATA was independently validated using FITC-Dextran (5 kDa). Statistical significance (p-value ≤ 0.05) was assessed using Welch’s t-test and effect size was calculated by Cohen’s D.ResultsIn rats, analyzed MRI scans showed a significant trend of increase in the % gadolinium in brain tissues as a result of hyperbaric oxygen pressures (p-value = 0.0079). The most significant increase was measured at 4 ATA compared to air (adjusted p-value = 0.0461). Significant increased FITC-Dextran levels were measured in the rats’ brains under 100% oxygen at 5 ATA versus air (p-value = 0.0327; Effect size = 2.0). In mice, a significant increase in gadolinium penetration into the hippocampus and frontal cortex was measured over time (adjusted p-value < 0.05) under 100% oxygen at 3 and 5 ATA versus air, and between the treatments (adjusted p-value < 0.0001).ConclusionsThe BBB is increasingly disrupted due to higher levels of hyperbaric oxygen in rodents, indicating a direct relation between hyperbaric oxygen and BBB dysregulation for the first time. We suggest considering this risk in different diving activities, and protocols using a hyperbaric chamber. On the other hand, this study highlights the potential therapeutic usage of hyperbaric oxygen for controlled drug delivery through the BBB into brain tissues in different brain-related diseases.

Physiological and chaos effect on dynamics of neurological disorder with memory effect of fractional operator: A mathematical study

Background and objective:To study the dynamical system, it is necessary to formulate the mathematical model to understand the dynamics of various diseases that are spread worldwide. The main objective of our work is to examine neurological disorders by early detection and treatment by taking asymptomatic. The central nervous system (CNS) is impacted by the prevalent neurological condition known as multiple sclerosis (MS), which can result in lesions that spread across time and place. It is widely acknowledged that multiple sclerosis (MS) is an unpredictable disease that can cause lifelong damage to the brain, spinal cord, and optic nerves. The use of integral operators and fractional order (FO) derivatives in mathematical models has become popular in the field of epidemiology. Method:The model consists of segments of healthy or barian brain cells, infected brain cells, and damaged brain cells as a result of immunological or viral effectors with novel fractal fractional operator in sight Mittag Leffler function. The stability analysis, positivity, boundedness, existence, and uniqueness are treated for a proposed model with novel fractional operators. Results:Model is verified the local and global with the Lyapunov function. Chaos Control will use the regulate for linear responses approach to bring the system to stabilize according to its points of equilibrium so that solutions are bounded in the feasible domain. To ensure the existence and uniqueness of the solutions to the suggested model, it makes use of Banach’s fixed point and the Leray Schauder nonlinear alternative theorem. For numerical simulation and results the steps Lagrange interpolation method at different fractional order values and the outcomes are compared with those obtained using the well-known FFM method. Conclusion:Overall, by offering a mathematical model that can be used to replicate and examine the behavior of disease models, this research advances our understanding of the course and recurrence of disease. Such type of investigation will be useful to investigate the spread of disease as well as helpful in developing control strategies from our justified outcomes.

Utilizing Siamese 4D-AlzNet and Transfer Learning to Identify Stages of Alzheimer’s Disease

Alzheimer's disease (AD) is the general form of dementia, leading to a progressive neurological disorder characterized by memory loss due to brain cell damage. Artificial Intelligence (AI) assists in the early identification and prediction of AD patients, determining future risks and benefits for radiologists and doctors to save time and cost. Since deep learning (DL) approaches work well with massive datasets and have recently become helpful for AD detection, there remains an area for improvement in automating detection performance. Present approaches somehow addressed the challenges of limited annotated data samples for binary classification. This contrasts with prior state-of-the-art techniques, which were constrained by their incapacity to capture abstract-level information. In this paper, we proposed a Siamese 4D-AlzNet model comprised of four parallel convolutional neural network (CNN) streams (Five CNN layer blocks) and customized transfer learning models (Frozen VGG-19, Frozen VGG-16, and customized AlexNet). Siamese 4D-AlzNet was vertically and horizontally stored, and the spatial features were passed to the final layer for classification. For experiments, T1-weighted MRI images comprised of four distinct subject classes, normal control (NC), mild cognitive impairment (MCI), late mild cognitive impairment (LMCI), and AD, have been employed. Our proposed models achieved outstanding accuracy, with a remarkable 95.05% accuracy distinguishing between normal and AD subjects. The performance across remaining binary class pairs consistently exceeded 90%. We thoroughly compared our model with the latest methods using the same dataset as our reference. Our proposed model improved NC-AD and MCI-AD classification accuracy by 2% 7%.

Electroacupuncture regulates histone acetylation of Bcl-2 and Caspase-3 genes to improve ischemic stroke injury

BackgroundImbalances between Bcl-2 and caspase-3 are significant evidence of apoptosis, which is considered an influential factor in rapidly occurring neuronal cell death and the decline of neurological function after stroke. Studies have shown that acupuncture can reduce poststroke brain cell damage via either an increase in Bcl-2 or a reduction in caspase-3 exposure. The current study aimed to investigate whether acupuncture could modulate Bcl-2 and caspase-3 expression through histone acetylation modifications, which could potentially serve as a neuroprotective mechanism. MethodsThis study used TTC staining, Nissl staining, Clark neurological system score, and Evans Blue (EB) extravasation to evaluate neurological damage following stroke. The expression of Bcl-2/caspase-3 mRNA was detected by real-time fluorescence quantification of PCR (real-time PCR), whereas the protein expression levels of Bcl-2, Bax, caspase-3, and cleaved caspase-3 were assessed using western blotting. TUNEL staining of the ischemic cortical neurons determined apoptosis in the ischemic cortex. Histone acetyltransferase (HAT) and histone deacetylase (HDAC) activities, along with the protein performance of AceH3, H3K9ace, and H3K27ace, were detected to evaluate the degree of histone acetylation. The acetylation enrichment levels of H3K9 and K3K27 in the Bcl-2/caspase-3 gene were assessed using Chromatin Immunoprecipitation (ChIP) assay. ResultsOur data demonstrated that electroacupuncture (EA) exerts a significant neuroprotective effect in middle cerebral artery occlusion (MCAO) rats, as evidenced by a reduction in infarct volume, neuronal damage, Blood-Brain Barrier (BBB) disruption, and decreased apoptosis of ischemic cortical neurons. EA treatment can promote the mRNA and protein expression of the Bcl-2 gene in the ischemic brain while reducing the mRNA and protein expression levels of caspase-3 and effectively decreasing the protein expression levels of Bax and cleaved caspase-3. More importantly, EA treatment enhanced the level of histone acetylation, including Ace-H3, H3K9ace, and H3K27ace, significantly enhanced the occupancy of H3K9ace/H3K27ace at the Bcl-2 promoter, and reduced the enrichment of H3K9ace and H3K27ace at the caspase-3 promoter. However, the Histone Acetyltransferase inhibitor (HATi) treatment reversed these effects. ConclusionsOur data demonstrated that EA mediated the expression levels of Bcl-2 and caspase-3 in MCAO rats by regulating the occupancy of acetylated H3K9/H3K27 at the promoters of these two genes, thus exerting a cerebral protective effect in ischemic reperfusion (I/R) injury.

Quantum mayfly optimization based feature subset selection with hybrid CNN for biomedical Parkinson’s disease diagnosis

Parkinson's disease (PD) arises from brain cell damage and necessitates early detection for effective treatment and symptom management. While various methods such as voice, speech, and written exams have been explored, utilizing automated tools is crucial to enhance accuracy. Recent advancements in artificial intelligence (AI) and deep learning (DL) provide an opportunity for precise early-stage PD identification. This study introduces a novel approach known as Quantum Mayfly Optimization-based feature subset selection with hybrid convolutional neural network (QMFOFS-HCNN) to improve PD detection and classification. QMFOFS-HCNN is designed to identify optimal feature subsets and overcome the dimensionality challenge. It combines a quantum mayfly optimization approach for feature selection with a convolutional neural network with attention-based long short-term memory for PD detection and classification. Additionally, hyperparameter selection is optimized using the Nadam optimizer. Experimental validation using benchmark datasets yielded compelling results. The QMFOFS-HCNN technique achieved accuracy rates: 96.35% for HandPD Spiral, 96.7% for HandPD Meander, 98.5% for Speech PD, and a perfect 100% for Voice PD datasets. These quantitative findings underscore the potential of AI and DL to enhance early PD detection accuracy significantly. These results offer promising prospects for improving healthcare outcomes in managing PD and related neurological disorders.

Selenium Nanoparticles in Protecting the Brain from Stroke: Possible Signaling and Metabolic Mechanisms.

Strokes rank as the second most common cause of mortality and disability in the human population across the world. Currently, available methods of treating or preventing strokes have significant limitations, primarily the need to use high doses of drugs due to the presence of the blood-brain barrier. In the last decade, increasing attention has been paid to the capabilities of nanotechnology. However, the vast majority of research in this area is focused on the mechanisms of anticancer and antiviral effects of nanoparticles. In our opinion, not enough attention is paid to the neuroprotective mechanisms of nanomaterials. In this review, we attempted to summarize the key molecular mechanisms of brain cell damage during ischemia. We discussed the current literature regarding the use of various nanomaterials for the treatment of strokes. In this review, we examined the features of all known nanomaterials, the possibility of which are currently being studied for the treatment of strokes. In this regard, the positive and negative properties of nanomaterials for the treatment of strokes have been identified. Particular attention in the review was paid to nanoselenium since selenium is a vital microelement and is part of very important and little-studied proteins, e.g., selenoproteins and selenium-containing proteins. An analysis of modern studies of the cytoprotective effects of nanoselenium made it possible to establish the mechanisms of acute and chronic protective effects of selenium nanoparticles. In this review, we aimed to combine all the available information regarding the neuroprotective properties and mechanisms of action of nanoparticles in neurodegenerative processes, especially in cerebral ischemia.

Neurotoxic effects of type II-diabetes mellitus and the possible preventive effects of olive leaves supplement in male rats.

Diabetes mellitus (DM) is a common metabolic disorder with well-known serious secondary complications. It is also associated with central nervous system damage. This damage is characterized by impairments in brain functions, with neurochemical and structural abnormalities. The study was conducted to clarify the neuroprotective effects of olive leaf supplements on the brain and brain histological structure of diabetic adult rats. Thirty adult male rats were allocated into three groups, the first group (CC), received an oral supplement containing olive leaves supplements (OLS) and served as a control; in the other group , DM was induced in these animals and left for 40 days; and the third group was DM+OL, which induced DM, then treated with oral OLS for 40 days. The investigation included serum glycemic index measurements, in addition to the level of malondialdehyde (MDA), glutathione (GSH), dopamine (DOP), acetylcholinesterase (AchE) in brain tissue, and histopathology of brain and pancreas. We demonstrated a significant increase in glycemic index measurements in diabetic groups (DM, DM+OL) at the beginning of a trial; however, the same parameters were significantly decreased after treatment with OLS in only the DM+OL group after 40 days. The study also showed differences in the levels of MDA, and GSH, in the diabetic groups, which returned to normal levels after being treated with OLS. Moreover, AchE and DOP exhibited a significant decline in diabetic rats. However, OLS induced a considerable rise in these neurotransmitters after treatment with it in the DM+OL group. The histopathological section of the pancreas and brain showed histopathological changes in DM groups; whereas, the tissue was shielded from chemical damage from DM by the OLS treatment in DM+OL animals. Overall, diabetes impairs glucose hemostasis by affecting glucose concentration, insulin level, and insulin resistance. However, olive leaf supplements restored the glucose hemostasis close to normal in diabetic rats. Furthermore, diabetes affects neurotransmitters by increasing the level of oxidative stress in brain tissue, and brain cell damage. Nevertheless, olive leaf supplements can ameliorate DM harmful effects by retrieving the normal oxidative environment in the brain.

Caveolae with serotonin and NMDA receptors as promising targets for the treatment of Alzheimer's disease.

Alzheimer's disease is the most general type of cognitive impairments. Until recently, strategies that prevent its clinical progression have remained more elusive. Consequently, research direction should be for finding effective neuroprotective agents. It has been suggested oxidative stress, mitochondrial injury, and inflammation level might lead to brain cell death in many neurological disorders. Therefore, several autophagy-targeted bioactive compounds may be promising candidate therapeutics for the prevention of brain cell damage. Interestingly, some risk genes to Alzheimer's disease are expressed within brain cells, which may be linked to cholesterol metabolism, lipid transport, endocytosis, exocytosis and/or caveolae formation, suggesting that caveolae may be a fruitful therapeutic target to improve cognitive impairments. This review would highlight the latest advances in therapeutic technologies to improve the treatment of Alzheimer's disease. In particular, a paradigm that serotonin and N-methyl-d-aspartate (NMDA) receptors agonist/antagonist within caveolae structure might possibly improve the cognitive impairment. Consequently, cellular membrane biophysics should improve our understanding of the pathology of the cognitive dysfunction associated with Alzheimer's disease. Here, this research direction for the purpose of therapy may open the potential to move a clinical care toward disease-modifying treatment strategies with certain benefits for patients.

Multitarget Protective Effects of JUB on Aβ-Induced Neurotoxicity and the Mechanism Predication Using Network Pharmacology Analysis.

Amyloid-β (Aβ) is one of the core factors in the pathogenesis of Alzheimer's disease (AD), and the accumulation of its aggregates in the brain can form age-related plaques, leading to brain cell damage and intellectual decline, which may be the common intersection of all causes of neurotoxicity. Jujuboside B (JUB) has many characteristics such as hypnosis, sedation, antianxiety, and antioxidant stress. However, it is still unclear whether JuB can alleviate the neurotoxicity caused by Aβ. Our study demonstrates that JUB improves learning and memory deficits in the nematode model. At the same time, JUB increases the antioxidant activity, prevents excessive accumulation of lipid synthesis, and resists endogenous lipofuscin deposition, thereby inhibiting the toxic effect of Aβ. In vitro, JUB can improve Aβ1-42-induced neuronal apoptosis level through the Bax/Bcl-2/caspase-3 signaling pathway and restore mitochondrial function in SH-SY5Y cells. The network pharmacology has been used to predict the potential neuroprotective mechanism of JUB. In summary, JUB exhibits neuroprotective properties employing both a neural cell and a nematode, which provides a basis for screening candidate ingredients for preventing AD.