Metabolic brain disease最新文献

{"title":"Ginkgo biloba extract mediates HT22 cell proliferation and migration after oxygen-glucose deprivation/reoxygenation via regulating RhoA-ROCK2 signalling pathway.","authors":"Dexiu Wang, Xin Zhao, Jinghan Li, Yang Song, Weida Chen, Xin Cai, Ruofan Liu, Zetao Chen","doi":"10.1007/s11011-024-01502-9","DOIUrl":"https://doi.org/10.1007/s11011-024-01502-9","url":null,"abstract":"<p><p>Vascular dementia (VD) is a neurocognitive disorder resulting from cerebral vascular disorders, leading to the demise of neurons and cognitive deficits, posing significant health concerns globally. Derived from Ginkgo biloba leaves, EGb761 is a potent bioactive compound widely recognized for its benefits in treating cerebrovascular diseases. Previous studies have demonstrated that the administration of EGb761 to VD rats enhances the proliferation, differentiation, and migration of neurons, effectively alleviating cognitive dysfunction. However, the specific mechanisms by which EGb761 exerts its remedial influence on VD persist in ambiguity. This investigation utilized an integrated approach incorporating network pharmacology with experimental procedures on HT-22 mouse hippocampal neuronal cells amidst oxygen-glucose deprivation and reoxygenation (OGD/R) to delve into certain repercussions of EGb761 on cell proliferation and migration. Results revealed that ras homolog family member A (RHOA) and B-cell lymphoma 2 (BCL-2) are potential targets of Ginkgo biloba leaves. Target genes are mainly enriched in pathways including those involved in growth hormone synthesis, secretion and action and the neurotrophin signalling pathway. Cellular experiments further demonstrated that the application of EGb761 notably enhanced the viability, proliferation, and migration of HT22 cells subjected to OGD/R through RhoA-ROCK2 pathway. In conclusion, our findings indicated that EGb761 significantly enhances neuronal proliferation and migration following OGD/R injury by targeting the RhoA-ROCK2 signalling pathway, thus offering valuable insights into its potential as a treatment for VD.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"91"},"PeriodicalIF":3.2,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11706868/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143055996","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":"Metabolic disorders after traumatic brain injury: a narrative review of systemic consequences.","authors":"Amanda C S Kursancew, Cristiano Julio Faller, Eloa M Piva-Uchida, Isadora B Benedet, Pedro M Maciel, Shaiane M de Figueredo, Fabricia Petronilho, Luciane B Ceretta, Emilio Streck, Jaqueline S Generoso","doi":"10.1007/s11011-024-01524-3","DOIUrl":"10.1007/s11011-024-01524-3","url":null,"abstract":"<p><p>Traumatic brain injury (TBI) is characterized as a heterogeneous and pathological remodeling of brain physiology because of various external mechanisms, including blows, falls, and rapid acceleration and deceleration of the skull. Its pathophysiology consists of two distinct moments, beginning with a primary lesion resulting from the impact that evolves into a secondary lesion as biochemical and molecular mechanisms are activated. The severity and prognosis after TBI vary widely, depending on factors such as the site of the injury, the patient's premorbid history, and the severity of the injury, and can result in long-term sequelae impacting multiple organs and systems, with a reduction in the life expectancy of these individuals. A relevant point to be investigated is the correlation between metabolic syndrome (MS), defined as the combination of glucose intolerance, dyslipidemia, systemic arterial hypertension (SAH), and acute or chronic coronary heart disease, and the prognosis of these individuals after a TBI. Therefore, this review seeks to verify the correlation between the occurrence of MS in patients who have suffered TBI as a pre-existing comorbidity and whether it develops later, looking for evidence in studies based on animal models and cohort follow-ups of individuals who have suffered TBI in the short and long term to assess the prognosis presented.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"93"},"PeriodicalIF":3.2,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142951773","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":"New insights on the regulators and inhibitors of RhoA-ROCK signalling in Parkinson's disease.","authors":"Nandita Ravichandran, Mahalaxmi Iyer, Deenathayalan Uvarajan, Laxmi Kirola, Sindduja Muthu Kumra, Harysh Winster Suresh Babu, Dibbanti HariKrishnaReddy, Balachandar Vellingiri, Arul Narayanasamy","doi":"10.1007/s11011-024-01500-x","DOIUrl":"10.1007/s11011-024-01500-x","url":null,"abstract":"<p><p>A multifaceted and widely prevalent neurodegenerative disease, Parkinson's disease (PD) is typified by the loss of dopaminergic neurons in the midbrain. The discovery of novel treatment(s) that can reverse or halt the course of the disease progression along with identifying the most reliable biomarker(s) in PD remains the crucial concern. RhoA in its active state has been demonstrated to interact with three distinct domains located in the central coiled-coil region of ROCK. RhoA appears to activate effectors most frequently by breaking the intramolecular autoinhibitory connections, which releases functional domains from the effector protein. Additionally, RhoA is highly expressed in the nervous system and it acts as a central molecule for its several downstream effector proteins in multiple signalling pathways both in neurons and glial cells. Mitochondrial dysfunction, vesicle transport malfunction and aggregation of α-Synuclein, a presynaptic neuronal protein genetically and neuropathologically associated with PD. While the RhoA-ROCK signalling pathway appears to have a significant role in PD symptoms, suggesting it could be a promising target for therapeutic interventions. Thus, this review article addresses the potential involvement of the RhoA-ROCK signalling system in the pathophysiology of neurodegenerative illnesses, with an emphasis on its biology and function. We also provide an overview of the state of research on RhoA regulation and its downstream biological activities, focusing on the role of RhoA signalling in neurodegenerative illnesses and the potential benefits of RhoA inhibition as a treatment for neurodegeneration.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"90"},"PeriodicalIF":3.2,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142951774","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":"Jaranol alleviates cognitive impairment in db/db mice through the PI3K/AKT pathway.","authors":"Ye Qian, Yue Xu, Qiuyu Zhang, Chengyu Huang, Hui Li, Lin Gao, Shidi Wu, Chengyu Qi, Xiangru Wen, Xiaoyan Zhou, Changjiang Ying","doi":"10.1007/s11011-024-01527-0","DOIUrl":"https://doi.org/10.1007/s11011-024-01527-0","url":null,"abstract":"<p><p>The widely used Radix Astragali (RA) has significant therapeutic effects on cognitive impairment (CI) caused by type 2 diabetes (T2DM). However, the effective active ingredients and the precise mechanism underly RA alleviation of T2DM-induced CI still require further study. In this study, we aim to elucidate whether and how jaranol, a key effective active ingredient in RA, influences CI in db/db mice. We used various online databases and Cytoscape to screen jaranol as the most active ingredient of RA in the treatment of T2DM-induced CI. The fear conditioning experiment, new object recognition (NOR) test, and Morris water maze (MWM) test were conducted to assess the improvement effect of jaranol on CI in diabetic mice. The protein-protein interaction (PPI) network, Cytoscape, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to identify key genes. The levels of AKT and caspase-3 were determined by Western blotting. The number of surviving hippocampal neurons was verified through Nissl staining. AutoDock was utilized for predicting potential binding sites between jaranol and key genes.As a result, jaranol attenuated CI in db/db mice probably through activation of PI3K-AKT signaling pathway by inhibiting cell apoptosis in hippocampus. Furthermore, A329 near the active site of AKT1 had hydrogen bond with jaranol. In conclusion, we suggest that jaranol may have therapeutic applications in T2DM-induced CI by targeting the PI3K-AKT signaling pathway directly via key sites. Our study provides alternative drugs and potential therapeutic targets for the prevention and treatment of T2DM-induced CI.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"88"},"PeriodicalIF":3.2,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142932276","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":"Resilience mechanisms underlying Alzheimer's disease.","authors":"Chu Shi Chew, Jia Yee Lee, Khuen Yen Ng, Rhun Yian Koh, Soi Moi Chye","doi":"10.1007/s11011-024-01507-4","DOIUrl":"https://doi.org/10.1007/s11011-024-01507-4","url":null,"abstract":"<p><p>Alzheimer's disease (AD) consists of two main pathologies, which are the deposition of amyloid plaque as well as tau protein aggregation. Evidence suggests that not everyone who carries the AD-causing genes displays AD-related symptoms; they might never acquire AD as well. These individuals are referred to as non-demented individuals with AD neuropathology (NDAN). Despite the presence of extensive AD pathology in their brain, it was found that NDAN had better cognitive function than was expected, suggesting that they were more resilient (better at coping) to AD due to differences in their brains compared to other demented or cognitively impaired patients. Thus, identification of the mechanisms underlying resilience is crucial since it represents a promising therapeutic strategy for AD. In this review, we will explore the molecular mechanisms underpinning the role of genetic and molecular resilience factors in improving resilience to AD. These include protective genes and proteins such as APOE2, BDNF, RAB10, actin network proteins, scaffolding proteins, and the basal forebrain cholinergic system. A thorough understanding of these resilience mechanisms is crucial for not just comprehending the development of AD but may also open new treatment possibilities for AD by enhancing the neuroprotective pathway and targeting the pathogenic process.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"86"},"PeriodicalIF":3.2,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142932294","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":"Eugenol attenuates aluminium-induced neurotoxicity in rats by inhibiting the activation of STAT3 and NF-кB.","authors":"Chandra Prakash, Jyoti Tyagi, Kumari Vandana Singh, Gautam Kumar, Deepak Sharma","doi":"10.1007/s11011-024-01526-1","DOIUrl":"https://doi.org/10.1007/s11011-024-01526-1","url":null,"abstract":"<p><p>Aluminium is a common metallic toxicant that easily penetrates the brain and exerts severe pathological effects e.g., oxidative stress, inflammation and neurodegeneration. Eugenol is a natural phenolic compound possessing numerous therapeutic properties including antioxidant, anti-inflammatory and neuroprotective. The compound has also been reported to interfere with important transcription factors like STAT3 and NF-кB. Thus, the present study intended to explore the therapeutic potential of eugenol in aluminium neurotoxicity. Rats were administered AlCl₃ (100 mg/kg b. wt., orally) and eugenol (200 mg/kg b. wt., orally) alone or in combination for 45 days. The results revealed that AlCl₃ administration increases acetylcholinesterase (AChE) activity, lipid peroxidation (LPO), and protein oxidation (PO) along with decreasing superoxide dismutase (SOD) and catalase (CAT) activities, and glutathione (GSH) content in the cortex and hippocampus regions of the brain. Moreover, AlCl₃ induces neuronal loss and astroglial activation in both brain areas. The study further revealed that AlCl₃ also increases the expression of transcription factors STAT3 and NF-кB in neurons and astrocytes of the cortex and hippocampus. However, co-administration of eugenol with AlCl₃ restored the enzymatic activities of AChE, SOD and CAT, and GSH content, and rescued the cortex and hippocampus from LPO, PO, neuronal loss and astroglial activation. Furthermore, the study reported that eugenol reverses the expression pattern of STAT3 and NF-кB in AlCl₃-intoxicated rats. In conclusion, the study suggests that eugenol ameliorates oxidative stress, neuronal loss and reactive astrogliosis in aluminium-induced neurotoxicity by inhibiting signalling molecules, STAT3 and NF-кB.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"87"},"PeriodicalIF":3.2,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142932272","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":"Metabolomics analyses and comparative insight to neuroprotective potential of unripe fruits and leaves of Citrus aurantium ethanolic extracts against cadmium-induced rat brain dysfunction: involvement of oxidative stress and akt-mediated CREB/BDNF and GSK3β/NF-κB signaling pathways.","authors":"Doaa A H Deabes, Eman A W El-Abd, Sara M Baraka, Zeinab A El-Gendy, Reda M S Korany, Marwa M Elbatanony","doi":"10.1007/s11011-024-01513-6","DOIUrl":"10.1007/s11011-024-01513-6","url":null,"abstract":"<p><p>Serious neurological disorders were associated with cadmium toxicity. Hence, this research aimed to investigate the potential neuroprotective impacts of the ethanolic extracts of Citrus aurantium unripe fruits and leaves (CAF and CAL, respectively) at doses 100 and 200 mg/kg against cadmium chloride-provoked brain dysfunction in rats for 30 consecutive days. HPLC for natural pigment content revealed that CAF implied higher contents of Chlorophyll B, while the CAL has a high yield of chlorophyll A and total carotenoid. Fifty-seven chromatographic peaks were identified by UPLC/MS/MS; 49 and 29 were recognized from CAF or CAL, respectively. Four compounds were isolated from CAF: 3',4',7 -trihydroxyflavone, isorhainetin, vitexin, and apigenin. In vitro studies outlined the antioxidant capacity of studied extracts where CAF showed better scavenging radical DPPH activity. Results clarified that both extracts with a superior function of CAF at the high adopted dose significantly ameliorated CdCl₂-induced neuro-oxidative stress and neuro-inflammatory response via restoring antioxidant status and hindering nuclear factor kappa B (NF-κB) stimulation. Moreover, it up-regulated the levels of phospho-protein kinase B (p-Akt), phospho- cAMP-response element binding protein (p-CREB), and brain-derived neurotropic factor (BDNF) levels, and elicited a marked decrease in the content of glycogen synthase kinase 3 beta (GSK3β), besides amending Caspase-3 and hyperphosphorylation of tau protein in brain tissues. Moreover, a significant improvement in the rats' behavioral tasks of the CAL and CAF-treated groups has been recorded, as indicated by marked preservation in locomotion, exploratory, and memory functions of the experimental rats. In conclusion, the reported neuroprotective impacts of C. aurantium extracts may be through modulating p-AKT/p-CREB/BDNF and / or p-Akt/ GSK3β/NF-κB signaling pathways.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"89"},"PeriodicalIF":3.2,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11703990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142932290","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":"Associations between stress hyperglycemia and outcomes in patients with ischemic stroke and TIA: the data comes from the Third China National Stroke Registry (CNSR-III).","authors":"Guojuan Chen, Xue Xia, Yijun Zhang, Xiaoli Zhang, Jing Li, Xia Meng, Anxin Wang","doi":"10.1007/s11011-024-01499-1","DOIUrl":"https://doi.org/10.1007/s11011-024-01499-1","url":null,"abstract":"<p><p>In the acute stage of stroke, stress hyperglycemia is common in both diabetic and nondiabetic patients. The associations between stress hyperglycemia and functional outcomes, as well as stroke recurrence were heterogeneous in previous studies. We aimed to demonstrate these associations in a general population of patients with ischemic stroke and transient ischemic attack (TIA). We included patients with complete data on blood glucose and hemoglobin from The Third China National Stroke Registry. The stress hyperglycemia ratio (SHR) was calculated using fasting blood glucose (mmol/L) divided by glycosylated hemoglobin A1c (%). Outcomes included functional disability, recurrent ischemic stroke and TIA, combined vascular events, and all-cause mortality at 90 days. In total, 7186 patients were included (median age: 62 [54-70] years, male: 4864 [67.69%], TIA: 589 [8.20%]). SHR levels were significantly associated with functional disability (adjusted OR: 1.69, 95%CI: 1.22-2.33). For every 1 standard deviation increment in SHR, the risk of functional disability increased by 13%. Compared to the patients in SHR Tertile 1, those in Tertile 3 had a 1.31-fold increased risk of functional disability (95%CI: 1.08-1.60). There was a trend indicating that the risk of functional disability increased with higher SHR tertiles (P for trend = 0.0074). Stroke severity explained 42.94% of the total excess association between SHR and functional disability. However, neither SHR levels nor SHR tertiles were associated with recurrent ischemic stroke and TIA, combined vascular events, or all-cause mortality. This study found that admission stress hyperglycemia was associated with functional disability, which was partially mediated by stroke severity.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"82"},"PeriodicalIF":3.2,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927608","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":"Alzheimer's disease and diabetes-associated cognitive dysfunction: the microglia link?","authors":"Yaqiong Liu, Tao Li, Juliang Xiong","doi":"10.1007/s11011-024-01516-3","DOIUrl":"https://doi.org/10.1007/s11011-024-01516-3","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is characterized by the accumulation of amyloid-β (Aβ) plaques and the aggregation of tau protein, resulting in intense memory loss and dementia. Diabetes-associated cognitive dysfunction (DACD) is a complication of diabetes mellitus, which is associated with decreased cognitive function and impaired memory. A growing body of literature emphasize the involvement of microglia in AD and DACD. Although AD and DACD share some common features related to symptomatology and pathophysiology, the characteristics and heterogeneity of microglia remain largely unknown in these two diseases. In this study, multiple bioinformatics analyses were performed to analyze the frequency, altered genes, cell-cell communication, and subtypes of microglia in AD and DACD mouse models based on two publicly single-nucleus RNA sequencing (snRNA-Seq) datasets. The results revealed that the frequency of microglia was increased in both AD and DACD mouse models when compared with control mice. After analyzing the differentially expressed genes of microglia from the two mouse models, only six common upregulated genes were found. The CellChat analysis revealed the complex cell-cell communication network (microglia clusters with other cell types) in 5XFAD vs. control mice and db/db vs. control mice. The microglia subtypes and their transcription factor activity profile in 5XFAD mice were different from that in db/db mice. In summary, this study provided some insights into the alterations of microglia in 5XFAD and db/db mice, which might open up potential avenues for the microglial-targeted therapy in AD and DACD.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"85"},"PeriodicalIF":3.2,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927574","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":"Exosomes and non-coding RNAs: bridging the gap in Alzheimer's pathogenesis and therapeutics.","authors":"Guo Chunhui, You Yanqiu, Chen Jibing, Luo Ning, Li Fujun","doi":"10.1007/s11011-024-01520-7","DOIUrl":"10.1007/s11011-024-01520-7","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a neurodegenerative disease that primarily affects the elderly population and is the leading cause of dementia. Meanwhile, the vascular hypothesis suggests that vascular damage occurs in the early stages of the disease, leading to neurodegeneration and hindered waste clearance, which in turn triggers a series of events including the accumulation of amyloid plaques and Tau protein tangles. Non-coding RNAs (ncRNAs), including long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs), have been found to be involved in the regulation of AD. Furthermore, lncRNAs and circRNAs can act as competitive endogenous RNAs to inhibit miRNAs, and their interactions can form a complex regulatory network. Exosomes, which are extracellular vesicles (EVs), are believed to be able to transfer ncRNAs between cells, thus playing a regulatory role in the brain by crossing the blood-brain barrier (BBB). Exosomes are part of the intercellular carrier system; therefore, utilizing exosomes to deliver drugs to recipient cells might not activate the immune system, making it a potential strategy to treat central nervous system diseases. In this review, we review that AD is a multifactorial neurological disease and that ncRNAs can regulate its multiple pathogenic mechanisms to improve our understanding of the etiology of AD and to simultaneously regulate multiple pathogenic mechanisms of AD through the binding of ncRNAs to exosomes to improve the treatment of AD.</p>","PeriodicalId":18685,"journal":{"name":"Metabolic brain disease","volume":"40 1","pages":"84"},"PeriodicalIF":3.2,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11700052/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927609","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}