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Despite extensive preclinical research over the years, a significant gap remains in our understanding of the specific effects of methamphetamine (METH) and amphetamine (AMPH) withdrawal. Understanding these differences could be pivotal to unveiling the unique pathophysiology underlying each stimulant. This may facilitate the development of targeted and effective treatment strategies tailored to the specific characteristics of each substance. Following PRISMA guidelines, this systematic review was conducted to examine alterations in spontaneous locomotor activity, specifically horizontal activity, in animals experiencing withdrawal from extended and repeated administration of AMPH or METH. Original articles were retrieved from four electronic databases, supplemented by a review of the references cited in the published papers. A total of thirty-one full-length articles (n = 31) were incorporated in the analysis. The results indicated that six studies documented a significant increase in horizontal activity among animals, seven studies reported decreased locomotion, and eighteen studies (8 AMPH; 10 METH) reported no significant alterations in the animals' locomotor activity. Studies reporting heightened locomotion mainly employed mice undergoing withdrawal from METH, studies reporting diminished locomotion predominantly involved rats undergoing withdrawal from AMPH, and studies reporting no significant changes in horizontal activity employed both rats and mice (12 rats; 6 mice). Drug characteristics, routes of administration, animal models, dosage regimens, duration, and assessment timing seem to influence the observed outcomes. Despite more than 50% of papers enlisted in this review indicate no significant changes in the locomotion during the stimulant withdrawal, the unique reactions of animals to withdrawal from METH and AMPH reported by some underscore the need for a more nuanced understanding of stimulant withdrawal.
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Alzheimer's disease (AD) poses a major worldwide health challenge because of its profound impact on cognitive abilities and overall well-being. Despite extensive research and numerous clinical trials, therapeutic options remain limited. Our study aimed to investigate the potential of Kelulut honey (KH) as a novel therapeutic agent for addressing the multifactorial pathology of AD. We tried to evaluate the disease-attenuating and neuroprotective potential of KH in the intrahippocampally induced AD rat model by utilizing histochemistry and enzyme-linked immunosorbent assay (ELISA) studies. A total of 26 male Sprague Dawley rats weighing ~280-380 g were randomly divided into three groups: Control, AD-induced (Aß), and AD-induced and treated with KH (Aß+KH). The latter two groups underwent stereotaxic surgery, where 6.25 µg of amyloid ß1-42 peptides were injected intrahippocampally. One-week post-surgery, KH was administered to the treatment group at a dose of 1 g/kg body weight for a period of four weeks, after which the rats went through behavior tests. After completion of behavior analysis, the rats were sacrificed, and the brains were processed for histochemistry and ELISA studies. The open field test analysis demonstrated that KH improved the locomotion of Aß+KH compared to Aß (p = 0.0013). In comparison, the Morris water maze did not show any nootropic effects on cognition with a paradoxical increase in time spent in the target quadrant by the Aß group (p = 0.029). Histochemical staining showed markedly increased Congo-red-stained amyloid plaques, which were significantly reduced in dentate gyrus of Aß+KH compared to Aß (p < 0.05). Moreover, significantly higher apoptosis was seen in the Aß group compared to Aß+KH (p < 0.01) and control groups (p < 0.001). Furthermore, the ELISA studies deduced more phosphorylated tau in the diseased group compared to Aß+KH (p = 0.038) and controls (p = 0.016). These findings suggest that KH consumption for twenty-eight days has the potential to attenuate the pathological burden of disease while exerting neuroprotective effects in rodent models of AD.
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Advanced atherosclerosis is linked to plaque instability, which can result in rupture and the onset of a heart attack. Evidence gathered from human atheroma plaques indicates that intraplaque neovascularization poses a risk to plaque stability and may lead to plaque hemorrhage. Hence, targeting the neovascularization within the atheroma plaque has the potential to mitigate the plaque's vulnerability. While neovascularization has been extensively explored in the context of cancer, research on pharmacological inhibition of this phenomenon in atherosclerosis remains limited. This systematic review aimed to comprehensively assess current and emerging pharmacological interventions for inhibiting intraplaque neovascularization in preclinical settings. Electronic databases (Web of Science, PubMed, Scopus, and Ovid) were searched from January 2013 until February 1, 2024. Preclinical studies reporting the effect of any pharmacological interventions targeting intraplaque neovascularization were included. A total of 10 articles involving in vivo animal studies were eligible for inclusion, with five of them incorporating in vitro experiments to complement their in vivo findings. The pharmacological interventions studied were axitinib, ghrelin, K5, rosuvastatin, atorvastatin, 3PO, everolimus, melatonin, Si-Miao-Yong-A, and protocatechuic aldehyde. All the interventions showed a positive impact in inhibiting intraplaque neovascularization in various atherosclerotic animal models through various signaling pathways. This review provides valuable insights into pharmacological approaches to attenuate intraplaque neovascularization that could serve as a promising therapeutic avenue to enhance plaque stability.
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Atherosclerosis , Neovascularization, Pathologic , Plaque, Atherosclerotic , Animals , Plaque, Atherosclerotic/drug therapy , Humans , Atherosclerosis/drug therapy , Neovascularization, Pathologic/drug therapy , Angiogenesis Inhibitors/pharmacology , Angiogenesis Inhibitors/therapeutic useABSTRACT
INTRODUCTION: Smoking among medical, dental, and pharmacy students is an issue in every university worldwide, which will impact future smoking cessation services as they are future healthcare providers. This study investigates the smoking prevalence, exposure to secondhand smoke, and factors associated with smoking among medical, dental, and pharmacy students at a public university in Malaysia. METHODS: The self-administered online survey utilized in this cross-sectional study was derived from the Global Health Professions Students Survey (GHPSS), which involved medical, dental, and pharmacy students. A total of 328 participants completed a questionnaire from June to August 2022, with a response rate of 91.1%. RESULTS: The overall smoking prevalence was 4.6% among the medical, dental, and pharmacy students who participated in this study; 46.7% of current smokers were exposed to secondhand smoke at home compared to 17.6% of non-smokers (p=0.011); and 66.7% of smokers were exposed to secondhand smoke in public compared to 40.3% of non-smokers (p=0.043). In all, 99.1% of respondents supported the smoking ban and 46.7% of current smokers supported the smoking ban in discos/bars/pubs, compared to 82.0% of non-smokers (p=0.002). Of the participants, 96.6% received lessons on the danger of tobacco, and 65.5% received smoking cessation training. Among factors associated with current smoking was gender; male students had a 19-fold higher likelihood of smoking than female students (adjusted odds ratio, AOR=19.25; 95% CI: 4.25-87.19, p<0.001). In addition, home exposure to secondhand smoke was four times more common for current smokers (OR=4.11; 95% CI: 1.43-11.79, p=0.009). CONCLUSIONS: Although smoking prevalence was low among the students in this study, there was a higher percentage of them exposed to secondhand smoke at home and in public.
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Traumatic brain injury (TBI) is a major global health issue that affects millions of people every year. It is caused by any form of external force, resulting in temporary or permanent impairments in the brain. The pathophysiological process following TBI usually involves excitotoxicity, mitochondrial dysfunction, oxidative stress, inflammation, ischemia, and apoptotic cell death. It is challenging to find treatment for TBI due to its heterogeneous nature, and no therapeutic interventions have been approved thus far. Neurotrophins may represent an alternative approach for TBI treatment because they influence various functional activities in the brain. The present review highlights recent studies on neurotrophins shown to possess neuroprotective roles in TBI. Neurotrophins, specifically brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) have demonstrated reduced neuronal death, alleviated neuroinflammatory responses and improved neurological functions following TBI via their immunomodulatory, anti-inflammatory and antioxidant properties. Further studies are required to ensure the efficacy and safety of neurotrophins to be used as TBI treatment in clinical settings.
Subject(s)
Brain Injuries, Traumatic , Nerve Growth Factors , Neuroprotective Agents , Brain Injuries, Traumatic/metabolism , Brain Injuries, Traumatic/drug therapy , Humans , Nerve Growth Factors/therapeutic use , Nerve Growth Factors/metabolism , Neuroprotective Agents/therapeutic use , Neuroprotective Agents/pharmacology , Animals , Brain-Derived Neurotrophic Factor/metabolism , Nerve Growth Factor/metabolism , Oxidative Stress/drug effects , Oxidative Stress/physiology , Brain/metabolism , Brain/drug effectsABSTRACT
Introduction: Neurotrophin-3 (NT3) is a neuroprotective growth factor that induces the development, maintenance and survival of neurons. This study aims to localize NT3-expressing cells in the adult zebrafish brain and examine the role of NT3 in a zebrafish Parkinson's disease (PD) model. Methods: Cellular localization of NT3 in adult zebrafish brains was conducted using in situ hybridization. Subsequently, adult zebrafish were injected intraperitoneally with 100 µg/g of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and treated with 400 ng/g body weight of recombinant NT3 (rNT3) via intracranial injection 24 h following MPTP injection. The fish were assessed for neurobehavioral, gene expression, immunohistology, and protein analysis on days 3, 5 and 10 post-MPTP injection. Results: Our findings showed that NT3 was extensively expressed throughout the adult zebrafish brain in neurons. Administration of rNT3 has significantly improved locomotor activity, with upregulation of th1, dat, ntf3 and bdnf gene expressions compared to MPTP-induced zebrafish. Dopaminergic neurons were also significantly increased in the zebrafish brain following rNT3 treatment. ELISA analysis reported raised GST and decreased caspase-3 levels on day 3 of assessment. The trophic changes of rNT3, however, decline as the assessment day progresses. Conclusion: This study is the first to examine the role of NT3 in the adult zebrafish PD model. NT3 has remarkable trophic effects in the zebrafish PD model. However, further study is needed to examine the dosage requirements and long-term effects of NT3 in PD.
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Plukenetia volubilis Linneo or Sacha Inchi (SI), a traditional natural remedy indigenous to Peru and Brazil, has garnered global attention due to its exceptional nutritional composition. Its protective effects against various non-communicable diseases, notably cardiovascular disease (CVD), have become a subject of interest in recent research. This comprehensive review summarizes the existing evidence from 15 relevant articles concerning the impact of SI on common CVD risk factors, including dyslipidemia, obesity, diabetes, and hypertension. The relevant articles were derived from comprehensive searches on PubMed, Scopus, Google Scholar, and Web of Science using predefined criteria and keywords related to the topic. Overall, SI demonstrated positive effects in attenuating dyslipidemia, obesity, diabetes, and hypertension. The multifaceted mechanisms responsible for the protective effects of SI against these CVD risk factors are primarily attributed to its antioxidative and anti-inflammatory properties. While preclinical studies dominate the current scientific literature on SI, there are limited clinical trials to corroborate these findings. Therefore, future well-designed, large-scale randomized clinical trials are highly recommended to establish the efficacy of SI and determine its optimal dosage, potential drug and food interactions, and practical integration into preventive strategies and dietary interventions for the high-risk populations.
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Alzheimer's disease (AD) is characterized by the pathologic deposition of amyloid and neurofibrillary tangles in the brain, leading to neuronal damage and defective synapses. These changes manifest as abnormalities in cognition and behavior. The functional deficits are also attributed to abnormalities in multiple neurotransmitter systems contributing to neuronal dysfunction. One such important system is the dopaminergic system. It plays a crucial role in modulating movement, cognition, and behavior while connecting various brain areas and influencing other neurotransmitter systems, making it relevant in neurodegenerative disorders like AD and Parkinson's disease (PD). Considering its significance, the dopaminergic system has emerged as a promising target for alleviating movement and cognitive deficits in PD and AD, respectively. Extensive research has been conducted on dopaminergic neurons, receptors, and dopamine levels as critical factors in cognition and memory in AD. However, the exact nature of movement abnormalities and other features of extrapyramidal symptoms are not fully understood yet in AD. Recently, a previously overlooked element of the dopaminergic system, the dopamine transporter, has shown significant promise as a more effective target for enhancing cognition while addressing dopaminergic system dysfunction in AD.
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Introduction: Parkinson's disease (PD) is the second most common neurodegenerative disease that severely affects the quality of life of patients and their family members. Exposure to 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been shown to reflect behavioral, molecular, and proteomic features of PD. This study aimed to assess the protocol for inducing PD following MPTP injection in adult zebrafish. Methods: Fish were injected with 100 µg/g of MPTP intraperitoneally once or twice and then assessed on days 1 to 30 post-injection. Results: Between one-time and two-time injections, there was no significant difference in most locomotor parameters, expressions of tyrosine hydroxylase-2 (th2) and dopamine transporter (dat) genes, and dopaminergic neurons (tyrosine hydroxylase positive, TH+ cells) counts. However, caspase-3 levels significantly differed between one- and two-time injections on the day 1 assessment. Discussion: Over a 30-day period, the parameters showed significant differences in swimming speed, total distance traveled, tyrosine hydroxylase-1 (th1) and dat gene expressions, caspase-3 and glutathione protein levels, and TH+ cell counts. Days 3 and 5 showed the most changes compared to the control. In conclusion, a one-time injection of MPTP with delayed assessment on days 3 to 5 is a good PD model for animal studies.
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BACKGROUND: Sepsis, a life-threatening infection-induced inflammatory condition, has significant global health impacts. Timely detection is crucial for improving patient outcomes as sepsis can rapidly progress to severe forms. The application of machine learning (ML) and deep learning (DL) to predict sepsis using electronic health records (EHRs) has gained considerable attention for timely intervention. METHODS: PubMed, IEEE Xplore, Google Scholar, and Scopus were searched for relevant studies. All studies that used ML/DL to detect or early-predict the onset of sepsis in the adult population using EHRs were considered. Data were extracted and analyzed from all studies that met the criteria and were also evaluated for their quality. RESULTS: This systematic review examined 1942 articles, selecting 42 studies while adhering to strict criteria. The chosen studies were predominantly retrospective (n = 38) and spanned diverse geographic settings, with a focus on the United States. Different datasets, sepsis definitions, and prevalence rates were employed, necessitating data augmentation. Heterogeneous parameter utilization, diverse model distribution, and varying quality assessments were observed. Longitudinal data enabled early sepsis prediction, and quality criteria fulfillment varied, with inconsistent funding-article quality correlation. CONCLUSIONS: This systematic review underscores the significance of ML/DL methods for sepsis detection and early prediction through EHR data.
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Obesity is known as a transgenerational vicious cycle and has become a global burden due to its unavoidable complications. Modern approaches to obesity management often involve the use of pharmaceutical drugs and surgeries that have been associated with negative side effects. In contrast, natural antioxidants, such as flavonoids, have emerged as a promising alternative due to their potential health benefits and minimal side effects. Thus, this narrative review explores the potential protective role of flavonoids as a natural antioxidant in managing obesity. To identify recent in vivo studies on the efficiency of flavonoids in managing obesity, a comprehensive search was conducted on Wiley Online Library, Scopus, Nature, and ScienceDirect. The search was limited to the past 10 years; from the search, we identified 31 articles to be further reviewed. Based on the reviewed articles, we concluded that flavonoids offer novel therapeutic strategies for preventing obesity and its associated co-morbidities. This is because the appropriate dosage of flavonoid compounds is able to reduce adipose tissue mass, the formation of intracellular free radicals, enhance endogenous antioxidant defences, modulate the redox balance, and reduce inflammatory signalling pathways. Thus, this review provides an insight into the domain of a natural product therapeutic approach for managing obesity and recapitulates the transgenerational inheritance of obesity, the current available treatments to manage obesity and its side effects, flavonoids and their sources, the molecular mechanism involved, the modulation of gut microbiota in obesity, redox balance, and the bioavailability of flavonoids. In toto, although flavonoids show promising positive outcome in managing obesity, a more comprehensive understanding of the molecular mechanisms responsible for the advantageous impacts of flavonoids-achieved through translation to clinical trials-would provide a novel approach to inculcating flavonoids in managing obesity in the future as this review is limited to animal studies.
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Introduction: Stress and infertility form a complex relationship. In line with this, various stress-related biological markers have been investigated in infertility. Methods: This systematic review was performed using PRISMA guidelines (i) to report whether cortisol is highly present in infertile patients compared to fertile control; (ii) to report whether there is any significant difference in the cortisol level in infertile subjects that conceive and those that didn't at the end of assisted reproduction treatments. Original articles involving human (male and female) as subjects were extracted from four electronic databases, including the list of references from the published papers. Sixteen original full-length articles involving male (4), female (11), and both genders (1) were included. Results: Findings from studies that compared the cortisol level between infertile and fertile subjects indicate that (i) Male: three studies reported elevated cortisol level in infertile patients and one found no significant difference; (ii) Female: four studies reported increased cortisol level in infertile subjects and three studies found no significant difference. Findings from studies that measured the cortisol level from infertile patients that conceived and those that didn't indicate that (i) Male: one study reported no significant difference; (ii) Female: one study reported elevated cortisol in infertile patients that conceived, whereas two studies reported increased cortisol in infertile patients that was unable to conceive. Five studies found no significant difference between the groups. Discussion: In the present review we only included the cortisol value that was measured prior to stimulation or IVF treatment or during natural or spontaneous cycles, despite this, there are still variations in the sampling period, assessment techniques and patients' characteristics. Hence, at present, we are still unable to conclude that cortisol is significantly elevated in infertile patients. We warrant future studies to standardize the time of biological sample collection and other limitations that were addressed in the review to negate the unwanted influencing factors.
Subject(s)
Hydrocortisone , Infertility , Humans , Female , Male , Fertilization , FertilityABSTRACT
High-mobility group box 1 (HMGB1) has been implicated as a key player in two critical factors of Parkinson's disease (PD): mitochondrial dysfunction and neuroinflammation. However, the specific role of HMGB1 in PD remains elusive. We investigated the effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration on mitochondrial dysfunction and HMGB1-associated inflammatory genes as well as locomotor activity in zebrafish, aiming to elucidate the role of HMGB1 in PD. Adult zebrafish received MPTP injections, and locomotor activity was measured at 24- and 48-h post-administration. Gene expression levels related to mitophagy (fis1, pink1, and park2) and HMGB1-mediated inflammation (hmgb1, tlr4, and nfkb) were quantified through RT-qPCR analysis. Following MPTP injection, the significant increase in transcript levels of fis1, pink1, and park2 indicated notable changes in PINK1/Parkin mitophagy, while the upregulation of hmgb1, tlr4, and nfkb genes pointed to the activation of the HMGB1/TLR4/NFκB inflammatory pathway. Furthermore, MPTP-injected zebrafish exhibited decreased locomotor activity, evident through reduced distance travelled, mean speed, and increased freezing durations. HMGB1 plays a major role in cellular processes as it is involved in both the mitophagy process and functions as a pro-inflammatory protein. MPTP administration in adult zebrafish activated mitophagy and inflammatory signaling, highlighting the significant role of HMGB1 as a mediator in both processes and further emphasizing its significant contribution to PD pathogenesis.
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Multiple alcohol use disorder (AUD)-related behavioral alterations are governed by protein kinase C epsilon (PKCε), particularly in the amygdala. Protein kinase C (PKC) is readily phosphorylated at Ser729 before activation by the mTORC2 protein complex. In keeping with this, the current study was conducted to assess the variations in mTORC2 and PKCε during different ethanol exposure stages. The following groups of rats were employed: control, acute, chronic, ethanol withdrawal (EW), and EW + ethanol (EtOH). Ethanol-containing and non-ethanol-containing modified liquid diets (MLDs) were administered for 27 days. On day 28, either saline or ethanol (2.5 g/kg, 20% v/v) was intraperitoneally administered, followed by bilateral amygdala extraction. PKCε mRNA levels were noticeably increased in the amygdala of the EW + EtOH and EW groups. Following chronic ethanol consumption, the stress-activated map kinase-interacting protein 1 (Sin1) gene expression was markedly decreased. In the EW, EW + EtOH, and chronic ethanol groups, there was a profound increase in the protein expression of mTOR, Sin1, PKCε, and phosphorylated PKCε (Ser729). The PKCε gene and protein expressions showed a statistically significant moderate association, according to a correlation analysis. Our results suggest that an elevated PKCε protein expression in the amygdala during EW and EW + EtOH occurred at the transcriptional level. However, an elevation in the PKCε protein expression, but not its mRNA, after chronic ethanol intake warrants further investigation to fully understand the signaling pathways during different episodes of AUD.
Subject(s)
Alcoholism , Substance Withdrawal Syndrome , Rats , Animals , Alcoholism/metabolism , Protein Kinase C-epsilon/genetics , Protein Kinase C-epsilon/metabolism , Rodentia , Mechanistic Target of Rapamycin Complex 2/metabolism , Ethanol , Amygdala , Substance Withdrawal Syndrome/metabolism , RNA, Messenger/metabolismABSTRACT
Glia, which was formerly considered to exist just to connect neurons, now plays a key function in a wide range of physiological events, including formation of memory, learning, neuroplasticity, synaptic plasticity, energy consumption, and homeostasis of ions. Glial cells regulate the brain's immune responses and confers nutritional and structural aid to neurons, making them an important player in a broad range of neurological disorders. Alzheimer's, ALS, Parkinson's, frontotemporal dementia (FTD), and epilepsy are a few of the neurodegenerative diseases that have been linked to microglia and astroglia cells, in particular. Synapse growth is aided by glial cell activity, and this activity has an effect on neuronal signalling. Each glial malfunction in diverse neurodegenerative diseases is distinct, and we will discuss its significance in the progression of the illness, as well as its potential for future treatment.
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Hyperglycemia is the hallmark of diabetes mellitus that results in oxidative stress, apoptosis, and diabetic vascular endothelial dysfunction. An increasing number of microRNAs (miRNAs) have been found to be involved in the pathogenesis of diabetic vascular complications. However, there is a limited number of studies that characterize the miRNA profile of endothelial cells exposed to hyperglycemia. Therefore, this study aims to analyze the miRNA profile of human umbilical-vein endothelial cells (HUVECs) exposed to hyperglycemia. HUVECs were divided into two groups: the control (treated with 5.5 mM glucose) and hyperglycemia (treated with 33.3 mM glucose) groups. RNA sequencing identified 17 differentially expressed miRNAs between the groups (p < 0.05). Of these, 4 miRNAs were upregulated, and 13 miRNAs were downregulated. Two of the most differentially expressed miRNAs (novel miR-1133 and miR-1225) were successfully validated with stem-loop qPCR. Collectively, the findings show that there is a differential expression pattern of miRNAs in HUVEC following exposure to hyperglycemia. These 17 differentially expressed miRNAs are involved in regulating cellular functions and pathways related to oxidative stress and apoptosis that may contribute to diabetic vascular endothelial dysfunction. The findings provide new clues on the role of miRNAs in the development of diabetic vascular endothelial dysfunction, which could be useful in future targeted therapy.
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Heart failure is a devastating disease that has high mortality rates and a negative impact on quality of life. Heart failure patients often experience emergency readmission after an initial episode, often due to inadequate management. A timely diagnosis and treatment of underlying issues can significantly reduce the risk of emergency readmissions. The purpose of this project was to predict emergency readmissions of discharged heart failure patients using classical machine learning (ML) models based on Electronic Health Record (EHR) data. The dataset used for this study consisted of 166 clinical biomarkers from 2008 patient records. Three feature selection techniques were studied along with 13 classical ML models using five-fold cross-validation. A stacking ML model was trained using the predictions of the three best-performing models for final classification. The stacking ML model provided an accuracy, precision, recall, specificity, F1-score, and area under the curve (AUC) of 89.41%, 90.10%, 89.41%, 87.83%, 89.28%, and 0.881, respectively. This indicates the effectiveness of the proposed model in predicting emergency readmissions. The healthcare providers can intervene pro-actively to reduce emergency hospital readmission risk and improve patient outcomes and decrease healthcare costs using the proposed model.
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Emerging evidence suggests that cognitive impairments may result from various factors, such as neuroinflammation, oxidative stress, mitochondrial damage, impaired neurogenesis, synaptic plasticity, blood-brain barrier (BBB) disruption, amyloid ß protein (Aß) deposition, and gut dysbiosis. Meanwhile, dietary polyphenol intake in a recommended dosage has been suggested to reverse cognitive dysfunction via various pathways. However, excessive intake of polyphenols could trigger unwanted adverse effects. Thus, this review aims to outline possible causes of cognitive impairments and how polyphenols alleviate memory loss via various pathways based on in vivo experimental studies. Thus, to identify potentially relevant articles, the keywords (1) nutritional polyphenol intervention NOT medicine AND neuron growth OR (2) dietary polyphenol AND neurogenesis AND memory impairment OR (3) polyphenol AND neuron regeneration AND memory deterioration (Boolean operators) were used in the Nature, PubMed, Scopus, and Wiley online libraries. Based on the inclusion and exclusion criteria, 36 research papers were selected to be further reviewed. The outcome of all the studies included supports the statement of appropriate dosage by taking into consideration gender differences, underlying conditions, lifestyle, and causative factors for cognitive decline, which will significantly boost memory power. Therefore, this review recapitulates the possible causes of cognitive decline, the mechanism of polyphenols involving various signaling pathways in modulating the memory, gut dysbiosis, endogenous antioxidants, bioavailability, dosage, and safety efficacy of polyphenols. Hence, this review is expected to provide a basic understanding of therapeutic development for cognitive impairments in the future.
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Maternal obesity can be considered an intergenerational cycle and is also an important indicator of cognitive impairments. It is thought that using natural products is the best and safest way to combat maternal obesity and associated complications. Recent studies have shown that Elateriospermum tapos (E. tapos) contains bioactive compounds with anti-obesity effects, and yoghurt is a convenient medium for supplementing obese maternal rats with E. tapos extract. Thus, the aim of this study is to investigate the impact of E. tapos in yoghurt on maternally obese rats' cognitive function supplemented with a high-fat diet (HFD). In this study, 48 female Sprague-Dawley rats were used. The rats were fed HFD for a period of 16 weeks to induce obesity, after which they were allowed to mate. Upon confirmation of pregnancy, obese rats were given varying doses of E. tapos (5, 50, and 500 mg/kg) in yoghurt until postnatal (PND) day 21. On PND 21, the dams' body mass index (BMI), Lee index, abdominal circumference, oxidative status, and metabolic profile were measured. The behavioral tests (open field, place, and object recognition) were conducted on PND 21 to access memory. The results show that the 50 and 500 mg/kg E. tapos in yoghurt supplemented groups had similar BMI, Lee index, abdominal circumference, lipid profile, FBG, insulin, FRAP, and GSH levels, as well as a similar recognition index, in comparison with the control group supplemented with saline. In conclusion, the results of this study indicate that the newly formulated E. tapos in yogurt can act as an anti-obesity agent in maternal obesity, alleviate anxiety, and enhance hippocampal-dependent memory.