Sudipta Chakrabarti, Malabendu Jana, Avik Roy, Kalipada Pahan
{"title":"Corrigendum to: Upregulation of Suppressor of Cytokine Signaling 3 in Microglia by Cinnamic Acid","authors":"Sudipta Chakrabarti, Malabendu Jana, Avik Roy, Kalipada Pahan","doi":"10.2174/156720502103240830145259","DOIUrl":"https://doi.org/10.2174/156720502103240830145259","url":null,"abstract":"In the online version of the article, a change was made in Figure 1 of the article titled “Upregulation of Suppressor of Cytokine Signaling 3 in Microglia by Cinnamic Acid”, published in Current Alzheimer Research, 2018, 15(10), 894-904. The author informed the publisher that an incorrect image was provided for Figure 1. The correct image was from the P-CREB experiment of Figure 5 [1]. <p> Now, the revised Figure 1 has been updated in the article, and it can be found online at: https://www.eurekaselect.com/article/90209","PeriodicalId":10810,"journal":{"name":"Current Alzheimer research","volume":"59 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142216421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Debasis Sen, Sunny Rathee, Vishal Pandey, Sanjay K. Jain, Umesh K. Patil
{"title":"Comprehensive Insights into Pathophysiology of Alzheimer's Disease: Herbal Approaches for Mitigating Neurodegeneration","authors":"Debasis Sen, Sunny Rathee, Vishal Pandey, Sanjay K. Jain, Umesh K. Patil","doi":"10.2174/0115672050309057240404075003","DOIUrl":"https://doi.org/10.2174/0115672050309057240404075003","url":null,"abstract":": Alzheimer's disease [AD] is a progressive neurodegenerative disorder characterized by cognitive decline, memory loss, and functional impairment. Despite extensive research, the exact etiology remains elusive. This review explores the multifaceted pathophysiology of AD, focusing on key hypotheses such as the cholinergic hypothesis, hyperphosphorylated Tau Protein and Amyloid β hypothesis, oxidative stress hypothesis, and the metal ion hypothesis. Understanding these mechanisms is crucial for developing effective therapeutic strategies. Current treatment options for AD have limitations, prompting the exploration of alternative approaches, including herbal interventions. Cholinesterase inhibitors, targeting the cholinergic hypothesis, have shown modest efficacy in managing symptoms. Blocking Amyloid β [Aβ] and targeting hyperphosphorylated tau protein are under investigation, with limited success in clinical trials. Oxidative stress, implicated in AD pathology, has led to the investigation of antioxidants. Natural products, such as Punica granatum Linn, Radix Scutellariae, and Curcuma longa have demonstrated antioxidant properties, along with anti-inflammatory effects, offering potential neuroprotective benefits. Several herbal extracts, including Ginkgo biloba, Bacopa monnieri, and Withania somnifera, have shown promise in preclinical studies. Compounds like Huperzine A, Melatonin, and Bryostatin exhibit neuroprotective effects through various mechanisms, including cholinergic modulation and anti-inflammatory properties. However, the use of herbal drugs for AD management faces limitations, including standardization issues, variable bioavailability, and potential interactions with conventional medications. Additionally, the efficacy and safety of many herbal products remain to be established through rigorous clinical trials. This review also highlights promising natural products currently in clinical trials, such as Resveratrol and Homotaurine, and their potential impact on AD progression. DHA, an omega-3 fatty acid, has shown cognitive benefits, while Nicotine is being explored for its neuroprotective effects. In conclusion, a comprehensive understanding of the complex pathophysiology of AD and the exploration of herbal interventions offer a holistic approach to managing this devastating disease. Future research should address the limitations associated with herbal drugs and further evaluate the efficacy of promising natural products in clinical settings.","PeriodicalId":10810,"journal":{"name":"Current Alzheimer research","volume":"25 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140568445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Post-Translational Modifications in Tau and Their Roles in Alzheimer's Pathology","authors":"Subha Kalyaanamoorthy, Stanley Kojo Opare, Xiaoxiao Xu, Aravindhan Ganesan, Praveen P.N. Rao","doi":"10.2174/0115672050301407240408033046","DOIUrl":"https://doi.org/10.2174/0115672050301407240408033046","url":null,"abstract":":: Microtubule-Associated Protein Tau (also known as tau) has been shown to accumulate into paired helical filaments and neurofibrillary tangles, which are known hallmarks of Alzheimer’s disease (AD) pathology. Decades of research have shown that tau protein undergoes extensive post-translational modifications (PTMs), which can alter the protein's structure, function, and dynamics and impact the various properties such as solubility, aggregation, localization, and homeostasis. There is a vast amount of information describing the impact and role of different PTMs in AD pathology and neuroprotection. However, the complex interplay between these PTMs remains elusive. Therefore, in this review, we aim to comprehend the key post-translational modifications occurring in tau and summarize potential connections to clarify their impact on the physiology and pathophysiology of tau. Further, we describe how different computational modeling methods have helped in understanding the impact of PTMs on the structure and functions of the tau protein. Finally, we highlight the tau PTM-related therapeutics strategies that are explored for the development of AD therapy.","PeriodicalId":10810,"journal":{"name":"Current Alzheimer research","volume":"1 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140568862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kathleen Angela Willoughby-Dudley, Marielle L. Darwin, Deana B. Davalos
{"title":"The Postoperative Effects of Anesthesia Exposure on Cognitive Decline in Older Adults: A Narrative Review","authors":"Kathleen Angela Willoughby-Dudley, Marielle L. Darwin, Deana B. Davalos","doi":"10.2174/0115672050288199240408035201","DOIUrl":"https://doi.org/10.2174/0115672050288199240408035201","url":null,"abstract":"Background:: As modern medicine continues to make strides in effective surgical treatments, we must also consider the critical impact of anesthesia on neuropsychological outcomes. Recent evidence suggests that anesthesia exposure may be a risk factor for postoperative cognitive decline and the eventual development of dementia. Objectives:: To explore the vulnerability of the aging brain in the context of anesthesia exposure in surgery, studies will be reviewed, and pertinent findings will be highlighted and explored to better understand risks and possible factors that need to be considered when contemplating surgery. Methods: A narrative review was conducted using a combination of MEDLINE and APA PsycINFO databases to shed light on themes across studies assessing general trends regarding the influence of anesthesia on postoperative cognitive decline. Results:: A search of relevant literature identified 388 articles. Excluding results outside the parameters of this study, the review includes quality assessments for 24 articles. Conclusion:: While findings are inconclusive, suggestions for further investigation into the relationship between anesthesia exposure and increased risk for postoperative cognitive decline are discussed, in addition to factors that may allow for greater informed disclosure of potential risks of anesthesia in older adults.","PeriodicalId":10810,"journal":{"name":"Current Alzheimer research","volume":"202 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2024-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140568547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sanjana Padala, Sharay Setti, James Raymick, Joseph Hanig, Sumit Sarkar
{"title":"Evaluation and Characterization of Modified K114 Method to Localize Plaques in Rodent and Plaques and Tangles in Human Brain Tissue","authors":"Sanjana Padala, Sharay Setti, James Raymick, Joseph Hanig, Sumit Sarkar","doi":"10.2174/0115672050295561240327055835","DOIUrl":"https://doi.org/10.2174/0115672050295561240327055835","url":null,"abstract":"Background: A plethora of studies has shown the utility of several chemical dyes due to their affinity to bind Aβ to enable visualization of plaques under light or fluorescence microscope, and some of them showed affinity to bind neurofibrillary tangles (NFT) as well. However, only a few of them have the propensity to bind both senile plaques (SP) and NFT simultaneously. Objective: In our current study, we aimed to modify the K114 dye and the staining procedure to substantially improve the staining of amyloid plaques in both human and rodent brains and neurofibrillary tangles in the human brain Methods: We modified the K114 solution and the staining procedure using Sudan Black as a modifier. Additionally, to evaluate the target of the modified K114, we performed double labeling of K114 and increased Aβ against three different epitopes. We used 5 different antibodies to detect phosphorylated tau to understand the specific targets that modified K114 binds. method: We have modified the K114 solution and the staining procedure using Sudan Black as modifier. Additionally, to evaluate the target of the modified K114, we performed double labeling of K114, and Aβ raised against three different epitopes. We used 5 different antibodies to detect phosphorylated Tau to understand the potential binding targets. Results: Dual labeling using hyperphosphorylated antibodies against AT8, pTau, and TNT1 revealed that more than 80% hyperphosphorylated tau colocalized with tangles that were positive for modified K114, whereas more than 70% of the hyperphosphorylated tau colocalized with modified K114. On the other hand, more than 80% of the plaques that were stained with Aβ MOAB-2 were colocalized with modified K114. result: We have found more than 80% hyperphosphorylated Tau against AT8, PTau and TNT1 colocalized with K114 labeled tangles, whereas more than 70% of the hyperphosphorylated Tau colocalized with modified K114. On the other hand, more than 80% of the plaques that were stained with amyloid beta MOAB-2 were colocalized with modified K114. Conclusion: Our modified method can label amyloid plaques within 5 min in the rat brain and within 20 min in the human brain. Our results indicated that modified K114 could be used as a valuable tool for detecting amyloid plaques and tangles with high contrast and resolution relative to other conventional fluorescence markers.","PeriodicalId":10810,"journal":{"name":"Current Alzheimer research","volume":"26 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2024-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140568831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Uncovering the Impact of Aggrephagy in the Development of Alzheimer's Disease: Insights Into Diagnostic and Therapeutic Approaches from Machine Learning Analysis","authors":"Jiayu Xu, Siqi Gou, Xueyuan Huang, Jieying Zhang, Xuancheng Zhou, Xiangjin Gong, Jingwen Xiong, Hao Chi, Guanhu Yang","doi":"10.2174/0115672050280894231214063023","DOIUrl":"https://doi.org/10.2174/0115672050280894231214063023","url":null,"abstract":"Background:: Alzheimer's disease (AD) stands as a widespread neurodegenerative disorder marked by the gradual onset of memory impairment, predominantly impacting the elderly. With projections indicating a substantial surge in AD diagnoses, exceeding 13.8 million individuals by 2050, there arises an urgent imperative to discern novel biomarkers for AD. Methods:: To accomplish these objectives, we explored immune cell infiltration and the expression patterns of immune cells and immune function-related genes of AD patients. Furthermore, we utilized the consensus clustering method combined with aggrephagy-related genes (ARGs) for typing AD patients and categorized AD specimens into distinct clusters (C1, C2). A total of 272 candidate genes were meticulously identified through a combination of differential analysis and Weighted Gene Co-Expression Network Analysis (WGCNA). Subsequently, we applied three machine learning algorithms-namely random forest (RF), support vector machine (SVM), and generalized linear model (GLM)-to pinpoint a pathogenic signature comprising five genes associated with AD. To validate the predictive accuracy of these identified genes in discerning AD progression, we constructed nomograms. Results:: Our analyses uncovered that cluster C2 exhibits a higher immune expression than C1. Based on the ROC(0.956). We identified five characteristic genes (PFKFB4, PDK3, KIAA0319L, CEBPD, and PHC2T) associated with AD immune cells and function. The nomograms constructed on the basis of these five diagnostic genes demonstrated effectiveness. In the validation group, the ROC values were found to be 0.760 and 0.838, respectively. These results validate the robustness and reliability of the diagnostic model, affirming its potential for accurate identification of AD. Conclusion:: Our findings not only contribute to a deeper understanding of the molecular mechanisms underlying AD but also offer valuable insights for drug development and clinical analysis. The limitation of our study is the limited sample size, and although AD-related genes were identified and some of the mechanisms elucidated, further experiments are needed to elucidate the more in-depth mechanisms of these characterized genes in the disease. result: Our analyses revealed that in the machine learning training group (GSE33000 dataset), the RF, SVM, and GLM models achieved an area under the receiver operating characteristic curve (ROC AUC) values of 0.934, 0.956, and 0.728, respectively. Based on the ROC AUC, we selected the SVM model as our experimental method and identified five characteristic genes associated with AD. The validation group (GSE122063 and GSE109887 datasets) yielded ROC AUC values of 0.760 and 0.838, respectively.","PeriodicalId":10810,"journal":{"name":"Current Alzheimer research","volume":"19 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2023-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139030875","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Interactions of Polyphenolic Gallotannins with Amyloidogenic Polypeptides Associated with Alzheimer’s Disease: From Molecular Insights to Physiological Significance","authors":"Jihane Khalifa, Steve Bourgault, Roger Gaudreault","doi":"10.2174/0115672050277001231213073043","DOIUrl":"https://doi.org/10.2174/0115672050277001231213073043","url":null,"abstract":": Polyphenols are natural compounds abundantly found in plants. They are known for their numerous benefits to human health, including antioxidant properties and anti-inflammatory activities. Interestingly, many studies have revealed that polyphenols can also modulate the formation of amyloid fibrils associated with disease states and can prevent the formation of cytotoxic oligomer species. In this review, we underline the numerous effects of four hydrolysable gallotannins (HGTs) with high conformational flexibility, low toxicity, and multi-targeticity, e.g., tannic acid, pentagalloyl glucose, corilagin, and 1,3,6-tri-O-galloyl-β-D-glucose, on the aggregation of amyloidogenic proteins associated with the Alzheimer’s Disease (AD). These HGTs have demonstrated interesting abilities to reduce, at different levels, the formation of amyloid fibrils involved in AD, including those assembled from the amyloid β-peptide, the tubulin-associated unit, and the islet amyloid polypeptide. HGTs were also shown to disassemble pre-formed fibrils and to diminish cognitive decline in mice. Finally, this manuscript highlights the importance of further investigating these naturally occurring HGTs as promising scaffolds to design molecules that can interfere with the formation of proteotoxic oligomers and aggregates associated with AD pathogenesis","PeriodicalId":10810,"journal":{"name":"Current Alzheimer research","volume":"38 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2023-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138744907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Virendra Tiwari, Akanksha Mishra, Sonu Singh, Shubha Shukla
{"title":"Caffeine improves memory and cognition via modulating neural progenitor cell survival and decreasing oxidative stress in Alzheimer's rat model.","authors":"Virendra Tiwari, Akanksha Mishra, Sonu Singh, Shubha Shukla","doi":"10.2174/1567205020666230605113856","DOIUrl":"https://doi.org/10.2174/1567205020666230605113856","url":null,"abstract":"<p><strong>Aims: </strong>Caffeine possesses potent antioxidant, anti-inflammatory and anti-apoptotic activities against a variety of neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD). The goal of this study was to investigate the protective role of a psychoactive substance like caffeine on hippocampal neurogenesis and memory functions in streptozotocin (STZ)-induced neurodegeneration in rats.</p><p><strong>Background: </strong>Caffeine is a natural CNS stimulant, belonging to the methylxanthine class, and is a widely consumed psychoactive substance. It is reported to abate the risk of various abnormalities that are cardiovascular system (CVS) related, cancer related, or due to metabolism dysregulation. Short-term caffeine exposure has been widely evaluated, but its chronic exposure is less explored and pursued. Several studies suggest a devastating role of caffeine in neurodegenerative disorders. However, the protective role of caffeine on neurodegeneration is still unclear.</p><p><strong>Objective: </strong>Here, we examined the effects of chronic caffeine administration on hippocampal neurogenesis in intracerebroventricular STZ injection induced memory dysfunction in rats. The chronic effect of caffeine on proliferation and neuronal fate determination of hippocampal neurons was evaluated by co-labeling of neurons by thymidine analogue BrdU that labels new born cells, DCX (a marker for immature neurons) and NeuN that labels mature neurons.</p><p><strong>Method: </strong>STZ (1 mg/kg, 2 μl) was injected stereotaxically into the lateral ventricles (intracerebroventricular injection) once on day 1, followed by chronic treatment with caffeine (10 mg/kg, i.p) and donepezil (5 mg/kg, i.p.). Protective effect of caffeine on cognitive impairment and adult hippocampal neurogenesis was evaluated.</p><p><strong>Result: </strong>Our findings show decreased oxidative stress burden and amyloid burden following caffeine administration in STZ lesioned SD rats. Further, double immunolabeling with bromodeoxyuridine+/doublecortin+ (BrdU+/DCX+) and bromodeoxyuridine+/ neuronal nuclei+ (BrdU+/NeuN+) has indicated that caffeine improved neuronal stem cell proliferation and long term survival in STZ lesioned rats.</p><p><strong>Conclusion: </strong>Our findings support the neurogenic potential of caffeine in STZ induced neurodegeneration.</p>","PeriodicalId":10810,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2023-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9942147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eid Abo Hamza, Ahmed A Moustafa, Richard Tindle, Rasu Karki, Shahed Nalla, Mohamed S Hamid, Mohamad El Haj
{"title":"Effect of APOE4 Allele and Gender on the Rate of Atrophy in the Hippocampus, Entorhinal Cortex, and Fusiform Gyrus in Alzheimer's Disease.","authors":"Eid Abo Hamza, Ahmed A Moustafa, Richard Tindle, Rasu Karki, Shahed Nalla, Mohamed S Hamid, Mohamad El Haj","doi":"10.2174/1567205020666230309113749","DOIUrl":"10.2174/1567205020666230309113749","url":null,"abstract":"<p><strong>Background: </strong>The hippocampus, entorhinal cortex, and fusiform gyrus are brain areas that deteriorate during early-stage Alzheimer's disease (AD). The ApoE4 allele has been identified as a risk factor for AD development, is linked to an increase in the aggregation of amyloid ß (Aß) plaques in the brain, and is responsible for atrophy of the hippocampal area. However, to our knowledge, the rate of deterioration over time in individuals with AD, with or without the ApoE4 allele, has not been investigated.</p><p><strong>Method: </strong>In this study, we, for the first time, analyze atrophy in these brain structures in AD patients with and without the ApoE4 using the Alzheimer's Disease Neuroimaging Initiative (ADNI) dataset.</p><p><strong>Results: </strong>It was found that the rate of decrease in the volume of these brain areas over 12 months was related to the presence of ApoE4. Further, we found that neural atrophy was not different for female and male patients, unlike prior studies, suggesting that the presence of ApoE4 is not linked to the gender difference in AD.</p><p><strong>Conclusion: </strong>Our results confirm and extend previous findings, showing that the ApoE4 allele gradually impacts brain regions impacted by AD.</p>","PeriodicalId":10810,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2023-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9138091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ayşe Hande Arpacı, Hasan Çalıskan, Emel Güneş, Berrin Işık
{"title":"Effects of the Recurrent and Different Doses of Ketamine Exposure on Anxiety-like Behaviors and Locomotor Activity in Juvenile Rats.","authors":"Ayşe Hande Arpacı, Hasan Çalıskan, Emel Güneş, Berrin Işık","doi":"10.2174/1567205020666230308123718","DOIUrl":"10.2174/1567205020666230308123718","url":null,"abstract":"<p><strong>Background: </strong>Ketamine is a widely used anesthetic agent. Although the potential adverse\u0000effects of ketamine use in juvenile age are uncertain, certain studies reported that children exposed to\u0000recurrent anesthesia could face an increased risk of neurodevelopmental deficits in motor function and\u0000behavioral risks. We aimed to investigate the long-term effects of repeated exposure to various ketamine\u0000doses on anxious behavior and locomotor activity in juvenile rats.</p><p><strong>Objective: </strong>We aimed to investigate the long-term effects of repeated exposure to various ketamine\u0000doses on anxious behavior and locomotor activity in juvenile rats.</p><p><strong>Methods: </strong>Thirty-two Wistar Albino juvenile male rats were randomized into 5 mg/kg, 20 mg/kg, and\u000050 mg/kg ketamine (KET) and saline (Group C) Groups and KET was administered for 3 consecutive\u0000days at 3-hour intervals in 3 doses. Ten days after the last KET dose, behavioral parameters were analyzed\u0000with an open field test (OFT), elevated plus maze (EPM), and light-dark box (LDB). Satistical\u0000analysis was conducted with Kruskall-Wallis test followed by Dunn's Multiple Comparison Test.</p><p><strong>Results: </strong>Unsupported rearing behavior decreased in 50 mg/kg KET Groups when compared to Group\u0000C. Incorrect transition time, total grooming time, and transfer latency time increased significantly in\u0000the 50 mg/kg KET Group when compared to Group C.</p><p><strong>Conclusion: </strong>These results suggested that 50 mg/kg KET led to anxiety-like behavior and destroyed\u0000memory and spatial navigation. Ketamine doses were associated with late effects of ketamine on anxiety-\u0000like behavior in juvenile rats. Further studies are needed to determine the mechanisms that play a\u0000role in the different effects of ketamine doses on anxiety and memory.</p>","PeriodicalId":10810,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2023-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9471195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}