Alzheimer’s disease (AD) is a progressive neurodegenerative disorder marked by amyloid-β plaque accumulation, tau tangles, and extensive neuroinflammation. Neuroinflammation, driven by glial cells like microglia and astrocytes, plays a critical role in AD progression. Initially, these cells provide protective functions, such as debris clearance and neurotrophic support. However, as AD progresses, chronic activation of these cells exacerbates inflammation, contributing to synaptic dysfunction, neuronal loss, and cognitive decline. Microglia release pro-inflammatory cytokines and reactive oxygen species (ROS), while astrocytes undergo reactive astrogliosis, further impairing neuronal health. This maladaptive response from glial cells significantly accelerates disease pathology. Current AD treatments primarily aim at symptomatic relief, with limited success in disease modification. While amyloid-targeting therapies like Aducanumab and Lecanemab show some promise, their efficacy remains limited. In this context, natural compounds have gained attention for their potential to modulate neuroinflammation and promote neuroprotection. Among these, butyrate and lauric acid are particularly notable. Butyrate, produced by a healthy gut microbiome, acts as a histone deacetylase (HDAC) inhibitor, reducing pro-inflammatory cytokines and supporting neuronal health. Lauric acid, on the other hand, enhances mitochondrial function, reduces oxidative stress, and modulates inflammatory pathways, thereby supporting glial and neuronal health. Both compounds have been shown to decrease amyloid-β deposition, reduce neuroinflammation, and promote neuroprotection in AD models. This review explores the mechanisms through which butyrate and lauric acid modulate glial and neuronal activity, highlighting their potential as therapeutic agents for mitigating neuroinflammation and slowing AD progression.

Short-chain fatty acids (SCFAs) hold exert many nutritional benefits on both physiological and pathological processes, including host metabolism, immune modulation, and appetite control. Originating from the microbial fermentation of resistant starches and dietary fibre in the colon, SCFAs have the capability to traverse the blood–brain barrier (BBB). It is evident that SCFAs play a critical role in the development of neurodegenerative disorders such as Alzheimer's disease (AD). AD is the most common form of dementia and is characterised by the deposition of amyloid β peptides (Aβ) and tau hyperphosphorylation. SCFAs have demonstrated the potential to interfere with the protein–protein interactions required for Aβ peptides to form neurotoxic oligomers. Moreover, research indicates that the SCFAs ability to maintain endothelial integrity and interact with neuroglial cells through the BBB may assist in downregulating excessive neuroinflammatory responses to amyloid peptides. This review summarises the research on SCFAs' potential role in AD and understand their mechanism of actions on astrocytes and microglia.

Aims: Stevia rebaudiana which is commonly known as sweet leaf herb is used to extract non caloric sweet steviol glycosides. Thus based on available reports about its chemical composition, biosynthesis of steviol glycosides, application, cultivation, and phytochemical screening an attempt has been made to review to Stevia rebaudiana in context of its medicinal and pharmaceutical importance. Methodology: Literature search have been done in the web using google scholar, PubMed as search platform. More than two-thirds of the references are within 15 years. Results: According to the literature search S. rebaudiana leaves contain non caloric steviol glycosides and pharmaceutically important other phytochemicals. Miccropropagation is the best propagation method to overcome difficulties in conventional propagation methods. Conclusion: It is concluded that in vitro cultures has potential to extract important phytochemicals used in various pharmaceutical, food (flavoring agents, food additives) and perfume industries.

Background: Low blood pressure and associated postural symptoms are well-recognized manifestations of anaphylaxis. Nonetheless, anaphylaxis can present with high blood pressure and is rarely reported in the literature. We report an unusual presentation of anaphylaxis with severe supine hypertension and orthostatic intolerance. Case presentation: A 43-year-old Asian female presented to the emergency department with generalized itching, hives, and postural dizziness after taking a slow-release diclofenac sodium 100 mg tablet. On admission, the patient was tachycardic with a supine blood pressure of 200/100 mmHg. She had urticaria and bilateral rhonchi. A clinical diagnosis of anaphylaxis was made. She was treated with intravenous hydrocortisone and chlorpheniramine, but intramuscular adrenaline was withheld owing to her high blood pressure. She was kept in the supine position, and her vital parameters were closely monitored. Although the respiratory and cutaneous symptoms improved with treatment, her blood pressure remained elevated. Forty minutes later, the postural dizziness recurred as she sat up on the bed and her blood pressure plummeted from 198/100 mmHg to 80/60 mmHg. She was put back in the supine position immediately, and the blood pressure was restored with three doses of intramuscular adrenaline and a fluid bolus. Her postural symptoms completely resolved after adrenaline, but her blood pressure remained elevated. Two weeks after the initial presentation, a diagnosis of essential hypertension was made, which probably had been undetected. In anaphylaxis, where the cardiovascular system is involved, a blood pressure reduction from baseline is expected in patients with preexisting hypertension. Despite cardiovascular involvement, our patients’ blood pressure on presentation to the emergency department was much higher than her pretreatment ambulatory blood pressure, thus making this presentation unusual. Conclusions: Diagnosis and treatment of anaphylaxis can be delayed in patients presenting with high blood pressure. Postural symptoms should alert the clinician to cardiovascular involvement despite elevated supine blood pressure. Early treatment with adrenaline should be considered in these patients with extreme caution.

Background: Recently, there has been substantial interest in investigating the role of short‐chain fatty acids (SCFAs) and, medium chain fatty acids (MCFA) in the neuroinflammation associated with Alzheimer’s disease (AD). Specifically, butyrate (SCFA) and lauric acid (MCFA) have demonstrated potential in alleviating neuroinflammation and reducing toxicity associated with amyloid proteins. Additionally, they have been found to enhance mitochondrial function and reduce neuronal hyperactivity. However, the mechanisms by which butyrate and lauric acid either suppress or activate astrocytes and neurons, as well as how they influence Aβ‐mediated activation of astrocytes and neurons, remain unclear. This study aims to address this knowledge gap by investigating the independent and synergistic effects of butyrate and lauric acid on AD pathogenesis—a research endeavour not undertaken previously.Method: Butyrate and lauric acid were administered independently and synergistically to cultures of astrocytes, neurons derived from induced pluripotent stem cells (iPSCs) obtained from healthy human control subjects. Inflammatory responses of astrocytes and neurons were measured under synthetic amyloid beta stimulating conditions similar to AD. Legend Plex Human Inflammatory Panel was used to quantify the response of inflammatory cytokines (Interleukin IL‐1β, IL‐6, IL‐8, IL‐18, IL‐33, etc.) to inflammatory stimuli. The statistical analysis was carried out using the GraphPad Prism version 10.1.2. One‐way ANOVA was used to analyse the data.Result: Butyrate and lauric acid, independently and synergistically demonstrate a positive association with pro‐inflammatory cytokines. There were negative association with anti‐inflammatory cytokines in neuron, astrocytes and spontaneous co‐cultures of astrocytes and neurons.Conclusion: The findings indicate that both butyrate and lauric acid inhibit inflammation in Alzheimer’s‐induced astrocytes and neurons. Ongoing investigations aim to evaluate their effects on various cytokines and determine the responsible genes through qPCR analysis.

Background: In Alzheimer’s disease (AD), astrocytes undergo reactive changes that can exert both protective and detrimental effects on neurons, thereby influencing neuronal survival and contributing to disease progression. Increasing attention has been directed toward elucidating the mechanisms underlying astrocyte dysfunction and neuroinflammation to identify novel therapeutic targets. Butyrate—a short‐chain fatty acid produced by gut microbiota—has demonstrated anti‐inflammatory and neuroprotective properties. Similarly, lauric acid (LA), a medium‐chain fatty acid, has shown potential in attenuating amyloid‐beta (Aβ)‐induced neurotoxicity, enhancing mitochondrial function, and modulating neuronal excitability. Despite these findings, the mechanisms by which they modulate astrocyte and neuronal function remain poorly understood. This study investigates the effects of butyrate and LA on oxidative stress, mitochondrial dysfunction, and lipidomic alterations in human‐induced pluripotent stem cells (iPSCs)‐derived astrocytes, neurons, and spontaneous cultures. Method: Astrocytes, neurons, and spontaneous co‐cultures were differentiated from iPSCs derived from a healthy donor. Cultures were treated with synthetic Aβ (20 µM), sodium butyrate (NaB) (100 µM), or LA (100 µM), alone and in combination. Oxidative stress, mitochondrial dysfunction and the lipidomic changes of these cells was measured using Quantitative PCR, Catalase activity, Mitochondrial ToxGlo™ Assay and Liquid Chromatography‐Mass Spectrometry (LC‐MS) respectively. Result: Aβ exposure significantly suppressed catalase expression in astrocytes, indicating elevated oxidative stress. Treatment with NaB and LA exhibit partial restoration of catalase expression, with the most effects observed in mixed cultures, suggesting enhanced cellular resilience. Furthermore, expression of Mitofusin‐1, a key regulator of mitochondrial fusion, was downregulated following Aβ treatment. Functional assays revealed butyrate and LA enhance antioxidant enzyme activity and improved mitochondrial integrity over time, with astrocytes and mixed cultures showing the most pronounced protective effect. The lipid profiles indicate that Aβ induces greater lipid variation in neurons compared to astrocytes and spontaneous cultures. Conclusion: This study highlights the modulatory roles of butyrate and lauric acid on oxidative stress pathways, mitochondrial dynamics, and lipidomic profiles in iPSC‐derived brain cell cultures subjected to amyloid‐beta toxicity. These results support further exploration of butyrate and LA as therapeutic agents targeting neuroinflammation and metabolic dysregulation in AD.