CEA, CA 15-3, and miRNA expression as potential biomarkers in canine mammary tumors.

The most often detected tumor in intact bitches is mammary tumors and represents a significant clinical problem throughout the world. Mammary neoplasms in canine have heterogeneous morphology, so the choice of the most appropriate biomarker is the biggest challenge in CMT detection. We performed a retrospective analysis and evaluated the canine cancer antigens and miRNA expression profiles as potential biomarkers. Sixty dogs based on histological examination divided into three groups, viz., dogs with a benign mammary tumor, malignant mammary tumor, and control/healthy. The CA 15-3 was found more sensitive than CEA but detection of both will increase sensitivity. miR-21 expression differed significantly in all three groups. miR-29b expression differed significantly between the control and benign group and control and malignant group. The miR-21 overexpression and miR-29b downregulation with CMT are associated with clinical stage and can be used as non-invasive diagnostic and prognostic biomarkers. Hence, evaluation of CA 15-3 along with CEA would be a non-invasive technique for detecting canine mammary tumors. Evaluation of deregulated circulating miR-21 could be a valuable prognostic marker for early detection of mammary tumors in canines while miR-29b can add sensitivity in the detection of the canine mammary tumors if evaluated with miR-21.

Pattern of liver function test variations in COVID-19 infection & its clinical significance: A study from a dedicated COVID-19 tertiary care centre from India.

Background & objectives: Coronavirus disease 2019 (COVID-19) affects respiratory, gastrointestinal, cardiovascular and other systems disease. Studies describing liver involvement and liver function test (LFT) abnormalities are sparse from our population. This study was undertaken to estimate the LFT abnormalities in patients with COVID-19 in a tertiary care set up in India. Methods: In this retrospective study conducted at a tertiary care centre in Mumbai, India, all consecutive patients with proven COVID-19 by reverse transcriptase-PCR from March 23 to October 31, 2020 were enrolled. Of the 3280 case records profiled, 1474 cases were included in the study. Clinical characteristics, biochemical parameters and outcomes were recorded. Results: Overall 681 (46%) patient had deranged LFTs. Hepatocellular type of injury was most common (93%). Patients with deranged LFTs had more probability of developing severe disease (P<0.001) and mortality (P<0.001). Advanced age (P<0.001), male gender (P<0.001), diabetes mellitus (P<0.001), lower oxygen saturation levels at admission (P<0.001), higher neutrophil-lymphocyte ratio (P<0.001), history of diabetes mellitus and cirrhosiss were associated with deranged LFTs. Acute liver injury was seen in 65 (4.3%) cases on admission and 57 (3.5%) cases during hospital stay. On multivariate analysis for predicting mortality, age >60 yr serum creatinine >2 mg%, PaO2/FiO2 ratio ≤200 and raised AST >50 IU/l (OR: 2.34, CI: 1.59-3.48, P<0.001) were found to be significant. Interpretation & conclusions: In COVID-19, LFT abnormalities were common, and derangement increased as severity progressed. The presence of deranged LFT worsens the clinical outcome and predicts in-hospital mortality.

Vinpocetine restores cognitive and motor functions in Traumatic brain injury challenged rats.

Traumatic brain damage is common worldwide and the treatments are not well-defined. Vinpocetine is a synthetic derivative of the vinca alkaloid vincamine and is clinically being used for various brain disorders. Here in the current study, we have investigated the neuroprotective potential of vinpocetine against traumatic brain injury. TBI was induced by the Marmarou weight drop method in rats. Brain damage was evaluated using cognitive and motor functions and the alterations in biomolecules. Injured rats were treated with different doses of vinpocetine (2.5, 5, and 10 mg/kg) for 4 weeks. Traumatic brain injury in rats produced significant deterioration of cognition and motor functions, which was accompanied by increased oxidative stress and significant alterations in brain monoamine levels as compared with the sham control group (p < 0.05). Vinpocetine alleviated TBI-induced oxidative burden, altered neurochemistry, and improved the cognitive and motor functions as compared with that of the TBI control group (p < 0.05). The observed neuroprotective potential of vinpocetine may be due to the observed antioxidant potential and its ability to restore the levels of brain neurochemicals under stressed conditions. The outcomes of the current study may help the repositioning of vinpocetine for preventing or treating traumatic brain injuries.

Artificial Intelligence in Medicine.

Artificial intelligence as the name suggests is intelligence given to machines by man. AI learns and performs like humans without human instructions. We encounter AI in daily activities, like music and video suggestions in video applications, and personalize what we see on Facebook, Twitter, Instagram. AI makes our day-to-day life easier, efficient and it increases the speed and accuracy of our efforts. In this article, we reviewed previous articles and internet sites to understand the general principles of artificial intelligence. We included general articles and few articles related to medicine to understand the basics of AI and its application in the medical field. A literature search was done using the following search terms: 'AI' and 'AI in medicine'.

Orienting an Organic Semiconductor into DNA 3D Arrays by Covalent Bonds.

A quasi-one-dimensional organic semiconductor, hepta(p-phenylene vinylene) (HPV), was incorporated into a DNA tensegrity triangle motif using a covalent strategy. 3D arrays were self-assembled from an HPV-DNA pseudo-rhombohedron edge by rational design and characterized by X-ray diffraction. Templated by the DNA motif, HPV molecules exist as single-molecule fluorescence emitters at the concentration of 8 mM within the crystal lattice. The anisotropic fluorescence emission from HPV-DNA crystals indicates HPV molecules are well aligned in the macroscopic 3D DNA lattices. Sophisticated nanodevices and functional materials constructed from DNA can be developed from this strategy by addressing functional components with molecular accuracy.

Neurobiology of traumatic brain injury.

Traumatic brain injury (TBI) involves structural damage to the brain regions causing death or disability in patients with lifelong sufferings. Accidental injuries to the brain, besides structural damage, if any, cause activation of various deleterious pathways leading to subsequent neuronal death and permanent dysfunction. However, immediate medical management/treatments could reduce the chances of disability and suffering to the patients. The objective of the current review is to review triggered molecular pathways following TBI and discuss possible targets that could restore brain functions. Understanding the pathologic process is always useful to device novel treatment strategies and may rescue the patient with TBI from death or associated co-morbidities. The current review significantly contributes to improve our understanding about the molecular pathways and neuronal death following TBI and helps us to provide possible targets that could be useful in the management/treatment of TBI.

Pharmacological potential of tocopherol and doxycycline against traumatic brain injury-induced cognitive/motor impairment in rats.

Primary Objective The primary objective of this study was to explore the pharmacological potential of tocopherol and doxycycline against traumatic brain injury-induced cognitive/motor impairment in rats. Research Design Weight drop model of traumatic brain injury. Methods and Procedures After TBI, the animals were treated with doxycycline (50 and 100 mg/kg; p.o), tocopherol (5 and 10 mg/kg; p.o) alone and in combination as doxycycline and tocopherol (50 and 10 mg/kg; p.o) from 1st day to 28th day. The behavioral parameters were performed on a weekly basis from 1st day to 28th day. On 29th day, animals were sacrificed and striatum and cortex were homogenized for the estimation of biochemical (LPO, nitrite, and GSH), neuroinflammatory (IL-6, IL-1ß, and TNF-α), and neurotransmitters (dopamine, norepinephrine, serotonin, GABA, and glutamate) analysis. Main Outcomes and Results Induction of TBI had significantly reduced locomotor activity, recognition memory, increased neuroinflammatory markers, and imbalance neurotransmitter levels. The treatment with doxycycline and tocopherol alone and in combination significantly attenuated locomotor activity, memory recognition, reduced neuroinflammation, preserved oxidative balance, and restored the level of neurotransmitters. Conclusions The neuroprotective effect of doxycycline and tocopherol might be due to its anti-inflammatory and free radical scavenging mechanisms. Abbreviations TBI: Traumatic brain injury; Doxy: Doxycycline; Toco: Tocopherol; LPO: Lipid peroxidation; MDA: Malondialdehyde; TNF-α: Tumor necrosis factor-alpha; IL-1b: Interleukin-1 beta; GSH: Glutathione; GABA: gamma-Aminobutyric acid.

Immunotherapies and Combination Strategies for Immuno-Oncology.

The advent of novel immunotherapies in the treatment of cancers has dramatically changed the landscape of the oncology field. Recent developments in checkpoint inhibition therapies, tumor-infiltrating lymphocyte therapies, chimeric antigen receptor T cell therapies, and cancer vaccines have shown immense promise for significant advancements in cancer treatments. Immunotherapies act on distinct steps of immune response to augment the body's natural ability to recognize, target, and destroy cancerous cells. Combination treatments with immunotherapies and other modalities intend to activate immune response, decrease immunosuppression, and target signaling and resistance pathways to offer a more durable, long-lasting treatment compared to traditional therapies and immunotherapies as monotherapies for cancers. This review aims to briefly describe the rationale, mechanisms of action, and clinical efficacy of common immunotherapies and highlight promising combination strategies currently approved or under clinical development. Additionally, we will discuss the benefits and limitations of these immunotherapy approaches as monotherapies as well as in combination with other treatments.

The War against Tuberculosis: A Review of Natural Compounds and Their Derivatives.

Tuberculosis (TB), caused by the bacterial organism Mycobacterium tuberculosis, pose a major threat to public health, especially in middle and low-income countries. Worldwide in 2018, approximately 10 million new cases of TB were reported to the World Health Organization (WHO). There are a limited number of medications available to treat TB; additionally, multi-drug resistant TB and extensively-drug resistant TB strains are becoming more prevalent. As a result of various factors, such as increased costs of developing new medications and adverse side effects from current medications, researchers continue to evaluate natural compounds for additional treatment options. These substances have the potential to target bacterial cell structures and may contribute to successful treatment. For example, a study reported that green and black tea, which contains epigallocatechin gallate (a phenolic antioxidant), may decrease the risk of contracting TB in experimental subjects; cumin (a seed from the parsley plant) has been demonstrated to improve the bioavailability of rifampicin, an important anti-TB medication, and propolis (a natural substance produced by honeybees) has been shown to improve the binding affinity of anti-TB medications to bacterial cell structures. In this article, we review the opportunistic pathogen M. tuberculosis, various potential therapeutic targets, available therapies, and natural compounds that may have anti-TB properties. In conclusion, different natural compounds alone as well as in combination with already approved medication regimens should continue to be investigated as treatment options for TB.

Avelumab: A Novel Anti-PD-L1 Agent in the Treatment of Merkel Cell Carcinoma and Urothelial Cell Carcinoma.

Long-term treatment in the setting of metastatic Merkel cell carcinoma (MCC) and urothelial carcinoma (UC) has shown that current first-line chemotherapeutic agents are losing effectiveness and that there are limited treatment options available outside of radiation therapy and surgical interventions. The use of immunotherapeutic agents such as monoclonal antibodies has been considered a promising alternative for cancers that progress despite treatment with radiation therapy, surgery, and/or chemotherapeutic agents. Cancer cells escape immune surveillance by interrupting immune checkpoint pathways, resulting in dysregulation of T-cell function and so preventing its antitumor effects. In early 2017, avelumab (BAVENCIO®), a PD-L1-blocking monoclonal antibody agent, was approved for the treatment of metastatic MCC and UC. Trials that evaluated avelumab for the treatment of metastatic MCC and UC were the JAVELIN Merkel 200 Trial and the JAVELIN Solid Tumor trial, respectively. Efficacy results for both trials showed positive overall response rate (ORR) and progression-free survival rate (PFS). A strong safety profile was also established for avelumab. This review provides a brief introduction to checkpoint inhibitors and focuses on the recently approved PD-L1 inhibitor, avelumab.

Activation of microglia and astrocytes: a roadway to neuroinflammation and Alzheimer's disease.

Alzheimer's disease (AD) is a neurodegenerative disease that is of high importance to the neuroscience world, yet the complex pathogenicity is not fully understood. Inflammation is usually observed in AD and could implicate both beneficial or detrimental effects depending on the severity of the disease. During initial AD pathology, microglia and astrocyte activation is beneficial since they are involved in amyloid-beta clearance. However, with the progression of the disease, activated microglia elicit detrimental effects by the overexpression of pro-inflammatory cytokines such as interleukin (IL)-1ß, IL-6, and tumor necrosis factor-α (TNF-α) bringing forth neurodegeneration in the surrounding brain regions. This results in decline in Aß clearance by microglia; Aß accumulation thus increases in the brain resulting in neuroinflammation. Thus, Aß accumulation is the effect of increased release of pro-inflammatory molecules. Reactive astrocytes acquire gain of toxic function and exhibits neurotoxic effects with loss of neurotrophic functions. Astrocyte dysfunctioning results in increased release of cytokines and inflammatory mediators, neurodegeneration, decreased glutamate uptake, loss of neuronal synapses, and ultimately cognitive deficits in AD. We discuss the role of intracellular signaling pathways in the inflammatory responses produced by astrocytes and microglial activation, including the glycogen synthase kinase-3ß, nuclear factor kappa B cascade, mitogen-activated protein kinase pathways and c-Jun N-terminal kinase. In this review, we describe the role of neuroinflammation in the chronicity of AD pathogenesis and an overview of the recent research towards the development of new therapies to treat this disorder.

Development and characterization of morin hydrate-loaded micellar nanocarriers for the effective management of Alzheimer's disease.

The aim of this study was to prepare and characterise oral delivery of morin hydrate-loaded micellar nanocarriers using Pluronic P127 and Pluronic F123 for the effective management of Alzheimer's disease. After administration of formulation brain and blood drug concentration were found to be highest for optimised morin hydrate-loaded micellar nanocarriers as compared to plain morin hydrate. Significant (p < 0.05) reduction in assessed pharmacodynamic parameters was observed after administration of morin hydrate-loaded micellar nanocarriers as compared to disease control group. Chronic treatment with morin-loaded micelles significantly increased the memory in AlCl3 induced Alzheimer's disease in Wistar rats.

P-Glycoprotein Inhibition Sensitizes Human Breast Cancer Cells to Proteasome Inhibitors.

Although effective for the treatment of hematological malignancies, the FDA approved proteasome inhibitors bortezomib and carfilzomib have limited efficacy in solid tumors including triple negative breast cancer (TNBC). Chemotherapy is the only option for treating TNBC due to the absence of specific therapeutic targets. Therefore, development of new TNBC therapeutic strategies has been warranted. We studied whether P-glycoprotein (P-gp) inhibition could sensitize TNBC cells to proteasome inhibitors. When verapamil, a P-gp inhibitor, was combined with the proteasome inhibitor MG132, bortezomib, or carfilzomib, the cytotoxic effects and apoptosis in TNBC MDA-MB-231 cells were enhanced, compared to each treatment alone. Furthermore, addition of verapamil improved proteasome-inhibitory properties of MG132, bortezomib, or carfilzomib in MDA-MB-231 cells, as shown by the increased accumulation of ubiquitinated proteins and proteasome substrates such as IκBα and p27kip1 . Additionally, when nicardipine, another P-gp inhibitor, was combined with bortezomib or carfilzomib, enhanced inhibition of MDA-MB-231 cell proliferation was observed. These findings indicate that P-gp inhibitors could sensitize TNBC cells to structurally and functionally diverse proteasome inhibitors and might provide new treatment strategy for TNBC. J. Cell. Biochem. 118: 1239-1248, 2017. © 2016 Wiley Periodicals, Inc.

Mouse oocytes nucleoli rescue embryonic development of porcine enucleolated oocytes.

It is well known that nucleoli of fully grown mammalian oocytes are indispensable for embryonic development. Therefore, the embryos originated from previously enucleolated (ENL) oocytes undergo only one or two cleavages and then their development ceases. In our study the interspecies (mouse/pig) nucleolus transferred embryos (NuTE) were produced and their embryonic development was analyzed by autoradiography, transmission electron microscopy (TEM) and immunofluorescence (C23 and upstream binding factor (UBF)). Our results show that the re-injection of isolated oocyte nucleoli, either from the pig (P + P) or mouse (P + M), into previously enucleolated and subsequently matured porcine oocytes rescues their development after parthenogenetic activation and some of these develop up to the blastocyst stage (P + P, 11.8%; P + M, 13.5%). In nucleolus re-injected 8-cell and blastocyst stage embryos the number of nucleoli labeled with C23 in P + P and P + M groups was lower than in control (non-manipulated) group. UBF was localized in small foci within the nucleoli of blastocysts in control and P + P embryos, however, in P + M embryos the labeling was evenly distributed in the nucleoplasm. The TEM and autoradiographic evaluations showed the formation of functional nucleoli and de novo rRNA synthesis at the 8-cell stage in both, control and P + P group. In the P + M group the formation of comparable nucleoli was delayed. In conclusion, our results indicate that the mouse nucleolus can rescue embryonic development of enucleolated porcine oocytes, but the localization of selected nucleolar proteins, the timing of transcription activation and the formation of the functional nucleoli in NuTE compared with control group show evident aberrations.

Animal models of hepatotoxicity.

INTRODUCTION: Liver is the largest and important organ in the body, involved in the metabolism of food and drugs. Liver diseases are potentially life threatening for humans. The etiology of liver disorder varied due to different reasons like autoimmune disorder, viral infection, toxic chemical, and due to changing diet style. Liver injury produces pathological changes like increase level of SGOT, SGPT, TB and generation of free radical radicals. METHODS: A better understanding of primary mechanisms is mandatory for designing of new therapeutic drugs. Therefore, animal models are being developed to mimic human liver diseases. Animal models are being used for several decades to study the pathogenesis of liver disorders and related toxicities. CONCLUSION: In this review, we revealed various animal models with their merits and demerits. Our main focus is to explore all new and traditional animal models under broad classification like non-invasive, invasive and genetic models which directly or indirectly produce hepatotoxicity.

Proteasome inhibitors induce AMPK activation via CaMKKß in human breast cancer cells.

The purpose of present study is to examine the mechanism of the 5'-AMP-activated protein kinase (AMPK) activation induced by proteasome inhibitors. AMPK activation and ubiquitin proteasome system (UPS) inhibition have gained great attention as therapeutic strategies for the treatment of certain types of cancers. While AMPK serves as a master regulator of cellular metabolism, UPS regulates protein homeostasis. However, the relationship between these two important pathways is not very clear. We observe that proteasome inhibition leads to AMPK activation in human breast cancer cells. siRNA transfection, western blotting, qPCR, and proteasomal inhibition assays were used to study the mechanism of proteasome inhibitor-induced AMPK activation using human triple-negative breast cancer, lung, and cervical cancer cell lines. We report that a variety of proteasome inhibitors activate AMPK in all the tested different cancer cell lines. Our data using liver kinase B1-deficient cancer cells suggest that proteasome inhibitor-induced AMPK activation is primarily mediated by Calcium/Calmodulin-dependent kinase kinase ß (CaMKKß). This hypothesis is supported by that pharmacological or genetic inhibition of CaMKKß leads to a decrease in proteasome inhibitor-induced AMPK activation. Additionally, the AMPK-activating function of the FDA-approved proteasome inhibitor bortezomib depends on an increase in intracellular calcium levels as calcium chelation abrogates its induced AMPK activation. Finally, bortezomib-mediated upregulation in CaMKKß levels is due to its enhanced protein synthesis. These data suggest that proteasome inhibitors indirectly activate AMPK in human cancer cells primarily via Ca(2+)-CaMKKß-dependent pathway.

L-Ornithine Schiff base-copper and -cadmium complexes as new proteasome inhibitors and apoptosis inducers in human cancer cells.

Ubiquitin-proteasome system (UPS) plays a crucial role in many cellular processes such as cell cycle, proliferation and apoptosis. Aberrant activation of UPS may result in cellular transformation or other altered pathological conditions. Previous studies have shown that metal-based complexes could inhibit proteasome activity and induce apoptosis in certain human cancer cells. In the current study, we report that the cadmium and copper complexes with heterocycle-ornithine Schiff base are potent inhibitors of proteasomal chymotrypsin-like (CT-like) activity, leading to induction of apoptosis in cancer cells. Two novel copper-containing complexes and two novel cadmium-containing complexes with different heterocycle-ornithine Schiff base structures as ligands were synthesized and characterized. We found that complexes Cu1, Cd1 and Cd2 show proteasome-inhibitory activities in human breast cancer MDA-MB-231 and human prostate cancer LNCaP cells, resulting in the accumulation of p27, a natural proteasome substrate and other ubiquitinated proteins, followed by the induction of apoptosis. Our results suggest that metal complexes with heterocycle-ornithine Schiff base have proteasome-inhibitory capabilities and have the potential to be developed into novel anticancer drugs.

Effect of GLT-1 modulator and P2X7 antagonists alone and in combination in the kindling model of epilepsy in rats.

INTRODUCTION: Multiple lines of investigation have explored the role of glutamatergic and purinergic systems in epilepsy, related cognitive impairment, and oxidative stress. Glutamate transporters, particularly GLT-1 expression, were found to be decreased, and purinergic receptor, P2X7 expression, was found to be increased in brain tissue associated with epilepsy. The present study was carried out to investigate the effect of ceftriaxone (GLT-1 upregulator) and Brilliant Blue G (P2X7 antagonist) against PTZ-induced kindling in rats. The study was further extended to elucidate the cross-link between glutamatergic and purinergic pathways in epilepsy. MATERIAL AND METHODS: Systemic administration of subconvulsant dose of PTZ (30 mg/kg) every other day for 27days (14 injections) significantly increased the mean kindling, and developed generalized tonic-clonic seizures, and reduced motor co-ordination, cognitive skills, oxidative defense (increases lipid peroxidation, nitrite levels and decreases GSH level) and acetylcholinesterase enzyme activities in the cortex and subcortical region. Treatments with CEF (100 and 200mg/kg) and BBG (15 and 30 mg/kg) alone and in combination (CEF 100mg/kg and BBG 15 mg/kg) significantly decreased the mean kindling score and restored behavioral and oxidative defense activities compared with treatment with PTZ. CONCLUSIONS: The combination of both the drugs was shown to have better effect in preventing kindled seizures and a significantly synergistic effect compared with their effect alone in PTZ-kindled rats. The present study elucidated the mechanistic role of GLT-1 modulator and selective P2X7 antagonist and their combination against PTZ-induced kindling. The study for the first time demonstrated the cross-link between glutamatergic and purinergic pathways in epilepsy treatment.

Impact of alogliptin on lipopolysaccharide-induced experimental Parkinson's disease: Unrevealing neurochemical and histopathological alterations in rodents.

BACKGROUND: Degeneration of the nigrostriatal dopaminergic pathway has been seen as a significant cause of movement disability in Parkinson's disease (PD) patients. However, the exact reason for these degenerative changes has remained obscure. In recent years, incretins have been neuroprotective in various pathologies. In the current study, we have investigated the neuroprotective potential of alogliptin (Alo), a dipeptidyl peptidase-IV (DPP-IV) inhibitor, in a lipopolysaccharide (LPS) induced experimental model of PD. EXPERIMENTAL APPROACH: LPS (5µg/5 µl) was infused intranigrally to induce PD in experimental rats. Post-LPS infusion, these animals were treated with Alo for 21 days in three successive dosages of 10, 20, and 40 mg/kg/day/per oral. The study is well supported with the determinations of motor functions biochemical, neurochemical, and histological analysis. KEY RESULTS: Intranigral infusion of LPS in rats produced motor deficit. It was accompanied by oxidative stress, elevation in neuroinflammatory cytokines, altered neurochemistry, and degenerative changes in the striatal brain region. While Alo abrogated LPS-induced biochemical/neurochemical alterations, improved motor functions, and preserved neuronal morphology in LPS-infused rats. CONCLUSION: The observed neuroprotective potential of Alo may be due to its antioxidant and anti-inflammatory actions and its ability to modulate monoaminergic signals. Nonetheless, current findings suggest that improving the availability of incretins through DPP-IV inhibition is a promising strategy for treating Parkinson's disease.

Embelin Mitigates Amyloid-ß-Induced Neurotoxicity and Cognitive Impairment in Rats: Potential Therapeutic Implications for Alzheimer's Disease.

Alzheimer's disease (AD) is a significant form of dementia. Embelin (EMB) is a natural compound with varied actions that could help prevent AD pathology. Herein, we have investigated the neuroprotective potential of EMB against Aß1-42-induced neurotoxicity in rats. In this experiment, Alzheimer-like dementia was induced in rats by infusing Aß1-42 oligomers directly into the brain's ventricles. Subsequently, the Aß1-42-intoxicated rats received treatment with varying doses of EMB (2.5, 5, and 10 mg/kg, administered intraperitoneally) over 2 weeks. The spatial and non-spatial memory of animals was assessed at different time intervals, and various biochemical, neurochemical, and neuroinflammatory parameters in the hippocampal brain tissue of the rats were analyzed. Infusion of Aß1-42 in rat brain caused cognitive impairment and was accompanied by increased acetylcholinesterase activity, oxidative stress, and elevated levels of pro-inflammatory cytokines (such as TNF-α, IL-1ß, and IL-6) in the hippocampal tissue. Moreover, a significant decline in the levels of monoamines and an imbalance of GABA and glutamate levels were also observed. EMB treatment significantly mitigated Aß1-42-induced cognitive deficit and other biochemical changes, including Aß levels. The EMB-treated rats showed improved learning and consolidation of memory. EMB also attenuated Aß-induced oxidative stress and neuroinflammation and restored the levels of monoamines and the balance between GABA and glutamate. The observed cognitive benefits following EMB treatment in Aß1-42-infused rats may be attributed to its antioxidant and anti-inflammatory properties and ability to restore hippocampal neurochemistry and Aß levels. The above findings indicate the therapeutic potential of EMB in neurodegenerative pathologies associated with cognitive decline, such as Alzheimer's disease.