Li-Qin Che, Zhen-Zhen Qu, Tao Xie, Yan-Ge Zhang, Dong-Juan Yuan, Qing Li, Li-Jing Jia, Wei-Ping Wang
{"title":"Effect of low‑frequency repetitive transcranial magnetic stimulation on cognitive function in rats with medial temporal lobe epilepsy.","authors":"Li-Qin Che, Zhen-Zhen Qu, Tao Xie, Yan-Ge Zhang, Dong-Juan Yuan, Qing Li, Li-Jing Jia, Wei-Ping Wang","doi":"10.55782/ane-2023-2471","DOIUrl":"10.55782/ane-2023-2471","url":null,"abstract":"<p><p>Epilepsy, especially the medial temporal lobe epilepsy (TLE), can result in cognitive impairment. Low‑frequency repetitive magnetic stimulation (rTMS) has been verified to suppress neural excitability and reduce seizures. Given its potential in modifying cortical activity, we aimed to investigate its impact on cognitive function in the context of epilepsy, a condition where the use of rTMS has not been extensively explored. However, the influence on cognitive function has not yet been investigated. Therefore, this study aimed to investigate the effects of low‑frequency rTMS on cognitive improvement in epileptic rats. Rats used in this study were randomly divided into five groups: the sham group, the epilepsy group, and three epilepsy groups treated with rTMS at different frequencies. Each group underwent the Morris water maze test to investigate hippocampus‑dependent episodic memory, to evaluate their cognitive performance. Further assessments included patch clamp and western blot techniques to estimate the synaptic function in the hippocampus. Comparison between groups showed that low‑frequency rTMS significantly reduced spontaneous recurrent seizures and improved spatial learning and memory impairment in epileptic rats. Additionally, rTMS remodeled the synaptic plasticity affected by seizures and notably enhanced the expression of AMPAR and synaptophysin. Low‑frequency rTMS can antagonize the cognitive impairment caused by TLE, and promote synaptic connections.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 4","pages":"395-403"},"PeriodicalIF":1.4,"publicationDate":"2023-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139465816","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":"Systematic review and meta‑analysis of observational studies to check the protective role of non‑steroidal anti‑inflammatory drugs in Alzheimer's disease.","authors":"Akash Asthana, Shashank Tripathi, Rachna Agarwal","doi":"10.55782/ane-2023-2467","DOIUrl":"10.55782/ane-2023-2467","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a major neurodegenerative disease, affecting more than two third cases of dementia in the world. Non‑steroidal anti‑inflammatory drugs (NSAIDs) are widely used anti‑inflammatory analgesic agents representing 7.7% of worldwide prescriptions of which 90% are in patients over 65 years old. Based on mixed findings a systematic review and meta‑analysis were conducted to develop a better understanding of the protective role of NSAIDs in AD. We used three database PubMed, Web of Science, and Embase to identify the literatures. The studies following cohort and case‑control design were investigated separately to check the effect of NSAIDs on AD, by the using their fundamental indicators (relative risk and odds ratio). The fixed effect or random effects model were used to estimate the pooled relative risk and pooled odds ratio separately for both the study design, based on magnitude of heterogeneity. A total of 14 studies were selected for meta‑analysis. Eight studies were following cohort study design, whereas, six studies were following case‑control study design. In meta‑analysis of cohort studies, the pooled relative risk was 0.67 with 95% C.I 0.39 to 1.15, which was statistically insignificant. In meta‑analysis of case‑control studies, the pooled odds ratio was 0.71 with 95% C.I 0.46 to 1.10, which was statistically insignificant. NSAIDs do not act as a protective factor for Alzheimer's disease. Additionally, methodologically sound randomized controlled trials are required to produce a robust result.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 4","pages":"386-394"},"PeriodicalIF":1.4,"publicationDate":"2023-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139465827","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":"The protective role of circ_0016760 downregulation against sevoflurane‑induced neurological impairment via modulating miR‑145 expression in aged rats.","authors":"Peiyu Shuai, Zhihong Hu, Wei Li, Guoliang You, Zhiye Liu, Niandong Zheng","doi":"10.55782/ane-2023-2464","DOIUrl":"10.55782/ane-2023-2464","url":null,"abstract":"<p><p>Sevoflurane can produce toxicity to the hippocampal tissues of brain, leading to nerve damage, causing learning and cognitive dysfunction. CircRNAs have been indicated to act as a key mediator in anesthetic neurotoxicity. This study focused on the effect of circ_0016760 on sevoflurane‑induced neurological impairment. The GEO database (GSE147277) and RT‑qPCR were used to predict and measure the circ_0016760 expression. The interaction of circ_0016760 and miR‑145 was verified by dual‑luciferase reporter assay. The CCK‑8 assay, flow cytometry, ELISA, ROS kit, MWM test were carried out to measure the cell viability, apoptosis, inflammation indicators, ROS level, and cognitive and memory function of the rats. Sevoflurane exacerbated neurotoxicity by restraining cell viability, inducing cell apoptosis, neuroinflammation, and ROS generation, and causing learning and cognitive dysfunction. Circ_0016760 expression was increased in POCD patients from the GEO database and upregulated after sevoflurane exposure. miR‑145 was a target miRNA of circ_0016760. Silencing of circ_0016760 weakened the effect of sevoflurane on cell viability, cell apoptosis, inflammation‑related factors, oxidative stress, which could be reversed by miR‑145 inhibitor. The animal experiments results showed that circ_0016760 played a protective effect on regulating the cognitive behavior of sevoflurane‑treated aged rats, expression of inflammation cytokine, and oxidative stress factors through targeting miR‑145 in sevoflurane‑treated aged rat's hippocampal neurons. Our results revealed that silencing of circ_0016760 attenuated sevoflurane‑induced hippocampal neuron injury by regulating miR‑145 expression, which may provide potential insights into the treatment of sevoflurane‑induced neurological impairment.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 4","pages":"377-385"},"PeriodicalIF":1.4,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139465833","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}
Monika Lewandowska, Krzysztof Tołpa, Marcin Hajnowski, Tomasz Piotrowski, Joanna Dreszer
{"title":"The less complex temporal patterns of resting‑state EEG activity, the lower the visual temporal order threshold.","authors":"Monika Lewandowska, Krzysztof Tołpa, Marcin Hajnowski, Tomasz Piotrowski, Joanna Dreszer","doi":"10.55782/ane-2023-2463","DOIUrl":"10.55782/ane-2023-2463","url":null,"abstract":"<p><p>Speech understanding, watching a movie, listening to music etc., requires perception of the temporal order of at least two incoming events. A history of performing these tasks may be reflected in spontaneous brain activity. Here, we examined the relationship between the complexity (temporal dynamics) of resting‑state EEG (rsEEG) signal, assessed using the multivariate MultiScale Entropy (mMSE) algorithm, and the perception of event ordering, indexed by a visual temporal order threshold (TOT), i.e., the minimum duration necessary to correctly identify the before‑after relation between two stimuli. Healthy adolescents and young adults performed a psychophysical task measuring the TOT and underwent an eyes‑closed rsEEG study. The features of mMSE vectors, namely the area under curve (AUC) that represents total signal complexity, as well as the MaxSlope and the AvgEnt, corresponding to the entropy at fine‑ and coarse‑grained timescales, respectively, were obtained for the central (midline), anterior, middle and posterior channel sets. The greater the AUC and AvgEnt values in the central, left and right posterior areas, and the higher AUC in the right middle region, the higher the TOT. The most significant relationships were found for the midline electrodes (Fz, Cz, Pz, Oz). There were no significant correlations between the MaxSlope values and the TOT. To the best of our knowledge, this is the first study demonstrating that spontaneous EEG signal complexity is associated with the temporal order perception of two stimuli presented in rapid succession. Our findings may indicate that low total and coarse entropy levels of rsEEG signal are beneficial for visual temporal order judgments.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 4","pages":"359-376"},"PeriodicalIF":1.4,"publicationDate":"2023-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139465830","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}
Magdalena Mlostek, Juan Zeng, Malgorzata Urbanska, Jacek Jaworski
{"title":"Dendritic arbor dynamics and stability in health and disease.","authors":"Magdalena Mlostek, Juan Zeng, Malgorzata Urbanska, Jacek Jaworski","doi":"10.55782/ane-2023-2456","DOIUrl":"10.55782/ane-2023-2456","url":null,"abstract":"<p><p>Dendritogenesis, a process of dendritic arbor development, is essential for the formation of functional neuronal networks, and in mammals, it begins in early life and continues into adulthood. It is a highly dynamic process in which dendritic branches form and regress until mature connectivity is achieved. Thereafter, dendritic branches are considered stable and do not undergo substantial rearrangements, although several exceptions have been described in the literature. After this long period of relative stability, significant changes in dendritic branching occur when the brain begins to age. Several neurological diseases, occurring both during development and in adulthood, have severe effects on the morphology of dendritic arbors, often associated with intellectual dysfunction. The molecular mechanisms of dendritogenesis are fairly well described. In contrast, knowledge of the molecular mechanisms of dendritic arbor stabilization and pathology‑induced instability is still quite incomplete, and several important questions remain unanswered. We describe the dynamic changes during development and adulthood and in different pathologies. Whenever possible, we also provide details on the molecular mechanisms behind dendritic dynamics and stability.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 4","pages":"331-358"},"PeriodicalIF":1.4,"publicationDate":"2023-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139465792","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":"IL‑4 alleviates CIRI by suppressing autophagy via the HIF‑1α/Bcl‑2/BNIP3 pathway in rats.","authors":"Yijun Suo, Lu Zhang, Yuanhang Che","doi":"10.55782/ane-2023-2429","DOIUrl":"10.55782/ane-2023-2429","url":null,"abstract":"<p><p>This paper was designed for delving into the mechanism adopted by interleukin‑4 (IL‑4) to relieve cerebral ischemia‑reperfusion injury (CIRI) in rats via suppressing autophagy. Herein, rats stochastically fell into sham operation (sham), model (RI), model + IL‑4 intervention (IL‑4), model + HIF‑1α inhibitor (2‑methoxyestradiol, 2ME2) and model + IL‑4 + 2ME2 (IL‑4 + 2ME2) groups. Next, western blotting was utilized to examine the protein expressions of microtubule‑associated protein 1 light chain 3 (LC3), p62, hypoxia‑inducible factor 1‑alpha (HIF‑1α) and Bcl‑2/adenovirus E1B 19 kDa‑interacting protein 3 (BNIP3). Relative to RI group, IL‑4 group had a significantly lower neurological impairment scale (NIS) score and an overtly lower apoptosis rate of neurons as well as a strikingly smaller cerebral infarction volume and number of autophagosomes (P<0.05). The LC3II/LC3I ratio and HIF‑1α and BNIP3 protein expressions dropped, but p62 protein expression rose pronouncedly in IL‑4 group (P<0.05). In contrast to those in RI group, the NIS score, neuronal apoptosis rate, cerebral infarction volume and autophagosome number were strikingly reduced (P<0.05). The NIS score, cerebral infarction volume, neuronal apoptosis rate, autophagosome number, LC3II/LC3I ratio and protein expressions of HIF‑1α and BNIP3 plummeted, while p62 protein expression sharply rose in IL‑4 + 2ME2 group relative to those in IL‑4 group (P<0.05). IL‑4 suppresses cell autophagy by inhibiting the HIF‑1α/BNIP3 pathway, thus relieving CIRI in rats.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 3","pages":"246-254"},"PeriodicalIF":1.4,"publicationDate":"2023-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49688305","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}
Bartłomiej Ptaszek, Szymon Podsiadło, Olga Czerwińska-Ledwig, Aneta Teległów, Wanda Pilch, Artur Wójcik, Ewa Sadowska-Krępa
{"title":"The effect of a series of whole‑body cryotherapy treatments on the activity of antioxidant enzymes in healthy women and women with multiple sclerosis.","authors":"Bartłomiej Ptaszek, Szymon Podsiadło, Olga Czerwińska-Ledwig, Aneta Teległów, Wanda Pilch, Artur Wójcik, Ewa Sadowska-Krępa","doi":"10.55782/ane-2023-2431","DOIUrl":"10.55782/ane-2023-2431","url":null,"abstract":"<p><p>The study aimed to compare the effect of a series of 20 sessions of whole‑body cryotherapy (WBC) on the level of CAT, GPx and SOD in women with multiple sclerosis and healthy women. The consent of the Bioethics Committee at the Regional Medical Chamber in Krakow was obtained, and the trial was registered in the Australian New Zealand Clinical Trials Registry. Thirty people took part in the study: the study group (MS) and the control group (CONT). All subjects participated in 20 cryotherapy sessions. Venous blood was collected for analysis before the WBC session and after 20 sessions. There were no changes in the examined parameters (CAT, GPx, SOD) after using WBC in the MS or control groups. There were also no differences between the groups in the first or the last study. There were no adverse changes in the parameters tested - WBC appeared to be a safe form of therapy, although the mechanisms of hypothermic protection are not fully understood.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 3","pages":"262-270"},"PeriodicalIF":1.4,"publicationDate":"2023-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49688309","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}
Seval Musuroglu Keloglan, Fatma Banu Aycik, Suleyman Emre Kocacan, Burak Yazgan, Mustafa Ayyildiz, Erdal Agar
{"title":"Nesfatin‑1 exerts anticonvulsant effect by reducing oxidative stress in experimental epilepsy model.","authors":"Seval Musuroglu Keloglan, Fatma Banu Aycik, Suleyman Emre Kocacan, Burak Yazgan, Mustafa Ayyildiz, Erdal Agar","doi":"10.55782/ane-2023-2419","DOIUrl":"10.55782/ane-2023-2419","url":null,"abstract":"<p><p>Neuropeptides play an important role in the pathogenesis of epilepsy. In the present study, the effect of nesfatin‑1, a neuropeptide, was investigated on penicillin‑induced epilepsy model. Epileptiform activity was induced by an injection of penicillin into the somatomotor cortex at 56 albino Wistar rats. Nesfatin‑1 (i.c.v.) was administered at five different doses (12.5, 25, 50, 100, and 200 pmol) 30 min after a penicillin administration. Astressin 2B, a corticotropin‑releasing factor (CRF) receptor antagonist, was administered 10 minutes later the effective dose of nesfatin‑1 (50 pmol, i.c.v.). Superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR) and malondialdehyde (MDA) levels in cerebrum were analysed by ELISA method. Nesfatin‑1, at the doses of 25, 50 and 100 pmol, significantly reduced the frequency of epileptiform activity. However, none of the doses of nesfatin‑1 had any effect on the amplitude of epileptiform activity. Astressin 2B alone did not show any effect on epileptiform activity. In addition, astressin 2B had no effect on the anticonvulsant effect of nesfatin‑1. Nesfatin‑1 (at the doses of 25, 50, 100 pmol) did not alter SOD and GSH levels, but significantly increased the GPx and GR levels. Nesfatin‑1 (at a dose of 50 pmol) significantly decreased the MDA level in the cerebrum. Nesfatin‑1 shows anticonvulsant effect and astressin 2B did not affect the anticonvulsant effect of nesfatin‑1. We suggest that nesfatin‑1 has oxidative stress‑mediated anticonvulsant effect in the penicillin‑induced epileptic activity.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":" ","pages":"227-235"},"PeriodicalIF":1.4,"publicationDate":"2023-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10553881","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}
Qiang Fu, Yuanqing Deng, Bo Zhou, Juan Lei, Ke Peng, Can Feng
{"title":"miR‑488‑3p alleviates neuropathic pain by regulating target gene ROCK1.","authors":"Qiang Fu, Yuanqing Deng, Bo Zhou, Juan Lei, Ke Peng, Can Feng","doi":"10.55782/ane-2023-2432","DOIUrl":"10.55782/ane-2023-2432","url":null,"abstract":"<p><p>The function of microRNA (miRNA) in neuropathic pain (NP) has received widespread attention. The current research sought to address the contribution of miR‑488‑3p in NP and its downstream mechanisms. The NP rat model was constructed by chronic constriction injury (CCI) surgery in rats. Regulation of miR‑488‑3p or Rho‑associated coiled‑coil‑containing protein kinase 1 (ROCK1) in rats by intrathecal injection of lentivirus or plasmid. Real‑time quantitative reverse transcription polymerase chain reaction (RT‑qPCR) to examine the levels of miR‑488‑3p and ROCK1 in the dorsal root ganglion (DRG). Enzyme‑linked immunosorbent assay (ELISA) to monitor the secretion of pro‑inflammatory and anti‑inflammatory factors. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) for the evaluation of mechanosensitive and thermal nociceptive hypersensitivity of NP behaviors. Validation of molecular mechanism between miR‑488‑3p and ROCK1 using RNA immunoprecipitation assay and dual‑luciferase reporter (DLR) assay. miR‑488‑3p was vigorously less expressed in the DRGs of CCI rats, while ROCK1 was upregulated. Elevated miR‑488‑3p alleviated the decrease of PWL and PWT in CCI rats, inhibited the secretion of pro‑inflammatory factors, and enhanced anti‑inflammatory factors levels. Mechanistically, ROCK1 was the target of miR‑488‑3p. Raised ROCK1 partially attenuated the mitigating effect of miR‑488‑3p on NP behavior and the suppression of inflammatory responses in rats. Current research demonstrated that miR‑488‑3p may be a novel therapeutic target for NP.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 3","pages":"271-279"},"PeriodicalIF":1.4,"publicationDate":"2023-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49688307","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}
Melike Uysal, Mert Celikten, Merve Beker, Nurhayat Polat, Onder Huseyinbas, Sule Terzioglu-Usak, Birsen Elibol
{"title":"Kaempferol treatment ameliorates memory impairments in STZ‑induced neurodegeneration by acting on reelin signaling.","authors":"Melike Uysal, Mert Celikten, Merve Beker, Nurhayat Polat, Onder Huseyinbas, Sule Terzioglu-Usak, Birsen Elibol","doi":"10.55782/ane-2023-2427","DOIUrl":"10.55782/ane-2023-2427","url":null,"abstract":"<p><p>Many treatment initiatives, like herbal products and their active ingredients, aim to alleviate neurodegeneration to increase cognitive functions. Kaempferol may be a candidate molecule for treating neurodegeneration because of its antioxidant effects. In the present study, we examined the molecular changes associated with kaempferol's memory‑enhancing effects on streptozotocin (STZ)‑induced neurodegeneration. After intracerebroventricular STZ injection in Long‑Evans male rats, intraperitoneal kaempferol was administered for 12 days. The Morris water maze (MWM) was used to measure learning and memory performance in the rats, and proteins related to memory formation were investigated in the hippocampi with western blotting. Kaempferol improved learning performance and memory decline in STZ‑treated rats. At the molecular level, STZ‑induced neurodegeneration resulted in a decrease in the expression of GAD67, reelin, and phosphorylated‑NMDAR. However, kaempferol treatment ameliorated these changes by enhancing their levels similar to the controls. While neither STZ injection nor kaempferol treatment produced any significant change in phosphorylated‑CAMKII levels, they increased the expression of klotho and prealbumin. These results show that kaempferol has positive effects on memory loss, affecting synaptic plasticity by ameliorating both the levels and activity of memory‑relevant molecules through reelin signaling. In summary, this study provides a guide to future studies by examining in detail the healing effect of kaempferol as a candidate molecule in the treatment of neurodegeneration, such as that observed in Alzheimer's disease.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 3","pages":"236-245"},"PeriodicalIF":1.4,"publicationDate":"2023-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49688306","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}