Protect Brain Cells Research Articles

Overexpression of BDNF Suppresses the Epileptiform Activity in Cortical Neurons of Heterozygous Mice with a Transcription Factor Sip1 Deletion.

Since genetic mutations during brain development play a significant role in the genesis of epilepsy, and such genetically determined epilepsies are the most difficult to treat, there is a need to study the mechanisms of epilepsy development with deletions of various transcription factors. We utilized heterozygous mice (Sip1wt/fl) with a neuronal deletion of the transcription factor Sip1 (Smad interacting protein 1) in the cerebral cortex. These mice are characterized by cognitive impairment and are prone to epilepsy. It is known that the brain-derived neurotrophic factor (BDNF) has a neuroprotective effect in various neurodegenerative diseases. Therefore, we created and applied an adeno-associated construct carrying the BDNF sequence selectively in neurons. Using in vitro and in vivo research models, we were able to identify a key gen, the disruption of whose expression accompanies the deletion of Sip1 and contributes to hyperexcitation of neurons in the cerebral cortex. Overexpression of BDNF in cortical neurons eliminated epileptiform activity in neurons obtained from heterozygous Sip1 mice in a magnesium-free model of epileptiform activity (in vitro). Using PCR analysis, it was possible to identify correlations in the expression profile of genes encoding key proteins responsible for neurotransmission and neuronal survival. The effects of BDNF overexpression on the expression profiles of these genes were also revealed. Using BDNF overexpression in cortical neurons of heterozygous Sip1 mice, it was possible to achieve 100% survival in the pilocarpine model of epilepsy. At the level of gene expression in the cerebral cortex, patterns were established that may be involved in the protection of brain cells from epileptic seizures and the restoration of cognitive functions in mice with Sip1 deletion.

Functional Changes in the Expression of the Aqp4 Gene in the Hypothalamus Under the Influence of Drinking Regimen and Arterial Hypertension in Rats

Aquaporin-4 (AQP4) is the main water channel in the central nervous system. AQP4 is densely expressed in brain structures suggesting a crucial role in water transport in normal conditions and in disease. The effect of changes in drinking regime (water-deprivation and hyperhydration) and inherited arterial hypertension on the expression of the AQP4 water channel gene in the hypothalamus, the center of regulation of visceral functions, was studied. It was shown that the level of the Aqp4 mRNA in hyperhydrated animals more than 1.5 times lower than in animals with water-deprivation. This decrease in the Aqp4 gene expression in the hypothalamus may be associated with the ability to prevent cytotoxic edema during increased fluid intake. Rats with inherited stress induced arterial hypertension (ISIAH) are characterized by an increased level of Aqp4 mRNA in the hypothalamus, which suggests the involvement of this channel in processes associated with the regulation of brain water balance during arterial hypertension and the prevention of vasogenic cerebral edema. Thus, the presence of the AQP4 water channel in the brain, associated with the protection of brain cells, is functionally determined by the state of the body. This may be evidenced by bidirectional changes in the Aqp4 gene expression during hyperhydration and arterial hypertension.

Astragaloside IV protects brain cells from ischemia-reperfusion injury by inhibiting ryanodine receptor expression and reducing the expression of P-Src and P-GRK2

Astragaloside IV, a prime active component of Astragalus membranaceus, has potential as a neuroprotectant. We aimed to identify the active ingredients in A. membranaceus and assess if Astragaloside IV can improve cerebral ischemia-reperfusion injury (CIRI) cell apoptosis by reducing P-Src and P-GRK2 via ryanodine receptor (RyR) expression inhibition. We used bioinformatics analysis to examine the effects of A. membranaceus on ischemic stroke. We studied brain samples from middle cerebral artery occlusion (MCAO) mice treated with normal saline, Astragaloside IV, and sham mice for pathology and Western blot tests. We also tested PC12 cells in vitro with or without Astragaloside IV or GSK180736A using Western blotting and fluorescence assays. Our bioinformatics analysis suggested a possible association between A. membranaceus, calcium ion pathways, and apoptosis pathways. Western blot data indicated Astragaloside IV significantly decreased RyR, p-Src, and downstream phosphorylated GRK2, PLC, CaMKII, and IP3R levels in MCAO mice brains. Astragaloside IV also considerably inhibited pro-apoptotic and oxidative stress-associated proteins’ expression while boosting anti-apoptotic protein expression. The results suggest Astragaloside IV can inhibit RyR expression, subsequently reducing brain cell apoptosis.

Virtual screening, molecular docking, MD simulation studies, DFT calculations, ADMET, and drug likeness of Diaza-adamantane as potential MAPKERK inhibitors.

Introduction: Multiple sclerosis (MS) is an autoimmune and inflammatory disease that destroys the protective coating of central nervous system (CNS) nerve fibers and affects over 2.8 million people worldwide. Despite several studies on new therapeutic targets and lead compounds, MS disease has limited treatment options. This condition may be caused by a complicated interaction of environmental and genetic variables. Studies showed that MS-associated microglial cells' increased MAPKERK activity may cause CNS inflammation and oligodendrocyte damage. Thus, screening for lead compounds that inhibit MAPKERK may protect brain cells and slow disease progression. Methods: The study aims to discover compounds that may inhibit MAPKERK as a novel approach for protecting the nervous system in managing MS. The study includes in silico methods, such as virtual screening, molecular docking, Density-functional theory (DFT) investigations (using the B3LYP/6-31++G(d,p) basis set in a gas phase environment), drug likeness scores, and molecular dynamic (MD) simulations. Results and Discussion:During the docking process with the MAPKERK protein, it was shown that the ligand L12 receptor had the best binding affinity, with a docking score of -6.18kcal/mol. To investigate the stability of the binding, a 100ns MD simulation was performed on the complex formed by the MAPKERK protein and L12. The receptor-ligand combination exhibited significant stability throughout the duration of the MD simulation. Additionally, the pharmacokinetic and drug-likeness properties of these ligands suggest that they have the potential to be considered viable candidates for future development in MS management.

Albiflorin alleviates neuroinflammation of rats after MCAO via PGK1/Nrf2/HO-1 signaling pathway

Ischemic stroke is acknowledged as one of the most frequent causes of death and disability, in which neuroinflammation plays a critical role. Emerging evidence supports that the PGK1/Nrf2/HO-1 signaling can modulate inflammation and oxidative injury. Albiflorin (ALB), a main component of Radix paeoniae Alba, possesses anti-inflammatory and antioxidative properties. However, how it exerts a protective role still needs further exploration. In our study, the middle cerebral artery occlusion (MCAO) model was established, and the Longa score was applied to investigate the degree of neurological impairment. Dihydroethidium (DHE) staining and Malondialdehyde (MDA) assay were used to detect the level of lipid peroxidation. 2, 3, 5-Triphenyltetrazolium chloride (TTC) staining was used to measure the infarct area. Evans blue staining was employed to observe the integrality of the blood–brain barrier (BBB). The injury of brain tissue in each group was observed via HE staining. Immunofluorescence staining, enzyme-linked immunosorbent assay (ELISA) and western blot assay were used for the measurement of inflammatory factors and protein levels. We finally observed that ALB relieved cerebral infarction symptoms, attenuated oxidative damage in brain tissues, and reduced neuroinflammation and cell injury in MCAO rats. The overexpression of PGK1 abrogated the protective effect of ALB after experimental cerebral infarction. ALB promoted PGK1 degradation and induced Nrf2 signaling cascade activation for subsequent anti-inflammatory and antioxidant damage. Generally speaking, ALB exerted a protective role in treating cerebral ischemia, and it might target at PGK1/Nrf2/HO-1 signaling. Thus, ALB might be a potential therapeutic agent to alleviate neuroinflammation and protect brain cells after cerebral infarction.

Ethanolic Extract of <i>Alternanthera Sessilis</i>: A Potential Therapeutic Agent for Behavioral Improvements in Reserpine-Induced Parkinsonian Rats

The present study evaluated the potential of an ethanol extract from Alternanthera sessilis to alleviate reserpine-induced Parkinson's disease (PD) like behavioural manifestations in rats. The animals were grouped into five: a control group, a group receiving only reserpine, a group treated with levodopa and carbidopa, and two groups given different doses of the Alternanthera sessilis extract. Reserpine was used to mimic PD symptoms, while the extract was administered orally at two different concentrations. The behavioral tests were conducted to assess locomotor activity, grip strength, catalepsy, and rearing activity. Locomotor activity was measured using an actophotometer, where interruptions in light beams caused by the rates were recorded over a 10-minute period. Grip strength was evaluated using a rotarod apparatus, measuring the time taken for rats to fall off individual rods. Catalepsy was assessed through a bar test, measuring the time for rats to descend from a horizontal bar to the base. Rearing activity was observed in a round open field arena, with parameters including the occurrence rate of rearing, general movements score, and duration spent in the center of the arena. The results revealed administration of reserpine led to a decrease in body weight, locomotor activity, muscle coordination, catalepsy score, rearing activity, and grip strength compared to the control group. Conversely, treatment with levodopa and carbidopa resulted in increased values for these parameters. Importantly, administration of Alternanthera sessilis extract showed a dose-dependent reversal of the effects induced by reserpine, with significant increases observed in body weight, locomotor activity, muscle coordination, rearing activity, general movement, and grip strength, indicating its potential therapeutic effects. In conclusion, the present study results suggest that the extract from the Alternanthera sessilis plant might protect brain cells and improve symptoms of Parkinson's disease. However, more research is needed to understand how it works and if it can be used safely and effectively clinical trails.

The impact of the ketogenic diet on Alzheimer’s disease

Alzheimer’s disease (AD) is a neurological illness that causes memory loss and mental decline. Many are contemplating a Ketogenic diet (KD) as an Alzheimer’s treatment due to its neuroprotective effects. By modifying brain metabolism, decreasing inflammation, and guarding against neurodegenerative processes, KD halts cognitive decline, enhances cognition, and gives therapeutic advantages. According to prior research, the KD combats inflammatory and apoptotic mediators in Alzheimer’s, protects brain cells, and influences amyloid plaques and tau protein. Animal and human research studies illustrate that the KD and supplements remedy brain inflammation, cognition, and metabolism. The KD works better with other AD treatments like exercise, forming a multi-domain strategy. However, the present research is frequently small and short-term, requiring big, long-term trials for more convincing data. This study suggests that optimizing the KD, evaluating particular fat sources, and constantly monitoring carbohydrate consumption are essential to achieve promising cognitive function and quality of life improvements. However, large-scale, long-term research and diet optimization is needed to fully understand the diet’s effect and potential to improve Alzheimer’s patients’ lives.

Glioblastoma and the CAR-T cell therapy: A review

Gliomas are the most common and aggressive tumors that develop from the brain. Glioblastomas are also known as grade IV gliomas, indicating them the most aggressive brain tumors. Unlike other cancers that are categorized by stage, gliomas are classified by grade which describes how aggressive the tumor appears under the microscope and its molecular profiles. The grade for gliomas ranges from I to IV, with I is the least aggressive gliomas and IV is the most aggressive one. Glioblastoma originated from glial cells which are a type of brain cells that support and protect brain cells. The common treatments for glioblastomas include surgery, chemotherapy with temozolomide, and radiotherapy. Though patients experience decreases in symptoms and improvement in emotions, the survival rate for the treatments is significantly low. Part of the reason for the situation is the poor efficiency of TMZ due to the medicine penetrating the blood-brain barrier insufficiently. CAR-T cell therapy, an innovative immunotherapy regarded as a self-duplicating drug to treat cancer, is considered to have a better blood-brain barrier penetration, making the therapy a potentially promising treatment for glioblastoma. Besides, the treatment targets and kills tumor cells directly and it is independent of the endogenous immune response, which is greatly repressed in glioblastoma. Unfortunately, due to the restricted number of specific antigens in glioblastoma and their heterogenous expression, results of CART cell therapy for glioblastoma have not indicated clinical benefit. Nevertheless, adjustments can be made in order to improve the CART cell therapy in glioblastoma.

Gut Microbiota. Neuropolen for Recovery after A Ischemic Stroke

Background The brain possesses an extraordinary ability to heal itself after a stroke. This ability is known as neuroplasticity. The relationship between the gut microbiota and stroke is recent, with early studies dating from 2013. Recent studies support that gut microbiota is associated with ischemic stroke through the gut-brain axis, thereby modulating stroke pathogenesis. Objectives Gut dysbiosis, defined as alterations to the gut microbial communities has been proposed in stroke. To determine whether Neuropolen can be a potential treatment for recovery after a stroke. Material and methods The 2-way communication between the gut and the brain, which involves the brain, the gut microbiota, and the intestinal tissue, has been suggested as a key component of stroke outcome. To arrive at these observations, authors examined how Neuropolen and diet solve disabilities. Results The gut microbiota can increase the risk of a cerebrovascular event, playing a role in the onset of stroke. Conversely, stroke can induce dysbiosis of the gut microbiota. We found that Neuropolen may be important for functional recovery after a stroke. Neuropolen that may help minimize the degree of complications, stimulation enhances plasticity of the brain, in which noninjured parts of the brain can pick up the job of the injured brain areas. Conclusion In this presentation, authors describe the role of the gut microbiota, microbiome and microbiota-derived metabolites in stroke, and their use as therapeutic targets. Neuropolen may be a potential therapy for recovery after a stroke, it can quickly feed oxygen to the brain and protect brain cells.

Lead Compounds for Brain Protection against Alzheimer’s

To find a promising drug for treatment of Alzheimer’s` is not that easy target. Although some medications have FDA approval for management of AD, all of them offer symptomatic benefits. This is because efforts to find the treatment are distributed among many targets in the brain which make it so difficult to find a drug that can correct all of them at once. The primary histopathologic lesions of Alzheimer’s pathology are amyloid plaques, NFTs and neuronal loss with a wide genetic background which deteriorate the patient condition so rapidly. In the current article, we highlight some lead compounds that protect brain cells from undergoing this dark pathway or, which is more important, to stop deterioration and worsening of the case after starting of the disease. sex lead compounds of natural sources suggested as anti-AD drugs with brief discussion of each of them regarding its chemistry, physiochemical properties, mechanism of action, bioavailability, derivatives and method of synthesis. These natural extracts can be expected as lead compounds for design and synthesis of more effective derivatives as prophylactic treatment against Alzheimer’s. The aim of our review is to help to direct efforts to treat AD toward the prophylactic choice according to research results and scientific facts.

CDNF overexpression prevents motor-cognitive dysfunction by intrastriatal CPP-based delivery system in a Parkinson's disease animal model

Parkinson's disease (PD) is characterized by the loss of dopaminergic neurons in the substantia nigra pars compact (SNpc), and no effective treatment has yet been established to prevent PD. Neurotrophic factors, such as cerebral dopamine neurotrophic factor (CDNF), have shown a neuroprotective effect on dopaminergic neurons. Previously, we developed a cell-penetrating-peptide-based delivery system that includes Asn194Lys mutation in the rabies virus glycoprotein-9R peptide (mRVG9R), which demonstrated a higher delivery rate than the wild-type. In this study, using a mouse PD-like model, we evaluated the intrastriatal mRVG9R-KP-CDNF gene therapy through motor and cognitive tests and brain cell analysis. The mRVG9R-KP-CDNF complex was injected into the striatum on days 0 and 20. To induce the PD-like model, mice were intraperitoneally administered Paraquat (PQ) twice a week for 6weeks. Our findings demonstrate that mRVG9R-KP-CDNF gene therapy effectively protects brain cells from PQ toxicity and prevents motor and cognitive dysfunction in mice. We propose that the mRVG9R-KP-CDNF complex inhibits astrogliosis and microglia activation, safeguarding dopaminergic neurons and oligodendrocytes from PQ-induced damage. This study presents an efficient CDNF delivery system, protecting neurons and glia in the nigrostriatal pathway from PQ-induced damage, which is known to lead to motor and cognitive dysfunction in neurodegenerative diseases such as PD.

Stem Cells from Human Exfoliated Deciduous Teeth Alleviate High-Altitude Cerebral Oedema by Shifting Microglial M1/M2 Polarisation.

To explore the high-efficiency and low-risk prevention and treatment strategies for stem cells from human exfoliated deciduous teeth (SHED) for high-altitude cerebral oedema. A low-pressure and low-oxygen tank mimicking high-altitude conditions was used to establish the high-altitude cerebral oedema animal model. The preventive effects of SHED for cerebral oedema were then evaluated by haematoxylin and eosin (H&E) and histological staining. In vitro, SHED was co-cultured with BV-2 to analyse the effects of SHED by western blot and immunofluorescence staining. SHED can prevent and treat cerebral oedema in a high altitude rat animal model. Mechanistically, SHED treatment can protect brain cells from apoptosis induced by high altitude condition. Moreover, SHED treatment can inhibit M1-type polarisation and promote M2-type polarisation of microglia cells via the suppression of hypoxia inducible factor (HIF)- 1α-mediated extracellular signal-regulated kinase (ERK) signalling activated in high altitude condition. SHED treatment can relieve high-altitude cerebral oedema via inhibiting HIF- 1α-mediated ERK signalling, which indicates that SHED is a promising alternative strategy to prevent and treat high-altitude cerebral oedema.

In silico analysis of Hsp70 genes in Ctenopharyngodon idella and their expression profiles in response to environmental stresses

Heat shock protein 70 (Hsp70) is a crucial member of the Hsp family, which is present in many animals, and acts as a chaperone to protect the organism from damage caused by various environmental stresses, particularly unfavorable temperatures. In this study, we used homologous gene search and domain analysis to identify sixteen Hsp70 genes (named as CiHSP genes) from the genome of grass carp (Ctenopharyngodon idella). These genes were classified into ten subfamilies based on their conserved structures and phylogenetic analysis. To investigate the biological functions of CiHSP genes in grass carp, we analyzed public RNA-Seq data, and found that most members of the CiHSP gene family were highly expressed in the brain and kidney, suggesting potential roles in protecting brain cells and participating in fish immunological processes. Additionally, these CiHSP genes were characterized as responding to high density and high temperature stress, with most members significantly upregulated under high temperature conditions. These findings demonstrate the critical roles of CiHSP genes in grass carp development and their response to environmental stress, which will provide valuable insights for determining their function and potential application in fish production in the future.

Caffeic Acid Phenethyl Ester (CAPE): Biosynthesis, Derivatives and Formulations with Neuroprotective Activities.

Neurodegenerative disorders are characterized by a progressive process of degeneration and neuronal death, where oxidative stress and neuroinflammation are key factors that contribute to the progression of these diseases. Therefore, two major pathways involved in these pathologies have been proposed as relevant therapeutic targets: The nuclear transcription factor erythroid 2 (Nrf2), which responds to oxidative stress with cytoprotecting activity; and the nuclear factor NF-κB pathway, which is highly related to the neuroinflammatory process by promoting cytokine expression. Caffeic acid phenethyl ester (CAPE) is a phenylpropanoid naturally found in propolis that shows important biological activities, including neuroprotective activity by modulating the Nrf2 and NF-κB pathways, promoting antioxidant enzyme expression and inhibition of proinflammatory cytokine expression. Its simple chemical structure has inspired the synthesis of many derivatives, with aliphatic and/or aromatic moieties, some of which have improved the biological properties. Moreover, new drug delivery systems increase the bioavailability of these compounds in vivo, allowing its transcytosis through the blood-brain barrier, thus protecting brain cells from the increased inflammatory status associated to neurodegenerative and psychiatric disorders. This review summarizes the biosynthesis and chemical synthesis of CAPE derivatives, their miscellaneous activities, and relevant studies (from 2010 to 2023), addressing their neuroprotective activity in vitro and in vivo.

Extracellular protein homeostasis: The dawning of a new age for human disease therapies?

Extracellular protein homeostasis: The dawning of a new age for human disease therapies?

Effect of hyperbaric oxygen on post-stroke depression.

In patients with post-stroke depression (PSD) in diabetes, the situation may be more complex, requiring simultaneous treatment of blood glucose, depressive symptoms, and neurological dysfunction. Hyperbaric oxygen (HBO) therapy can improve tissue oxygen content and improve the situation of ischemia and hypoxia, thus playing a role in protecting brain cells and restoring the function of brain cells. However, there are few studies on HBO therapy for patients with PSD. This study explores the clinical efficacy of such therapy for stroke complicated with depression and diabetes mellitus, and to provide reference and basis for clinical treatment and development through the application of relevant rating scales and laboratory test indicators. To evaluate the clinical effects of HBO therapy on patients with diabetes with PSD. A total of 190 diabetic patients with PSD were randomly divided into observation and control groups (95 patients per group). The control group received escitalopram oxalate 10mg once a day for eight weeks. In addition, the ob-servation group was also given HBO therapy, once a day, five times a week, for eight weeks. The Montgomery Depression Rating Scale (MADRS), National Institutes of Health Stroke Scale (NIHSS), hypersensitive C-reactive protein, tumor necrosis factor (TNF)-α, and fasting glucose levels were compared. There were no significant differences in age, sex, or depression course between the groups (P > 0.05). After HBO treatment, MADRS scores in both groups decreased significantly (14.3 ± 5.2), and were significantly lower in the control group (18.1 ± 3.5). After HBO treatment, NIHSS scores in both groups decreased significantly, and scores in the observation group (12.2 ± 4.0) decreased more than in the control group (16.1 ± 3.4), the difference was statistically significant (P < 0.001). The levels of hypersensitive C-reactive protein and TNF-α in both groups were significantly decreased, and the observation group was significantly lower than the control group (P < 0.001). Fasting blood glucose levels in both groups decreased significantly, and those in the observation group decreased more (8.02 ± 1.10) than in the control group (9.26 ± 1.04), with statistical significance (t = -7.994, P < 0.001). HBO therapy can significantly improve depressive symptoms and neurological dysfunction in patients with PSD, and reduce the levels of hypersensitive C-reactive protein, TNF-α and fasting blood glucose.

Bio-synthesized selenium nanoparticles ameliorateBrain oxidativestress in Parkinson disease rat models.

Parkinson disease (PD) is a prevalent central nervous system degenerative condition that impacts elderly people. Recent clinical and experimental study findings have established oxidative stress as one of the main pathogeneses of PD. Selenium, a trace metals with antioxidant effects, might reverse the neurobehavioral impairments and oxidative stress in rats. Thus, the goal of this study was to ascertain if Selenium Nano Particles (SeNPs) are also effective to protect brain cells from oxidative stress or not. SeNPs were synthesized utilizing Ascorbic acid and chitosan as a reducing and stabilizing agent. Next, eight groups (N: 6) of male Wistar rats were randomly assigned and injected by different dosage (0.1, 0,2, and 0.3mg/kg) of Se and SeNP. Finally, to ascertain the protective benefits of SeNP on PD rats, behavioral evaluation, clinical symptoms, antioxidant activity, and oxidant levels were examined. According to the findings, PD rats' motor functions had developed by SeNP injection. Higher MDA levels and inhibited antioxidant activities (SOD, CAT, and GPX) in lesion group are highlighting the significant role of oxidative stress in dopaminergic neuron death and neurobehavioral abnormalities. SeNP also protect against oxidative stress as compared to the lesion group. The levels of MDA had greatly reduced while the activities of enzymes, TAC, and SeNP both had significantly increased. By enhancing antioxidant activity, administration of SeNP can reduce the hazardousconsequences of oxidative stress.

Pharmacological Regulation of Endoplasmic Reticulum Structure and Calcium Dynamics: Importance for Neurodegenerative Diseases.

The endoplasmic reticulum (ER) is the largest organelle of the cell, composed of a continuous network of sheets and tubules, and is involved in protein, calcium (Ca2+), and lipid homeostasis. In neurons, the ER extends throughout the cell, both somal and axodendritic compartments, and is highly important for neuronal functions. A third of the proteome of a cell, secreted and membrane-bound proteins, are processed within the ER lumen and most of these proteins are vital for neuronal activity. The brain itself is high in lipid content, and many structural lipids are produced, in part, by the ER. Cholesterol and steroid synthesis are strictly regulated in the ER of the blood-brain barrier protected brain cells. The high Ca2+ level in the ER lumen and low cytosolic concentration is needed for Ca2+-based intracellular signaling, for synaptic signaling and Ca2+ waves, and for preparing proteins for correct folding in the presence of high Ca2+ concentrations to cope with the high concentrations of extracellular milieu. Particularly, ER Ca2+ is controlled in axodendritic areas for proper neurito- and synaptogenesis and synaptic plasticity and remodeling. In this review, we cover the physiologic functions of the neuronal ER and discuss it in context of common neurodegenerative diseases, focusing on pharmacological regulation of ER Ca2+ Furthermore, we postulate that heterogeneity of the ER, its protein folding capacity, and ensuring Ca2+ regulation are crucial factors for the aging and selective vulnerability of neurons in various neurodegenerative diseases. SIGNIFICANCE STATEMENT: Endoplasmic reticulum (ER) Ca2+ regulators are promising therapeutic targets for degenerative diseases for which efficacious drug therapies do not exist. The use of pharmacological probes targeting maintenance and restoration of ER Ca2+ can provide restoration of protein homeostasis (e.g., folding of complex plasma membrane signaling receptors) and slow down the degeneration process of neurons.

Nicotine's Potential to Protect Brain Cells: The Influence of Nicotine on Alzheimer's Disease Risk in the United States: A Scoping Review

Nicotine consumption increases brain excitability in a dispersed system of brain areas, such as the frontal cortex, amygdala, cingulate, and frontal lobes, in a dose-dependent manner. Stimulation in these areas is compatible with nicotine's ability to arouse and reinforce behaviour in humans. However, the effects of nicotine consumption on brain cells and the way it modifies them to either inhibit AD or facilitate AD is still unknown, therefore, the current scientific article aimed to address this research gap through analysing prior but latest research studies in this domain. Since there was a need to establish and explore more research regarding the positive impacts of Nicotine on patients with AD, a qualitative research design using secondary data was used to conduct the present scientific evidence. Four published papers within the year range 2017 to 2023 were acquired and thematically evaluated. Mixed findings regarding the impact of nicotine on brain cells and probability of getting AD were found however, there has been no clinical trials or enough empirical studies to support this assumption. Therefore, more research will be needed in the prospective to obtain credible and supporting results. Keywords: Nicotine, Brain cells, nicotinic receptors, Alzheimer’s disease.

Association between Edinburgh Postnatal Depression Scale and Serum Levels of Ketone Bodies and Vitamin D, Thyroid Function, and Iron Metabolism.

Suicide due to postpartum depression is the most common perinatal-related death and is a social concern in Japan. Nutritional deficiencies during pregnancy may contribute to postpartum depression; therefore, we investigated the relationship between postpartum depression and nutritional status during pregnancy and postpartum. We focused specifically on ketone bodies because they are known to protect brain cells. The relationship between the Edinburgh Postnatal Depression Scale (EPDS) scores and the serum levels of ketone bodies and vitamin D, thyroid function, and iron metabolism was examined. Overall, 126 pregnant women were identified for the study, and 99 were eventually included in the analysis. We defined an EPDS score of ≥9 as being positive for postpartum depression, and serum ketone levels were found to be higher in the group with an EPDS score of ≥9 during the second trimester; however, there were no other significant findings. We may be able to predict postpartum depression from a pregnant woman's serum ketone levels in the second trimester. There was a positive correlation between the EPDS scores at 3 days and 1 month postpartum (r = 0.534, p < 0.001). EPDS scores assessed in the early postpartum period may be useful for the timely detection of postpartum depression.