Metabolic brain disease最新文献

{"title":"Effects of a mitochondrial calcium uniporter and P-selectin inhibitors on neural injury induced by global cerebral ischemia-reperfusion in male rats.","authors":"Setareh Javanmardi, Farshad Moradpour, Mojgan Veisi, Neda Omidian, Rasoul Kavyannejad","doi":"10.1007/s11011-025-01570-5","DOIUrl":"10.1007/s11011-025-01570-5","url":null,"abstract":"<p><p>Neural injury following ischemia-reperfusion (I/R) is induced by multiple pathophysiological pathways. This study aimed to use mitochondrial calcium channel and p-selectin inhibitors to weaken these pathways. One hundred and two rats were randomly divided into six groups. In the sham group, cerebral I/R induction and drug intervention were not performed. In the I/R group, cerebral I/R induction was induced. In the RR + FCN group, animals received only ruthenium red (RR) and fucoidan (FCN) intraperitoneally without I/R induction. In the I/R + RR group, animals received RR during the cerebral I/R period. In the I/R + FCN group, FCN was administered along with cerebral I/R. In the I/R +(RR + FCN) group, animals exposed to cerebral I/R received a combination of RR and FCN simultaneously. The shuttle box and new object tests were used to assess learning and memory. The superoxide dismutase (SOD), malondialdehyde (MDA), interleukin-1 beta (IL-1β), and tumor necrosis factor-alpha (TNF-α) levels in the hippocampus were measured. Neuronal death in the hippocampal CA1 area was assessed via hematoxylin-eosin staining. FCN and RR significantly decreased the tissue MDA, IL-1β, TNF-α levels while increased the SOD level. These inhibitors significantly reduced learning disorders and cerebral edema following I/R. The rate of neuronal death was significantly lower in each of the receiving RR and FCN groups. This study revealed that the use of FCN and RR significantly attenuated the pathways associated with oxidative stress and inflammation as well as neuronal death following cerebral I/R, thereby reducing learning and memory impairments. The effects of neuroprotection were further determined when two inhibitors were used simultaneously. HIGHLIGHTS: Cerebral ischemia-reperfusion is associated with many neurological, sensory and motor defects. Multiple pathways of neural pathophysiology are activated during cerebral ischemia-reperfusion. The Administration of ruthenium and fucoidan weakens inflammatory pathways, oxidative stress, and learning dysfunctions caused by cerebral ischemia and reperfusion. Stronger Neuroprotective effects were observed during the simultaneous administration of ruthenium and fucoidan.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"150"},"PeriodicalIF":3.2,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of quercetin and derivatives on NAMPT/Sirtuin-1 metabolic pathway in neuronal cells: an approach to mitigate chemotherapy-induced cognitive impairment.","authors":"Jeena John, Subham Das, Anu Kunnath, Jayesh Mudgal, Krishnadas Nandakumar","doi":"10.1007/s11011-025-01567-0","DOIUrl":"10.1007/s11011-025-01567-0","url":null,"abstract":"<p><strong>Background: </strong> The cognitive alterations observed in individuals undergoing cancer treatments have garnered more attention recently. Chemotherapy can reduce nicotinamide adenine dinucleotide (NAD+) levels by inhibiting nicotinamide phosphoribosyl transferase (NAMPT). This reduction can make cancer cells more susceptible to oxidative damage and death and may also affect non-cancerous cells, particularly the brain cells. During chemotherapy-induced suppression, the downregulation of the NAMPT-mediated NAD+/Sirtuin 1 (SIRT1) pathway may cause dyscognition. Objective: This study aimed to assess the role of quercetin and analogues in chemobrain and the associated mechanisms. Methods: The potential of quercetin and its derivatives interaction with NAMPT and SIRT1 proteins was performed using computational studies followed by their in vitro evaluation in SH-SY5Y cells. Molecular docking and simulation studies of human SIRT1 and NAMPT proteins with quercetin and its derivatives were performed. Differentiated SH-SY5Y cell lines were treated with quercetin and selected derivatives against Methotrexate and 5-Fluorouracil (MF) toxicity, by subjecting to cytotoxicity assay, flow cytometry, and RT-PCR analysis. Results: Quercetin, Rutin, and Isoquercetin showed interactions necessary in the activation process of both proteins. Cytotoxicity and flow cytometric studies demonstrated that the phytochemicals shield the differentiated SH-SY5Y cells from MF toxicity. As determined by RT-PCR investigations, NAMPT and SIRT1 gene mRNA expression was higher in test drug-treated cells at quercetin (0.12, 0.6 µM), rutin, and isoquercetin (16, 80 µM) and lower in MF-treated cells. Conclusion: The treatment of phytochemicals alleviated CICI by targeting NAMPT and SIRT1 proteins, which could lead to the identification of effective treatment strategies for the chemobrain.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"151"},"PeriodicalIF":3.2,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11909064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quercetin inhibited chronic unpredictable mild stress-induced mouse depressive behaviors through attenuating lateral Habenula neuronal activities.","authors":"Yu-Ting Cai, Dong-Ni Chen, Ke-Xin Li, Jia-Jia Dong, Chong Li, Ying-Kui Liu, Yong Liu","doi":"10.1007/s11011-025-01569-y","DOIUrl":"10.1007/s11011-025-01569-y","url":null,"abstract":"<p><p>As a flavonoid, quercetin has shown anti-tumor, anti-inflammation, and anti-depressant effects. However, the exact anti-depressant mechanism of quercetin remains unclear. In this study, a combination of behavioral tests and neuropharmacological methods were used to investigate whether the endocannabinoid (eCB) system in the lateral habenula (LHb) mediated the anti-depressant pathogenesis of quercetin. Depressive model was prepared by chronic unpredictable mild stress (CUMS) in C57 mice. The CUMS exposure led to depressive-like behaviors and an increase of the miniature excitatory postsynaptic current (mEPSC) frequency in the LHb neurons, which were blocked by quercetin intragastrically administered for 14 days. As quercetin has been shown to upregulate the mRNA expression of cannabinoid receptor 1 (CB1) in cultured tumor cells, and the inhibitory effect of eCB system activation is related to glutamatergic neurons, depolarization-induced suppression of excitation (sDSE) was detected. The results showed that presynaptic inhibitory effect of eCB system was significantly down-regulated in the LHb of CUMS model, and the down-regulation was abolished by quercetin. Blocking eCB system in the LHb with CB1 antagonist AM251 rescued the neuroprotective effects of quercetin in CUMS mice. Taken together, the results suggested that eCB system in the LHb was involved in the anti-depressant effects of quercetin.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"149"},"PeriodicalIF":3.2,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"JNK inhibition mitigates sepsis-associated encephalopathy via attenuation of neuroinflammation, oxidative stress and apoptosis.","authors":"Riya Gagnani, Harshita Singh, Manisha Suri, Anjana Bali","doi":"10.1007/s11011-025-01563-4","DOIUrl":"10.1007/s11011-025-01563-4","url":null,"abstract":"<p><p>Sepsis-associated encephalopathy (SAE) is a severe complication of sepsis, leading to cognitive dysfunction and neuronal damage. C-Jun N-terminal kinases (JNKs), a subset of the MAP kinase family, have attracted substantial interest for their role in cellular events during sepsis conditions. Previous investigations have established the involvement of JNK signaling against memory impairment and abnormal synaptic plasticity. However, the present study is the first to investigate the effects of JNK inhibition in sepsis-associated cerebral injury and cognitive impairments. This study investigated the neuroprotective effects of SP600125, a selective JNK inhibitor, in cecal ligation and puncture (CLP) mouse model of sepsis. CLP-induced sepsis resulted in significant cognitive impairments, as assessed by the open field test, inhibitory avoidance test, morris water maze, and novel object recognition test. Additionally, septic mice exhibited increased serum levels of neuronal injury markers (S100B and NSE), pro-inflammatory cytokines (TNF-α and IL-1β), and oxidative stress markers (MDA), along with decreased antioxidant levels (GSH, SOD, and CAT). Histological analysis revealed neuronal pyknosis, degeneration, and loss of Nissl bodies in the cortex and hippocampus of septic mice. Furthermore, sepsis-induced blood-brain barrier dysfunction was evident from increased cerebral edema. Treatment with SP600125 (10, 30, and 50 mg/kg) significantly attenuated CLP-induced cognitive deficits, neuronal injury, neuroinflammation, oxidative stress, and apoptosis in a dose-dependent manner. The present study provides preliminary evidence that JNK inhibition by SP600125 exerts neuroprotective effects against sepsis-induced encephalopathy in vivo via suppression of neuroinflammation, oxidative stress, and apoptosis.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"148"},"PeriodicalIF":3.2,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gamma-aminobutyric acid and glutamate system dysregulation in a small population of Egyptian children with autism spectrum disorder.","authors":"Nagwa Meguid, Susan Roushdy Ismail, Mona Anwar, Adel Hashish, Yuliya Semenova, Ebtesam Abdalla, Mohamed S Taha, Amal Elsaeid, Geir Bjørklund","doi":"10.1007/s11011-025-01557-2","DOIUrl":"10.1007/s11011-025-01557-2","url":null,"abstract":"<p><p>Autism spectrum disorder (ASD) is associated with various symptoms, including repetitive behaviors, restricted interests, and deficits in proper communication. Earlier studies have linked these symptoms to abnormalities in the balance between excitatory (glutamatergic signaling) and inhibitory (GABAergic signaling) neurotransmission. The present study aimed to analyze the levels of different biomarkers in children with ASD compared to neurotypical (NT) controls. The study included 80 children, of whom 40 were cases (children with ASD) and 40 were age- and sex-matched NT controls. Serum levels of GABA_A, and GABA_B receptors, glutamate, zinc, potassium, and calcium were measured in both groups. ASD diagnosis was verified using the Childhood Autism Rating Scale (CARS) and Autism Diagnostic Interview-Revised (ADI-R). There was a significant decrease (P < 0.001) in the median serum levels of GABA_A (0.6) and GABA_B receptors (2.03) in children with ASD compared to controls. Additionally, a significant increase in median serum glutamate levels was observed in ASD children (102, P < 0.001) compared to controls. Children with ASD also showed a significant reduction (P < 0.001) in median levels of all studied blood minerals compared to controls, including potassium (3.8 vs. 4.6), calcium (9.0 vs. 9.7), and zinc (57.0 vs. 92.0). The roles of GABA_B and zinc as potential pathological biomarkers were investigated due to their highly significant inverse correlations with stereotypic and repetitive behaviors (ADI-R domain), with rho = -0.393 (P = 0.012) and rho = -0.488 (P = 0.001), respectively. Further analysis of pathways regulating these biomarkers may provide deeper insights into the etiology and pathophysiology of ASD, paving the way for potential therapeutic interventions.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"146"},"PeriodicalIF":3.2,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Suppression of miR-218 promotes SOCS3 expression to alleviate cognitive impairment and white matter injury after chronic cerebral hypoperfusion.","authors":"Yuanyuan Zhu, Juan Tong, Jianzhong Jiang, Keyun Shi, Jing Xie, Yan Zhu, Yuefeng Li, Yuhao Xu","doi":"10.1007/s11011-025-01572-3","DOIUrl":"10.1007/s11011-025-01572-3","url":null,"abstract":"<p><p>Chronic cerebral hypoperfusion-induced white matter injury (WMI) is a significant cause of vascular cognitive impairment. Emerging evidence suggests that miR-218 may be involved in the pathogenesis of WMI. However, understanding of the relationship between miR-218 and chronic hypoperfusion-induced WMI remains insufficient. Our study investigated the relationship between miR-218 and chronic hypoperfusion-induced WMI at clinical, animal, and cellular levels. We found that serum miR-218 expression was elevated in clinical WMI patients, had a certain diagnostic efficacy for WMI, and was correlated with the degree of WMI, cognitive scores, and serum inflammatory factors. In addition, we constructed a mouse model with bilateral carotid artery stenosis (BCAS) to simulate chronic hypoperfusion-induced WMI and detected an increase in miR-218 expression in the white matter of BCAS mice. Following administration of Lv-sh-miR-218 to the white matter of BCAS mice, improvements were observed in both cognitive impairment and WMI. Furthermore, Lv-sh-miR-218 also reduced M1 polarization of microglia and neuroinflammation within the white matter. Subsequently, we confirmed that SOCS3 is the specific target of miR-218 through bioinformatics analysis and luciferase reporter gene assays. Injection of LV-SOCS3 into the white matter also led to improvements in cognitive impairment and WMI in BCAS mice, along with reduced M1 polarization of microglia and neuroinflammation. Moreover, in primary cultured microglia cells, we demonstrated that after chronic hypoxia, miR-218 regulates inflammatory factors through the SOCS3/STAT3 pathway. In summary, our current results indicate a strong correlation between elevated miR-218 levels and chronic hypoperfusion-induced WMI, and downregulation of miR-218 expression can improve neuroinflammation by upregulating SOCS3, thereby ameliorating WMI and cognitive impairment.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"147"},"PeriodicalIF":3.2,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating cuproptosis and mitochondrial dysfunction in brain cells: uncovering novel mechanisms and biomarkers for Parkinson's disease.","authors":"Qiuhong Li, Dongliang Li, Yinghong Li, Kunli Yang, Yankai Ren","doi":"10.1007/s11011-025-01574-1","DOIUrl":"10.1007/s11011-025-01574-1","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a chronic neurodegenerative condition marked by the gradual degeneration of dopaminergic neurons, resulting in a range of disabling motor and non-motor symptoms. Despite advances, the molecular mechanisms underlying PD remain elusive, and effective biomarkers and therapeutic targets are limited. Recent studies suggest that mitochondrial dysfunction and dysregulated cellular metabolism are central to PD pathogenesis. This study investigated cuproptosis-related genes (CRGs), a class of genes linked to mitochondrial function and metabolic pathways, as potential contributors to PD using in silico and in vitro analyses. By analyzing Gene Expression Omnibus (GEO) datasets, we identified a consistent downregulation of CRGs, including DLD, FDX1, LIPT1, LIAS, PDHB, DLAT, PDHA1, CDKN2A, MTF1, and GLS, in PD samples. Immune infiltration analysis and subcellular localization studies highlighted significant correlations with immune cells and mitochondrial localization, implicating CRGs in immune and metabolic dysregulation. Functional assays confirmed that overexpression of DLD and FDX1 promotes cell proliferation and migration, suggesting their involvement in PD progression. Diagnostic model analysis further demonstrated the strong potential of CRGs as biomarkers, with high Area Under the Curve (AUC) values indicating accuracy in distinguishing PD from controls. Additionally, miRNA-mRNA interaction and drug sensitivity analyses identified key regulatory microRNAs (miRNAs) and drug sensitivities associated with CRGs expression. Pathway enrichment analysis linked CRGs to essential mitochondrial and metabolic processes, providing insights into PD's underlying mechanisms. The findings of this study emphasize the diagnostic and therapeutic potential of CRGs in PD, offering a novel avenue for understanding and managing this complex disease.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"144"},"PeriodicalIF":3.2,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tetrapleura tetraptera fruit extracts ameliorate pentylenetetrazol-induced seizures as well as ensuing cognitive deficit and oxidative stress.","authors":"Moses B Ekong, Okokon O Bassey, Nelly A Pessu, Godslove V Kpobari, Ekereobong I Okuku, Rosemary B Bassey, Ekemini I Johnson, Aniekan I Peter, Jude E Okokon, Monday I Akpanabiatu","doi":"10.1007/s11011-025-01576-z","DOIUrl":"10.1007/s11011-025-01576-z","url":null,"abstract":"<p><p>Kindling is an experimental-induced seizure consistent with epilepsy disease, a chronic neurological disorder characterised by spontaneous and repeated seizures. This disease is associated with oxidative stress, and most therapeutic strategies against epilepsy aim at improving the antioxidant defence mechanism in the brain. However, prolonged usage and associated adverse side effects limit antiepileptics, warranting natural antioxidant patronage. The present study investigated the behavioural and antioxidant actions of Tetrapleura tetraptera fruit extracts (TT) against pentylenetetrazol (PTZ)-kindling rats. Twenty-five male Wistar rats (150-180 g) were assigned into five groups (1-5, n = 5): Control (normal saline, 5 ml/kg body weight, b.w.), PTZ-only (40 mg/kg/b.w. i.p.), and groups 3-5 administered PTZ (40 mg/kg/b.w. i.p.) after, respectively, receiving oral TT (500 mg/kg/b.w.), TT flavonoid (fTT, 50 mg/kg/b.w.), and sodium valproate (SV, 15 mg/kg/b.w.). All administrations were carried out 48 hourly for 21 days. In the end, buried food, novel object recognition (NOR), Y-maze, elevated plus maze (EPM), and beam walk tests were done, and the rats were sacrificed. Whole brains were processed for antioxidant assays. The results showed a high (p <.05) seizure score and buried food test latency, preference for the familiar object in the NOR test, aversion to open-arm and reduced grooming in the EPM, reduced beam walk latency, elevated brain malondialdehyde (MDA), and decreased superoxide dismutase (SOD) in the PTZ group. The TT, fTT, and SV suppressed seizure, decreased buried food latency, `preference for the novel object and open-arm, increased grooming, decreased brain MDA, and elevated SOD. In conclusion, TT extracts protected against PTZ-induced cognitive deficits and brain oxidative stress, with results similar to those of the standard anticonvulsant drug, SV.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"143"},"PeriodicalIF":3.2,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143615021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Probiotics ameliorates hypothalamic amenorrhea in a rat model of PCOS.","authors":"Stephanie E Areloegbe, Nsisong N Obong, Olabimpe C Badejogbin, Adesola A Oniyide, Isaac O Ajadi, Chukwubueze L Atuma, Mary B Ajadi, Oluseyi E Adelekan, Kehinde S Olaniyi","doi":"10.1007/s11011-025-01573-2","DOIUrl":"10.1007/s11011-025-01573-2","url":null,"abstract":"<p><strong>Background: </strong>Polycystic ovary syndrome (PCOS) is a common endocrinometabolic disorder affecting women of reproductive age, characterized by hormonal imbalances, irregular menstrual cycles, and often, infertility. Hypothalamic amenorrhea, a condition marked by the cessation of menstruation due to disruptions in the hypothalamic-pituitary-gonadal axis, is a frequent manifestation in PCOS. Probiotics, beneficial microorganisms known for improving metabolic health, have shown promise in restoring hormonal balance and enhancing fertility. In this study, we hypothesize that probiotics would ameliorate hypothalamic amenorrhea by modulating hypothalamic kisspeptin and reducing inflammation in a rat model of PCOS.</p><p><strong>Methods: </strong>Eight (8)-week-old female Wistar rats were grouped into four with n = 5. Letrozole administration (1 mg/kg, p.o.) for 21 days induced PCOS, thereafter the animals were treated with probiotics (3 × 10⁹ CFU, p.o.), while control animals received distilled water. The treatment lasted for six weeks.</p><p><strong>Results: </strong>Reduced insulin sensitivity, hyperinsulinemia, ovarian dysfunction with evidence of disrupted steroid hormone levels (testosterone/17β-Estradiol) and cystic follicles as well as hypothalamic lipid accumulation, elevated inflammatory markers (NF-kB/TNF-α) and antioxidant depletion (GSH/NrF2), which are accompanied by decreased level of kisspeptin. Nonetheless, administration of probiotics reversed these pathological alterations by enhancement of hypothalamic kisspeptin and suppression of inflammatory response.</p><p><strong>Conclusions: </strong>Altogether, the present results demonstrate that probiotics significantly ameliorated hypothalamic amenorrhea by mitigating hypothalamic lipid accumulation, suppressed inflammation, and replenished antioxidants. Crucially, probiotics enhanced hypothalamic kisspeptin levels, a key regulator of reproductive function, highlighting their potential as a therapeutic strategy for restoring ovarian function in PCOS.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"145"},"PeriodicalIF":3.2,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nanomedicine: a cost-effective and powerful platform for managing neurodegenerative diseases.","authors":"Majid Hassanzadeh-Khanmiri, Amirreza Moshari, Reza Kheradmand, Tannaz Haghgouei, Maryam Homaei, Saeid Charsouei, Ahmad Mobed","doi":"10.1007/s11011-025-01564-3","DOIUrl":"10.1007/s11011-025-01564-3","url":null,"abstract":"<p><p>Neurodegenerative diseases (NDDs) are characterized by the chronic and progressive deterioration of the structure and function of the nervous system, imposing a significant burden on patients, their families, and society. These diseases have a gradual onset and continually worsen, making early diagnosis challenging. Current drugs on the market struggle to effectively cross the blood-brain barrier (BBB), leading to poor outcomes and limited therapeutic success. Consequently, there is an urgent need for new diagnostic tools and treatment strategies. To address these challenges, nanotechnology-based drug delivery systems-such as liposomes, micelles, dendrimers, and solid lipid nanoparticles (SLNs)-have emerged as promising solutions. This study provides a comprehensive review of recent advances in nanomedicine and nanotechnology-based platforms, alongside an exploration of ND mechanisms. The authors conducted a systematic literature search across relevant databases such as PubMed, Scopus, and Web of Science, focusing on peer-reviewed articles, reviews, and clinical studies published within the last 5 to 10 years. Additionally, this paper addresses the challenges faced by nanomedicines and delivery systems, offering insights into future directions in the field and the need for further research to establish their clinical viability as alternatives to current therapies.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"142"},"PeriodicalIF":3.2,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143605708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}