IBRO Neuroscience Reports最新文献

{"title":"Effects of the combination of melatonin and N-acetylcysteine on the inflammatory response in a rat model of cerebral ischemia","authors":"Pouria Soleimani ,&nbsp;Saied Nekoonam ,&nbsp;Fariba Zafari ,&nbsp;Fatemeh Sabbaghziarani","doi":"10.1016/j.ibneur.2025.06.004","DOIUrl":"10.1016/j.ibneur.2025.06.004","url":null,"abstract":"<div><div>Stroke is the second leading cause of death and long-term damage globally. Inflammation is a significant factor in the onset of ischemic stroke. This study investigated the simultaneous administration of melatonin and N-acetylcysteine (NAC) on inflammation in rat cerebral ischemia. First, 30 male Wistar rats were randomly divided into five groups (n = 6), including the sham group without ischemia, the ischemic group, and the ischemic groups treated with NAC, melatonin, and NAC + melatonin, respectively. To induce ischemia, a silicone-coated monofilament was placed from the common carotid artery towards the middle cerebral artery and stained for 60 min. The rats were treated by administering NAC (50 mg/kg), melatonin (5 mg/kg) and the combination of NAC + melatonin by intraperitoneal injection after ischemia induction. The animals were assessed for sensory-motor activity at 24 and 72 h. Following sacrifice, the rats' brain was dissected to estimate infarct volume after triphenyltetrazolium chloride (TTC) staining. Inflammatory parameters were then analyzed through gene expression analysis using reverse transcription quantitative polymerase chain reaction (RT-qPCR) for nuclear factor kappa B (NF-κB), tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), and nucleotide oligomerization domain (NOD)-like receptor family with pyrin domain 1 and 3 (NLRP1 and NLRP3). The results showed a significant decrease in mRNA expression of the target genes in the rats treated with NAC + melatonin compared to the ischemic group (p &lt; 0.05). The group that received the combined treatment exhibited enhanced sensory-motor function and a reduced brain infarct volume compared to the other groups (p &lt; 0.05). In summary, the combined use of NAC and melatonin has shown promise in enhancing neurobehavioral function and decreasing the volume of cerebral infarction by regulating the inflammatory signaling pathway.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 83-90"},"PeriodicalIF":2.0,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144298737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of L-theanine on cerebellar granule cell migration related to cognitive disorders","authors":"Mai Ibrahim ,&nbsp;Matsuda Tomoko ,&nbsp;Kuriya Kenji ,&nbsp;Ozeki Makoto ,&nbsp;Abe Aya ,&nbsp;Hayato Umekawa ,&nbsp;Masahiro Nishio","doi":"10.1016/j.ibneur.2025.05.015","DOIUrl":"10.1016/j.ibneur.2025.05.015","url":null,"abstract":"<div><h3>Introduction</h3><div>Cerebellar granule cell migration plays a crucial role in cerebellum development, and any abnormalities in CGC migration can lead to significant neurological disorders such as anxiety, a common psychological disorder that impacts a person's emotional, physical, and social health. <em>L</em>-theanine, an amino acid found in green tea, demonstrates neuroprotective properties and regulates the release of neurotransmitters by stimulating CGC migration. This study investigated the impact of <em>L</em>-theanine on CGC migration related to cognitive disorders.</div></div><div><h3>Methods</h3><div><em>ddY</em> male mice treated with a single oral dose of <em>L</em>-theanine at varying concentrations (10 mg/kg) were assessed for anxiety, learning, and memory using the maze test and the Morris Water Maze test, where the average completion time and escape time of the mice were considered indicators of cognitive performance. CGC microexplants were isolated from newly born <em>C57BL/N6</em> mice and treated with a series of increasing concentrations of <em>L</em>-theanine. The migration distance of the CGC under the different <em>L</em>-theanine concentrations was assessed after 24, 48, and 72 h post-treatment using phase-contrast microscopy and image analysis software.</div></div><div><h3>Results and conclusion</h3><div>Mice's anxiety symptoms improved based on their performance on the maze test after treatment with <em>L</em>-theanine at 5 mg/ml. However, <em>L</em>-theanine at 0.05 mg/ml enhanced learning and memory abilities. Compared to other concentrations, <em>L</em>-theanine at 1 µM yielded the longest migration distance for CGC <em>in vitro</em>. Therefore, <em>L</em>-Theanine may serve as a potential therapeutic agent in supporting cerebellar development and enhancing cognitive skills. Further investigation is required to fully elucidate the molecular mechanisms and therapeutic potential of <em>L</em>-theanine in neurodevelopmental disorders.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 63-71"},"PeriodicalIF":2.0,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144240997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microglia: Mediators of experience-driven corrective neuroplasticity","authors":"Lara Rogerson-Wood,&nbsp;Atomu Sawatari,&nbsp;Catherine A. Leamey","doi":"10.1016/j.ibneur.2025.05.013","DOIUrl":"10.1016/j.ibneur.2025.05.013","url":null,"abstract":"<div><div>Neural connectivity is essential for brain function: this is initially established via early axon guidance mechanisms and subsequently refined by synaptic pruning. Alterations in the patterns of neural connectivity, arising due to changes in either of these processes, are found in neurodevelopmental conditions. Microglia, the brain’s resident immune cell, are recognised mediators of synaptic pruning. Unlike axon guidance, synaptic pruning occurs over protracted periods of postnatal life and can be profoundly impacted by experience. Little is known about whether targeted microglial synaptic pruning could be recruited to compensate for alterations in neural connectivity arising due to deleterious changes in other neurodevelopmental processes, such as axon guidance. Here we review our recent work which has addressed this by examining the effect of Environmental Enrichment (EE) on the miswired visual circuitry of mice lacking the axon guidance molecule Ten-m3. Notably, exposure to EE commenced around birth (but not from weaning or later) triggered selective removal of miswired retinal inputs in the visual thalamus of these Ten-m3 knockout mice. Most importantly, our work identifies selective microglial engulfment of neural connections during a defined postnatal window, as a likely mediator of this effect of early EE. The findings reviewed here emphasise the importance of early life experience in shaping neural circuitry, particularly when early development has been compromised by genetic factors. They also provide a potential mechanistic underpinning for the results of recent clinical trials investigating the effectiveness of early, experience-based interventions for human neurodevelopmental conditions.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 91-100"},"PeriodicalIF":2.0,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144298738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cognitive functioning in young adults after mild COVID-19: A case-control study from Iran","authors":"Farzad Akbarzadeh ,&nbsp;Farhad Faridhosseini ,&nbsp;Mahboubeh eslamzadeh ,&nbsp;Mojtaba ghalandarzadeh ,&nbsp;Saeedeh Hajebikhaniki ,&nbsp;Alireza Ebrahimi","doi":"10.1016/j.ibneur.2025.06.003","DOIUrl":"10.1016/j.ibneur.2025.06.003","url":null,"abstract":"<div><h3>Introduction</h3><div>Since December 2019, the novel coronavirus (COVID-19) has caused widespread infection across global populations, characterized by its high transmissibility. Despite extensive research on the acute effects of COVID-19, the long-term psychological and neurological sequela remain inadequately explored. This study aimed to investigate cognitive function after COVID-19 infection compared to a control group of non-infected subjects.</div></div><div><h3>Methods</h3><div>This case-control study included 40 individuals who had recovered from COVID-19, referred to Imam Reza Referral and Educational Hospital in Mashhad, Iran, and 40 matched controls who had not experienced COVID-19 symptoms. All participants underwent an initial screening by a psychiatric assistant to exclude significant medical and psychiatric conditions and any history of drug use. A demographic checklist was administered, followed by cognitive assessments using the Stroop Test, Digit Span Test, and Wisconsin Card Sorting Test (WCST). Data were analysed using SPSS Version 20.</div></div><div><h3>Results</h3><div>No significant differences were observed between the two groups regarding age, sex, education level, marital status, or employment status (p &gt; 0.05). However, COVID-19-infected individuals exhibited significantly longer completion times for the congruent Stroop test and increased reaction times compared to healthy controls (p &lt; 0.05). Additionally, the duration for completing the Wisconsin Card Sorting Test was significantly longer in the infected group compared to the non-infected group (p &lt; 0.001). Although the longest digit span and scores on the Digit Span Test were lower in the infected group, these differences did not reach statistical significance (p &gt; 0.05). Furthermore, reaction times in the Continuous Performance Test (CPT) for the first, second, and third sets of 50 stimuli were significantly greater in the COVID-19 group (p &lt; 0.001).</div></div><div><h3>Conclusion</h3><div>This study underscores that cognitive performance post-COVID-19 is adversely affected, particularly in terms of processing speed and sustained attention, when compared to healthy individuals. Further research is warranted to elucidate the underlying mechanisms and to explore potential interventions for cognitive rehabilitation in this population.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 117-123"},"PeriodicalIF":2.0,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144306811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brain pericytes upregulate glutamate uptake by astrocytes in vitro through sodium-dependent transporter","authors":"Kenta Sakai ,&nbsp;Fuyuko Takata ,&nbsp;Takuro Iwao ,&nbsp;Miho Yasunaga ,&nbsp;Gaku Yamanaka ,&nbsp;Yasufumi Kataoka ,&nbsp;Shinya Dohgu","doi":"10.1016/j.ibneur.2025.05.017","DOIUrl":"10.1016/j.ibneur.2025.05.017","url":null,"abstract":"<div><div>Astrocytes maintain glutamate homeostasis in the central nervous system (CNS) via glutamate uptake through Na⁺-dependent excitatory amino acid transporters (EAAT1 and EAAT2), and this process is regulated by several CNS cell types. However, it is unclear whether brain pericytes regulate glutamate uptake by astrocytes. Therefore, in this study, we aimed to investigate the effects of pericytes on the uptake of extracellular glutamate by astrocytes using an <em>in vitro</em> co-culture model of human brain-derived pericytes and astrocytes (pericyte co-cultures). The [³H]-L-glutamate ([³H]-L-Glu) uptake rate of astrocytes in pericyte co-cultures was significantly higher than that in astrocyte monocultures. Under Na⁺-free conditions, [³H]-L-Glu uptake by astrocytes was significantly inhibited in astrocyte monocultures and pericyte co-cultures. The inhibitory effect of Na⁺ depletion on glutamate uptake by astrocytes was more pronounced in pericyte co-cultures than in astrocyte monocultures. These findings suggest that glutamate uptake by astrocytes through the Na⁺-dependent transporter EAATs is upregulated by pericytes. Treatment with dihydrokainic acid, a selective inhibitor of EAAT2, significantly inhibited [³H]-L-Glu uptake by astrocytes in pericyte co-cultures but not in astrocyte monocultures. Treatment with UCPH-101, a selective inhibitor of EAAT1, significantly inhibited [³H]-L-Glu uptake by astrocytes in both monocultures and pericyte co-cultures. The UCPH-101-induced reduction in [³H]-L-Glu uptake by astrocytes in pericyte co-cultures was similar to that observed in astrocyte monocultures. These results suggest that pericytes upregulate glutamate uptake via EAAT2 in astrocytes. Furthermore, [³H]-L-Glu uptake in astrocytes significantly increased when astrocytes were treated with pericyte-conditioned medium. This finding suggests that pericyte-derived soluble factors contribute to the upregulation of astrocytic glutamate uptake. To our knowledge, this is the first study to report that pericyte-released mediators upregulate the EAAT2-dependent uptake of extracellular glutamate in astrocytes.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 54-61"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144230955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toxoplasma TgCtwh3 Δrop16Ⅰ/Ⅲ accelerates neuronal apoptosis and APP production in mouse with acute infection","authors":"Di Yang ,&nbsp;Cong Wang ,&nbsp;Qing Tao ,&nbsp;Lei Liu ,&nbsp;Mengmeng Jin ,&nbsp;Haiping Cai ,&nbsp;Meijuan Zheng ,&nbsp;Mengtao Gong ,&nbsp;Li Yu ,&nbsp;Jian Du ,&nbsp;Qingli Luo ,&nbsp;Jilong Shen ,&nbsp;Kunpeng Qin ,&nbsp;Deyong Chu","doi":"10.1016/j.ibneur.2025.05.009","DOIUrl":"10.1016/j.ibneur.2025.05.009","url":null,"abstract":"<div><h3>Objective</h3><div>To explore the mechanism by which <em>rop16</em>_{<em>Ⅰ/Ⅲ</em>}-deficient/<em>gra15</em>_<em>Ⅱ</em>-dominant <em>toxoplasma gondii</em> Chinese 1 genotype Wh3 (TgCtwh3 Δ<em>rop16</em>_{<em>Ⅰ/Ⅲ</em>}) strain induced neuron apoptosis, APP and BACE1 production <em>in vivo</em> and <em>vitro</em>.</div></div><div><h3>Method</h3><div>BALB/c mice were infected by intraperitoneal injection with TgCtwh3 wild type (TgCtwh3 WT) and TgCtwh3 Δ<em>rop16</em>_{<em>Ⅰ/Ⅲ</em>} tachyzoites, respectively. One week after infection, the morphology and number of hippocampal neurons were examined by hematoxylin-eosin (H&amp;E) and Nissl staining. Expression levels of apoptosis-related proteins, APP, BACE1 as well as inflammatory factors proteins and genes in the hippocampus were evaluated using western blotting and qRT-PCR. The hippocampal neuron cell line HT22 was infected with TgCtwh3 WT and TgCtwh3 Δ<em>rop16</em>_{<em>Ⅰ/Ⅲ</em>} tachyzoite, respectively, and the expression of target proteins was analyzed through immunofluorescence staining and western blotting. Furthermore, HT22 apoptosis was assessed using flow cytometry.</div></div><div><h3>Result</h3><div>BALB/c mice injected with TgCtwh3 Δ<em>rop16</em>_{<em>Ⅰ/Ⅲ</em>} tachyzoites presented abnormal appearance and posture changes as well as declined vitality. The hippocampus assay demonstrated that TgCtwh3 Δ<em>rop16</em>_{<em>Ⅰ/Ⅲ</em>} <em>toxoplasma</em> caused neuron loss, neuron alignment disorder, neuronal nucleus abnormal deep-stained and neuron apoptosis. Furthermore, TgCtwh3 Δ<em>rop16</em>_{<em>Ⅰ/Ⅲ</em>} tachyzoites caused obvious production of APP, BACE1and expression increase of pro-inflammatory factors in hippocampal tissue compared to these in mice infected with TgCtwh3 WT tachyzoites. Contrarily, the expression of transforming growth factor beta 1 (TGF-β1), a pivotal anti-inflammatory cytokine was significantly decreased in TgCtwh3 Δ<em>rop16</em>_{<em>Ⅰ/Ⅲ</em>} infected mice. Further study showed that TgCtwh3 Δ<em>rop16</em>_{<em>Ⅰ/Ⅲ</em>} tachyzoites induced HT22 apoptosis through triggering ERS, meanwhile promoted HT22 to produce APP, BACE1 by activating NF-κB signaling pathway.</div></div><div><h3>Conclusion</h3><div>Our results indicated that the GRA15_Ⅱ effector may play a crucial part in neuron apoptosis, pro-inflammatory factors secretion, and APP, BACE1 production. Inversely, ROP16_Ⅰ/Ⅲ effector may play a potentially protective role in this process.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 830-843"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144178004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin D and brain volumetric changes: An updated systematic review and meta-analysis","authors":"Rozhina Tamannaeifar ,&nbsp;Salar Yousefzadeh ,&nbsp;Sana Rahmani ,&nbsp;Maedeh Bayani ,&nbsp;Mahdiyeh Nozad Varjovi ,&nbsp;Nima Eftekhari ,&nbsp;Mona Ranjkesh ,&nbsp;Mahsa Kohansal Vajargah ,&nbsp;Sajjad Hajihosseini ,&nbsp;Faezeh Ahanj ,&nbsp;Hadis Sarlak ,&nbsp;Komeil Aghazadeh-Habashi ,&nbsp;Melika Arab Bafrani ,&nbsp;Alaleh Alizadeh ,&nbsp;Yaser Khakpour ,&nbsp;Niloofar Deravi","doi":"10.1016/j.ibneur.2025.04.011","DOIUrl":"10.1016/j.ibneur.2025.04.011","url":null,"abstract":"<div><h3>Background</h3><div>In this systematic review and meta-analysis, we aimed to investigate the relationship between vitamin D levels and brain volumetric changes in human studies.</div></div><div><h3>Method</h3><div>We conducted a comprehensive search in PubMed, Scopus, and Google Scholar databases up to December 2024. A total of 450 studies were identified. Following title, abstract, and full-text screening, we included three studies for analysis. Data were extracted from these studies and analyzed using appropriate statistical methods.</div></div><div><h3>Result</h3><div>Our analysis revealed that the included case-control and cohort studies were conducted in the United States, Norway, and the Netherlands. The studies exhibited a range of characteristics, including sample size (number of patients: 183–240), demographic variables, and methods of assessing both vitamin D levels and brain volume. Brain volume assessments included gray matter, white matter, and total brain volume. The total follow-up duration across studies was 11 years. The age of participants ranged from 30 to 64 years in one study, while in another, they were aged 65 years or older. The meta-analysis indicated no significant association between vitamin D levels and brain volumetric changes across the included studies (effect size: 0.07, 95 % CI= [-0.01, 0.15], P = 0.07, I²=54.44 %).</div></div><div><h3>Conclusion</h3><div>This meta-analysis did not establish a significant association between vitamin D levels and brain volumetric changes. These findings highlighted the need for further large-scale studies to clarify the potential role of vitamin D in brain volume and to better understand the underlying mechanisms involved.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 844-852"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144185229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mapping the knowledge of epilepsy and Potassium Channels: A scientometric analysis in CiteSpace and VOSviewer","authors":"Zheng Li","doi":"10.1016/j.ibneur.2025.05.004","DOIUrl":"10.1016/j.ibneur.2025.05.004","url":null,"abstract":"<div><div>Epilepsy is one of the most common neurological diseases. Studies have suggested that epileptic seizures are directly related to ion channel abnormalities in the central nervous system. Activation of potassium ion channels may lead to increased cell excitability and abnormal neuronal excitation. Over the past decade, significant progress has been achieved in understanding the potassium ion channel abnormalities related to epilepsy. To facilitate further research, in this paper, we adopted the bibliometrics method (based on Web of Science database) and used CiteSpace and VOSviewer to visualize literature in the field (Potassium Channels-related epilepsy) from 2010 to 2023. A total of 2415 original research and summary papers were included, and the basic situation, subject theme, and knowledge structure evolution were analyzed and discussed step by step from macro to micro perspectives.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 1-16"},"PeriodicalIF":2.0,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144195622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The microbial guardians: Unveiling the role of gut microbiota in shaping neurodegenerative disease","authors":"Nour Abou Izzeddine ,&nbsp;Kawsar Ahmad ,&nbsp;Christine Bacha ,&nbsp;Maria Jabbour ,&nbsp;Mouin Najjar ,&nbsp;Sethrida Salhab ,&nbsp;Hilda E. Ghadieh ,&nbsp;Amjad Kanaan ,&nbsp;Sami Azar ,&nbsp;Ziad Abi Khattar ,&nbsp;Frederic Harb","doi":"10.1016/j.ibneur.2025.05.014","DOIUrl":"10.1016/j.ibneur.2025.05.014","url":null,"abstract":"<div><div>The gut microbiota, a complex community of microorganisms residing in the digestive tract, plays a pivotal role in human health. Recent studies have highlighted its significant impact on neurodegenerative diseases, conditions that pose profound challenges to affected individuals and society at large. This review explores the intricate relationship between gut microbiota and the progression of neurodegenerative disorders, such as Alzheimer's disease, Parkinson's disease, Huntington’s disease, and Amyotrophic Lateral Sclerosis. We delve into the dynamic ecosystem of gut microbiota, examining factors influencing its composition and the bidirectional communication established via the gut-brain axis. Emerging evidence suggests that gut microbiota can modulate neurodegenerative disease progression through mechanisms including inflammatory responses, production of neuroactive substances, and regulation of neurotransmitters. Furthermore, we discuss the potential therapeutic implications of targeting gut microbiota with probiotics, prebiotics, and postbiotics. While promising, these interventions face challenges and limitations that must be addressed through ongoing research. Understanding the role of gut microbiota in neurodegenerative diseases is crucial for developing innovative therapeutic strategies and improving patient outcomes.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 17-37"},"PeriodicalIF":2.0,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144203863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A meta-analysis update evaluating the treatment effects of donepezil alone versus donepezil combined with memantine for Alzheimer's disease","authors":"Sajjad Hajihosseini ,&nbsp;Seyed Amirali Zakavi ,&nbsp;Zahra Farrokhi ,&nbsp;Mahnaz Amanzadeh ,&nbsp;Parham Panahi ,&nbsp;Mina Mahram ,&nbsp;Nima Eftekhari ,&nbsp;Masoud Noroozi ,&nbsp;Mohammad Javad Ebrahimi ,&nbsp;Alaleh Alizadeh ,&nbsp;Pegah Refahi ,&nbsp;Melika Arab Bafrani ,&nbsp;Maral Moafi ,&nbsp;Niloofar Deravi","doi":"10.1016/j.ibneur.2025.05.016","DOIUrl":"10.1016/j.ibneur.2025.05.016","url":null,"abstract":"<div><h3>Background</h3><div>Alzheimer's disease (AD) remains a significant global health problem, with ongoing debates about the most effective treatment approach. While donepezil monotherapy has been traditionally used, recent interest has focused on combining it with memantine. This updated meta-analysis aimed to compare the efficacy of donepezil monotherapy versus its combination with memantine for treating AD.</div></div><div><h3>Method</h3><div>A literature search was conducted in the PubMed, Scopus, and Google Scholar databases up to February 14, 2024. Randomized controlled trials (RCTs) comparing donepezil monotherapy with donepezil combined with memantine in AD patients were included. The quality of each selected study was assessed using the Joanna Briggs Institute (JBI) risk-of-bias tool. Data on cognitive function, measured using the Mini-Mental State Examination (MMSE) and the Severe Impairment Battery (SIB), were extracted and analyzed using a random-effects model.</div></div><div><h3>Results</h3><div>A total of four RCTs, including 1930 patients, met the inclusion criteria. Analysis using a forest plot revealed no significant difference in MMSE scores between monotherapy and combination therapy (OR = 0.54, 95 % CI: 0.06–4.60, p &gt; 0.05). However, SIB scores showed a significant improvement with combination therapy (OR = 7.00, 95 % CI: 1.13–43.24, p &lt; 0.05). Both analyses exhibited high heterogeneity (I² = 72 % for MMSE; I² = 89 % for SIB). The funnel plots suggested minor publication bias for the MMSE outcomes, but some asymmetry was observed in the results for SIB.</div></div><div><h3>Conclusion</h3><div>This meta-analysis suggests that combination therapy with donepezil and memantine significantly benefits patients with severe cognitive impairment, as assessed by the SIB, compared to donepezil monotherapy. However, no significant advantage was observed in MMSE scores. The high heterogeneity among studies highlights the need for cautious interpretation and calls for larger, well-designed randomized controlled trials to further elucidate the comparative efficacy of these two therapeutic approaches in Alzheimer's disease.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 72-82"},"PeriodicalIF":2.0,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144262212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}