Metabolic brain disease最新文献_第4页

Manuscript title: unravelling the neuroprotective role of miR-27a-3p in the MAPK pathway in Parkinson's disease.

IF 3.2 3区医学

Metabolic brain disease Pub Date : 2025-03-11 DOI: 10.1007/s11011-025-01568-z

Zahra Moradi Vastegani, Rasoul Ghaedi-Heidari, Andisheh Oroujalian, Maryam Peymani, Kamran Ghaedi

{"title":"Manuscript title: unravelling the neuroprotective role of miR-27a-3p in the MAPK pathway in Parkinson's disease.","authors":"Zahra Moradi Vastegani, Rasoul Ghaedi-Heidari, Andisheh Oroujalian, Maryam Peymani, Kamran Ghaedi","doi":"10.1007/s11011-025-01568-z","DOIUrl":"10.1007/s11011-025-01568-z","url":null,"abstract":"Parkinson's disease (PD) is a multifaceted neurodegenerative disorder characterized by dopaminergic neuron loss and the presence of Lewy bodies. Beyond its hallmark motor symptoms, PD involves significant neuroinflammation and immune dysfunction, driven by dysregulated signalling pathways such as the Mitogen-Activated Protein Kinase (MAPK) pathway. This study investigates the therapeutic potential of hsa-miR-27a-3p in modulating these pathways, with a focus on its interaction with MKK7, a key MAPK component. Bioinformatics and experimental analyses, using miRNA-mRNA interactions and construct a protein-protein interaction (PPI) network, confirm that hsa-miR-27a-3p directly binds to the 3' untranslated region (3'UTR) of MKK7, reducing its expression. Overexpression of hsa-miR-27a-3p improves cell viability, mitigates morphological changes, and reduces neurotoxicity in SH-SY5Y (human neuroblastoma cell line for experimental validation) cells exposed to MPP +, a PD neurotoxin. The study further demonstrates that hsa-miR-27a-3p modulates apoptotic pathways by increasing anti-apoptotic BCL2 while downregulating pro-apoptotic BAX and P53, as assessed through Western blot analysis of protein expression in SH-SY5Y cells transfected with miR-27a-3p mimic or negative control, followed by quantification of protein levels. Additionally, hsa-miR-27a-3p suppresses neuroinflammatory responses by significantly reducing TNF-α and IL1β levels. Western blot analysis reveals that hsa-miR-27a-3p inhibits phosphorylation of MKK7 and other MAPK pathway components, such as JNK and p38, highlighting its role in attenuating neuroinflammation and oxidative stress. These findings establish a negative correlation between hsa-miR-27a-3p expression and key neurodegenerative processes, suggesting its potential as a therapeutic target. This study provides comprehensive insights into the neuroprotective mechanisms of hsa-miR-27a-3p, paving the way for innovative interventions in PD management.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"141"},"PeriodicalIF":3.2,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143605705","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}

引用次数: 0

Impact of L-thyroxine on hippocampal activity, morphology, and behavioral performance in thyroidectomized rats.

IF 3.2 3区医学

Metabolic brain disease Pub Date : 2025-03-10 DOI: 10.1007/s11011-025-01566-1

Lilit Darbinyan, Karen Simonyan, Lilia Hambardzumyan, Larisa Manukyan, Kristine Karapetyan, Margarita Danielyan

{"title":"Impact of L-thyroxine on hippocampal activity, morphology, and behavioral performance in thyroidectomized rats.","authors":"Lilit Darbinyan, Karen Simonyan, Lilia Hambardzumyan, Larisa Manukyan, Kristine Karapetyan, Margarita Danielyan","doi":"10.1007/s11011-025-01566-1","DOIUrl":"10.1007/s11011-025-01566-1","url":null,"abstract":"Thyroid hormones, particularly L-thyroxine, are integral to cognitive processes like learning and memory. However, electrophysiological and morphological evidence connecting thyroid hormone activity to hippocampal function remains limited. This study aims to investigate the electrophysiological, morphological, and behavioral effects of L-thyroxine treatment in thyroidectomized (TX) rats, addressing the complex interplay between thyroid hormone regulation and hippocampal function. Adult male and female Wistar rats were assigned to three groups: TX, TX + L-thyroxine (10 µg/100 g/day, i.p., administered one week post-surgery for 4 weeks), and vehicle-control. Behavioral assessments were conducted prior to electrophysiological and morphological recordings. Under urethane anesthesia, hippocampal electrical activity was recorded following entorhinal cortex stimulation, while morphological changes were assessed in the capillary networks of both the hippocampus and the paraventricular nucleus. Results revealed significant changes in hippocampal electrophysiological responses in the L-thyroxine-treated group, including enhanced synaptic plasticity, increased excitatory activity, and more frequent, synchronized neuronal firing in the CA1 and CA3 regions. Additionally, L-thyroxine treatment led to changes in capillary morphology. This integrative study bridges electrophysiological, morphological, and behavioral approaches, enhancing our understanding of thyroid hormone influence on hippocampal function. The findings suggest that the observed electrophysiological and morphological changes could contribute to the cognitive and memory-related symptoms reported by individuals with thyroid dysfunction.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"140"},"PeriodicalIF":3.2,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143597397","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}

引用次数: 0

Retraction Note: The effects of Cinnamaldehyde on early brain injury and cerebral vasospasm following experimental subarachnoid hemorrhage in rabbits.

IF 3.2 3区医学

Metabolic brain disease Pub Date : 2025-03-07 DOI: 10.1007/s11011-025-01561-6

Bora Gürer, Hayri Kertmen, Pınar Kuru Bektaşoğlu, Özden Çağlar Öztürk, Hüseyin Bozkurt, Abdullah Karakoç, Ata Türker Arıkök, Erhan Çelikoğlu

引用次数: 0

Hepatic encephalopathy: risk identification and prophylaxis approaches.

IF 3.2 3区医学

Metabolic brain disease Pub Date : 2025-03-07 DOI: 10.1007/s11011-025-01531-y

Aldo Torre, Jacqueline Córdova-Gallardo, Froylan David Martínez-Sánchez

{"title":"Hepatic encephalopathy: risk identification and prophylaxis approaches.","authors":"Aldo Torre, Jacqueline Córdova-Gallardo, Froylan David Martínez-Sánchez","doi":"10.1007/s11011-025-01531-y","DOIUrl":"10.1007/s11011-025-01531-y","url":null,"abstract":"Hepatic encephalopathy (HE) is a debilitating neurological condition associated with cirrhosis, characterized by cognitive impairment ranging from minimal to overt symptoms. It significantly impacts patients' quality of life and substantially burdens healthcare systems. This review examines current prophylactic strategies for HE, focusing on established treatments, emerging therapies, and predictive tools to identify high-risk patients. Traditional treatments such as lactulose and rifaximin remain the cornerstone of HE management, effectively reducing ammonia levels and preventing recurrence. However, novel approaches like L-ornithine L-aspartate, albumin infusions, and antioxidants like resveratrol show promise in further improving outcomes by addressing underlying pathophysiological mechanisms, including systemic inflammation and gut dysbiosis. Developing predictive models, such as the AMMON-OHE score and clinical-genetic risk assessments, enhances the ability to tailor preventive interventions to individual patient profiles. These advancements are crucial in mitigating the incidence of overt HE, reducing hospital admissions, and improving patient survival rates. The future of HE management lies in personalized medicine, targeting specific inflammatory and metabolic pathways, with the potential integration of genetic manipulation. Continued research is essential to refine these strategies, ultimately aiming to improve the prognosis and quality of life for cirrhotic patients at risk of HE.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"138"},"PeriodicalIF":3.2,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573474","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}

引用次数: 0

Astaxanthin nanoemulsion improves cognitive function and synaptic integrity in Streptozotocin-induced Alzheimer's disease model.

IF 3.2 3区医学

Metabolic brain disease Pub Date : 2025-03-06 DOI: 10.1007/s11011-025-01560-7

Mazzura Wan Chik, Meor Mohd Redzuan Meor Mohd Affandi, Nurul Aqmar Mohd Nor Hazalin, Gurmeet Kaur Surindar Singh

{"title":"Astaxanthin nanoemulsion improves cognitive function and synaptic integrity in Streptozotocin-induced Alzheimer's disease model.","authors":"Mazzura Wan Chik, Meor Mohd Redzuan Meor Mohd Affandi, Nurul Aqmar Mohd Nor Hazalin, Gurmeet Kaur Surindar Singh","doi":"10.1007/s11011-025-01560-7","DOIUrl":"10.1007/s11011-025-01560-7","url":null,"abstract":"Astaxanthin derived from natural sources has excellent antioxidant and anti-inflammatory effects, and it is currently being widely researched as a neuroprotectant. However, astaxanthin possesses low oral bioavailability, and thus, astaxanthin extract from Haematococcus pluvialis was formulated into a nanoemulsion to improve its bioavailability and administered to Alzheimer's disease (AD)-like rats to study its possible neuroprotective benefits. Astaxanthin nanoemulsion was administered orally once a day for 28 days to streptozotocin (STZ)-induced AD rats at concentrations of 160, 320, and 640 mg/kg of body weight (bw) and subsequently assessed for cognitive function using behavioral assessments. Brain samples were collected for the assessment of AD biomarkers. Astaxanthin nanoemulsion at a dosage of 640 mg/kg bw significantly improved spatial learning, spatial memory, and recognition memory against STZ-AD rats. At 320 and 640 mg/kg bw, astaxanthin nanoemulsion significantly reduced levels of hippocampus synaptosomal amyloid beta and paired-helical fibrillary tau protein while increasing neuron survival. Additionally, astaxanthin nanoemulsion at 640 mg/kg bw significantly increased acetylcholine levels in the hippocampus and cerebellum. Astaxanthin nanoemulsion at all treatment dosages significantly reduced malondialdehyde, a lipid peroxidation product, and neuroinflammatory mediators (GFAP and TNF-α). Astaxanthin nanoemulsion supplementation has the potential to improve cognitive function and synaptic function by lowering amyloid beta and tau levels, as well as preserve neuron integrity by reducing neuroinflammation and lipid peroxidation, indicating that it may be able to treat some of the underlying causes of AD.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"136"},"PeriodicalIF":3.2,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567502","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}

引用次数: 0

The impact and mechanisms of YL-IPA08, a potent ligand for the translocator protein (18 kDa) on protection against LPS-induced depression and cognitive dysfunction in rodents.

IF 3.2 3区医学

Metabolic brain disease Pub Date : 2025-03-06 DOI: 10.1007/s11011-025-01565-2

Lin-Yu Cui, Jing-Yao Duan, Jiao-Zhao Yan, Jing-Ya Wang, Peng Ren, Li-Ming Zhang, Wen-Zhi Guo, Wei Dai, Yun-Feng Li

{"title":"The impact and mechanisms of YL-IPA08, a potent ligand for the translocator protein (18 kDa) on protection against LPS-induced depression and cognitive dysfunction in rodents.","authors":"Lin-Yu Cui, Jing-Yao Duan, Jiao-Zhao Yan, Jing-Ya Wang, Peng Ren, Li-Ming Zhang, Wen-Zhi Guo, Wei Dai, Yun-Feng Li","doi":"10.1007/s11011-025-01565-2","DOIUrl":"10.1007/s11011-025-01565-2","url":null,"abstract":"Translocator protein (18 kDa) (TSPO) has been implicated in the development of depression and cognitive dysfunction. This study aimed to investigate the anti-depression/anti-anxiety and cognitive enhancing impacts and potential mechanisms of TSPO ligand YL-IPA08 in lipopolysaccharide (LPS)-induced inflammatory model. The effects of YL-IPA08 in LPS induced mice were identified by behavioral tests, and the target of YL-IPA08 was validated using the TSPO antagonist PK11195. The microglia in PFC were analyzed by immunofluorescence, and the inflammatory cytokines (IL-6, IL-1β and TNF-α) and anti-inflammatory factors (IL-4, IL-10, TGF-β1) in PFC was detected by ELISA or WB. Effect of TGF-β1 inhibitor Repsox on the actions of YL-IPA08 in LPS-treated mice was further verified. We found that YL-IPA08 administration ameliorated LPS-induced depression/anxiety-like behaviors and cognitive impairment, which were blocked by PK11195. YL-IPA08 reversed the increased number and inflammatory morphological changes of microglia in PFC of LPS mice by targeting TSPO. YL-IPA08 reversed the increased inflammatory cytokines (IL-6, IL-1β and TNF-α) and decreased anti-inflammatory factors (IL-4, IL-10) in the PFC of LPS mice by TSPO activation. In addition, YL-IPA08 elevated the suppressed levels of TGF-β1 and smad3 (member of TGF-β1 pathway) in PFC of LPS mice by TSPO activation. TGF-β1 inhibitor Repsox blocked the anti-depression/anxiety and cognition enhancing effects of YL-IPA08 in LPS mice. Our data implicated that central inflammation regulation and TSPO-TGF-β1/Smad pathway activation contributed to the anti-depressant/anxiety and cognitive promoting impacts of YL-IPA08.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"137"},"PeriodicalIF":3.2,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143567524","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}

引用次数: 0

Edaravone dextranol alleviates ferroptosis, Cuproptosis, and blood-brain barrier damage after acute cerebral infarction.

IF 3.2 3区医学

Metabolic brain disease Pub Date : 2025-03-03 DOI: 10.1007/s11011-025-01559-0

Guimin Jin, Wei Han, Tingting Duan, Zongwei Xue, Chenglin Song, Yuhao Xu, Ming Yu

{"title":"Edaravone dextranol alleviates ferroptosis, Cuproptosis, and blood-brain barrier damage after acute cerebral infarction.","authors":"Guimin Jin, Wei Han, Tingting Duan, Zongwei Xue, Chenglin Song, Yuhao Xu, Ming Yu","doi":"10.1007/s11011-025-01559-0","DOIUrl":"10.1007/s11011-025-01559-0","url":null,"abstract":"Edaravone dextrose (EDB) is a commonly used clinical treatment for cerebral infarction due to its anti-inflammatory and free radical scavenging properties. However, its potential additional neuroprotective mechanisms need to be further investigated. In this study, we evaluated the effects of EDB on ferroptosis, cuproptosis, and blood-brain barrier (BBB) disruption after cerebral infarction in vivo and in vitro by constructing a mouse middle cerebral artery occlusion (MCAO) model, and an oxygen-glucose deprivation/reperfusion (OGD/R) model of neurons and brain microvascular endothelium. Our results showed that EDB treatment improved neurological impairment and brain histopathology in MCAO mice. EDB treatment significantly alleviated ferroptosis and cuproptosis in MCAO mice and OGD/R models of neuronal, in vitro and in vivo, the protective pathway of ferroptosis SLC7A11/GPX4 was detected to be activated and the cuproptosis-promoting protein SLC31A1 and FDX1 were down-regulated. We also found that EDB treatment ameliorated BBB damage in MCAO mice. The endothelial cell protective pathway PDGFRβ/PI3K/AKT activation was also detected in MCAO mice and OGD/R models of endothelial cells after EDB treatment. In conclusion, our study demonstrated that EDB has a good ameliorating effect on ferroptosis, cuproptosis, and BBB damage after cerebral infarction, which provides more evidence for the clinical application of EDB and provides new theories and directions for the study of the mechanism of EDB.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"134"},"PeriodicalIF":3.2,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542613","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}

引用次数: 0

Correction to: Anti-inflammatory, anti-apoptotic, and neuroprotective potentials of anethole in Parkinson's disease-like motor and non-motor symptoms induced by rotenone in rats.

IF 3.2 3区医学

Metabolic brain disease Pub Date : 2025-03-03 DOI: 10.1007/s11011-025-01547-4

Sadegh Moradi Vastegani, Seyed Esmaeil Khoshnam, Esrafil Mansouri, Samireh Ghafouri, Nima Bakhtiari, Yaghoob Farbood, Alireza Sarkaki

引用次数: 0

Combined treatment of Ketogenic diet and propagermanium reduces neuroinflammation in Tay-Sachs disease mouse model.

IF 3.2 3区医学

Metabolic brain disease Pub Date : 2025-02-28 DOI: 10.1007/s11011-025-01553-6

Orhan Kerim Inci, Volkan Seyrantepe

{"title":"Combined treatment of Ketogenic diet and propagermanium reduces neuroinflammation in Tay-Sachs disease mouse model.","authors":"Orhan Kerim Inci, Volkan Seyrantepe","doi":"10.1007/s11011-025-01553-6","DOIUrl":"10.1007/s11011-025-01553-6","url":null,"abstract":"Tay-Sachs disease is a rare lysosomal storage disorder caused by β-Hexosaminidase A enzyme deficiency causing abnormal GM2 ganglioside accumulation in the central nervous system. GM2 accumulation triggers chronic neuroinflammation due to neurodegeneration-based astrogliosis and macrophage activity with the increased expression level of Ccl2 in the cortex of a recently generated Tay-Sachs disease mouse model Hexa-/-Neu3-/-. Propagermanium blocks the neuroinflammatory response induced by Ccl2, which is highly expressed in astrocytes and microglia. The ketogenic diet has broad potential usage in neurological disorders, but the knowledge of the impact on Tay-Sach disease is limited. This study aimed to display the effect of combining the ketogenic diet and propagermanium treatment on chronic neuroinflammation in the Tay-Sachs disease mouse model. Hexa-/-Neu3-/- mice were placed into the following groups: (i) standard diet, (ii) ketogenic diet, (iii) standard diet with propagermanium, and (iv) ketogenic diet with propagermanium. RT-PCR and immunohistochemistry analyzed neuroinflammation markers. Behavioral analyses were also applied to assess phenotypic improvement. Notably, the expression levels of neuroinflammation-related genes were reduced in the cortex of 140-day-old Hexa-/-Neu3-/- mice compared to β-Hexosaminidase A deficient mice (Hexa-/-) after combined treatment. Immunohistochemical analysis displayed correlated results with the RT-PCR. Our data suggest the potential to implement combined treatment to reduce chronic inflammation in Tay-Sachs and other lysosomal storage diseases.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"133"},"PeriodicalIF":3.2,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11870964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143523846","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}

引用次数: 0

Pharmacological modulation of PI3K/PTEN/Akt/mTOR/ERK signaling pathways in ischemic injury: a mechanistic perspective.

IF 3.2 3区医学

Metabolic brain disease Pub Date : 2025-02-26 DOI: 10.1007/s11011-025-01543-8

Heena Khan, Aditi Singh, Yashvardhan Singh, Diksha Sharma, Kamal Dua, Amarjot Kaur Grewal, Thakur Gurjeet Singh

{"title":"Pharmacological modulation of PI3K/PTEN/Akt/mTOR/ERK signaling pathways in ischemic injury: a mechanistic perspective.","authors":"Heena Khan, Aditi Singh, Yashvardhan Singh, Diksha Sharma, Kamal Dua, Amarjot Kaur Grewal, Thakur Gurjeet Singh","doi":"10.1007/s11011-025-01543-8","DOIUrl":"10.1007/s11011-025-01543-8","url":null,"abstract":"Ischemia, also known as ischemia, relates to the reduced blood movement to a cells, muscle group, or organ in the body, culminating in an insufficient amount of oxygen required for cellular metabolism and the maintenance of tissue viability. There are different types of stroke (ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage), and different causes of stroke (e.g., cardioembolic, atherothrombotic, lacunar ischemic strokes, aneurysmal subarachnoid hemorrhage). It also includes other disorders affecting the blood vessels in the brain (e.g., vascular malformations, unruptured aneurysms). Each of these conditions has different characteristics in terms of how common they are and how they are managed. Stroke is the primary and catastrophic clinical presentation of all cerebrovascular diseases. In this review we focused about the importance of PI3K/AKT signaling pathways which are important in the onset of ischemia-reperfusion (I/R) injury. In addition, mTOR, a target that is activated by the PI3K/Akt signaling pathway, is both required and capable of providing enough protection to the heart against harm caused by I/R. Moreover, the signaling pathways that involve PI3K/Akt/Erk/PTEN/mTOR play a crucial role in facilitating the proliferation and maintenance of neurons following an ischemic stroke. The current review summarizes the molecular mechanisms of various signaling pathways in ischemic diseases and suggests targeting its receptors as a preventive approach based on pre-clinical and clinical studies.","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 3","pages":"131"},"PeriodicalIF":3.2,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143502487","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}

引用次数: 0