METABOLIC BRAIN DISEASE代谢性脑病
METABOLIC BRAIN DISEASE(英文缩写 METAB BRAIN DIS),ISSN 0885-7490,eISSN 1573-7365,中文译名:代谢性脑病 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 3.655 | Q3 |
| 2022 | 3.600 | Q2 |
| 2023 | 3.200 | Q2 |
| 2024 | 3.500 | Q2 |
| 2025 | 3.800 | Q2 |
METABOLIC BRAIN DISEASE 最新收录文献
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1. Punica granatum L. peel extract mitigates hyperlipidemia-induced cognitive impairments in zebrafish larvae via modulating LXR signaling.
PMID:日期:2026-10-01Punica granatum L. is known to provide multiple health benefits against several diseased conditions, primarily hyperlipidemia, atherosclerosis, hyperglycemia and cognitive impairments. Many of its health benefits are attributed due to its antioxidant and anti-inflammatory properties. The purpose of the current study was to assess the in vivo effectiveness of an aqueous peel extract of Punica granatum (PuAq) against hyperlipidemia-induced cognitive impairments in a zebrafish larva model. The quantification of major bioactive metabolites of PuAq was done by a high-pressure liquid chromatography technique. The molecular association of the identified metabolites were assessed through in silico docking simulations. The lower confidence limit of the benchmark dose for PuAq in larvae was calculated to be 59.40 µg/mL. Thereafter, larvae at 4 days' post-fertilization were exposed to a 0.1% egg yolk solution with or without PuAq for the subsequent 5 days. Oil Red O staining showed reduced lipid deposition following PuAq treatment. Furthermore, PuAq incubation alleviated hyperlipidemia-induced cognitive decline in larvae subjected to the partition preference test. The extract treatment increased NeuN protein and bdnf expression within the larvae's cephalic region. The treatment modulated the expression of inflammation, oxidative stress, and lipid metabolism-related genes and reduced lipid peroxidation. The protective effects of PuAq were reverted following pre-exposure of GSK2033 (LXR antagonist), which suggested the involvement of LXR receptor activation for the observed changes. In silico docking simulations further supported the molecular interactions between the identified compounds of PuAq and LXR. The study concluded that PuAq protects against hyperlipidemia-induced cognitive impairments in zebrafish larvae.
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2. Metabolic and redox modulation by 2-deoxy-D-glucose and sodium selenite protects against pentylenetetrazole-kindled seizures, neuroinflammation and cognitive dysfunction.
PMID:日期:2026-09-29Cellular metabolism, disrupted brain bioenergetics adaptability and neuroinflammation are inextricably linked in epileptogenesis. Their pathological interplay exacerbates glutamatergic storming, free-radical induced excitotoxicity and glial reactivity leading to network hyperexcitability. Therefore, a novel metabolic approach concurrently targeting cerebral energy metabolism, oxidative stress and neuroinflammation represents a rationale approach for dual seizure control and neuroprotection. 2-deoxy-D-glucose (2DG) inhibits glycolysis while sodium selenite (NaSe) mediates potent anti-inflammatory and anti-oxidant effects. We assumed that the combined intervention would efficiently halt kindling, electroencephalographic ictal activity and associated progression of behavioral comorbidities in PTZ-induced murine model of epilepsy. Furthermore we also evaluated impact of 2DG+NaSe combination on neuroinflammatory markers, oxidative stress markers and histopathological changes in CA1, CA3 and DG subregions of cornu ammonis. Our results demonstrated that combination significantly reduced seizure scores with normalization of aberrant cortical epileptiform discharges and associated quantitative parameters (spike counts, average cyclic height and spiking frequency). This dual approach markedly halted PTZ-induced anxiety-like phenotype and cognitive decline as all animals showed good performance in relevant neurobehavioral assays (OFT, L/D, HBT, T-maze, NOR, and MWM). Mechanistically, combination might have altered glial reactivity and pro-inflammatory cytokines as evidenced by reduced mRNA expression levels of GFAP, IL-1β, and TNF-ɑ. In addition it prompts redox homeostasis (↑ SOD, CAT and GPx enzymatic activity and ↓ MDA levels) and preserved histoarchitecture across cornu ammonis subfields. These outcomes reinforces that concurrent metabolic and oxidative pathways targeting confers robust management of seizure burden and neuroprotection, positioning this combination as a potential multi-modal intervention for patients with DRE.
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3. Unraveling the role of FGF21 in epilepsy disease: mechanistic insights and therapeutic Potential.
3. 揭示FGF21在癫痫疾病中的作用：机制见解与治疗潜力PMID:日期:2026-09-29Epilepsy, progressive neurological disorder marked repeated seizures, producing aberrant neuronal excitability, followed by oxidative stress, mitochondrial malfunction, and neuroinflammation. Fibroblast growth factor 21 (FGF21), an endocrine member of the FGF family mainly secreted by liver, adipose tissue, and muscle, has turned out to be a potent neuromodulator in addition to its established as lipid and glucose homeostasis. According to studies, FGF21 can cross the Blood-brain barrier (BBB) and provide neuroprotection in experimental models of epilepsy via attenuation of neuronal hyperexcitability, inhibition of inflammation, and mitochondrial preservation. Mechanistically, FGF21 activates the Nrf2 antioxidant pathway, upregulating enzymes like catalase, thereby limiting production of reactive oxygen species. It further improves mitochondrial biogenesis dependent on Peroxisome Proliferator-Activated Receptor Gamma Coactivator-1 Alpha (PGC-1α) signaling, and suppresses ferroptosis, eventually decreasing susceptibility to seizures. Neuroinflammation is mediated by the downregulation of pro-inflammatory cytokines. Present evidence shows FGF21 administration significantly decreased seizure frequency and severity, underscoring its therapeutic promise. This review focuses on emerging evidence of FGF21's mechanistic actions in disease and its translational relevance novel adjunctive therapeutic strategy, offering opportunities for disease modification beyond conventional anti-seizure drugs.
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4. Randomized, placebo-controlled trial of N-acetylcysteine in Parkinson's disease patients: a pilot study.
4. N-乙酰半胱氨酸在帕金森病患者中的随机安慰剂对照试验：一项初步研究PMID:日期:2026-09-23This pilot trial evaluated the one-year tolerability of oral N-acetylcysteine (NAC) 1200 mg/day in Parkinson's disease (PD) and explored associations with clinical progression, levodopa dose, and striatal dopamine-transporter imaging. Forty-two patients were randomized to NAC or matching placebo twice daily for 12 months in addition to usual care. Completers (n = 32) were assessed at baseline and 12 months with the original UPDRS parts I-IV, 99mTc-TRODAT-1 SPECT, prescribed levodopa dose, and liver/kidney tests. Analyses included paired t-tests, Welch tests of change scores, and linear mixed-effects models with a group × time interaction adjusted for age, sex, and disease duration. No multiplicity correction was applied; results are exploratory. Thirty-two of 42 randomized patients completed both visits. Total UPDRS increased in both groups, but less with NAC than placebo (mean Δ + 5.4 vs. + 9.5 points; difference - 4.1, 95% CI - 7.6 to - 0.5; p = 0.028; mixed-model group × time p = 0.024). Mood-item change also differed (difference - 0.64, 95% CI - 1.17 to - 0.11; p = 0.020). TRODAT binding declined less with NAC (difference in change + 5.5 units, 95% CI 1.7 to 9.3; p = 0.006; group × time p = 0.004). The ≤ 4-year subgroup comprised 9/17 (53%) NAC and 7/15 (47%) placebo participants and showed a similar pattern. Levodopa-dose change was not significant between groups after ANCOVA adjustment for baseline dose, age, sex, and disease duration (adjusted difference - 86 mg/day, 95% CI - 235 to + 64; p = 0.25). Completer laboratory values were stable; discontinuations were not characterized for adverse events. One-year oral NAC was associated with more favorable exploratory clinical and imaging trajectories than placebo. Completer laboratories were unremarkable, but safety cannot be established from completers alone. These data do not establish disease modification and require confirmation in a larger, prospectively powered trial.
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5. Behavioral, neuroanatomic, and neuroinflammatory characteristics of metabolic syndrome in cafeteria diet-induced obese male rats.
PMID:日期:2026-09-23Obesity and metabolic syndrome are associated with low-grade systemic inflammation and neuroinflammation, potentially contributing to structural brain alterations and cognitive decline. This study evaluated brain volumetry, metabolic disturbances, neuroinflammation markers, and behavioral outcomes in a rat model of diet-induced obesity. Male Wistar rats were fed either a standard diet (CTRL; n = 6) or a cafeteria diet (CAF; n = 6) for five months from weaning. Metabolic parameters (weight, glucose tolerance, blood pressure, lipids), behavior (Open Field, Novel Object Recognition), and brain regional volumes (4.7 T MRI) were assessed. Neuroinflammatory markers (tumor necrosis factor-α levels (TNF-α) and glial fibrillary acidic protein (GFAP)) were quantified in the hypothalamus and olfactory bulb. CAF rats developed a metabolic syndrome-like phenotype characterized by abdominal adiposity, insulin resistance, hypertension, and dyslipidemia (p < 0.05). They also showed higher hypothalamic GFAP and TNF-α levels, higher relative orbitofrontal cortex volume (p < 0.05) than controls, whereas lower relative hypothalamic and corpus callosum volumes did not reach significance. Behaviorally, CAF rats exhibited reduced locomotor activity, impaired short-term memory, and higher grooming activity (p < 0.05). Multivariate modeling identified hypothalamic neuroinflammation, severity of continuous metabolic syndrome z-score, and reduced corpus callosum volume as key predictors of cognitive and behavioral impairments. Long-term consumption of a CAF diet induces key features of human metabolic syndrome, hypothalamic neuroinflammation, region-specific brain volumetric alterations, and cognitive deficits. These findings support a role for the metabolic-inflammatory axis in brain vulnerability and suggest that preservation of neuroimmune homeostasis may be important for maintaining cognitive health in obesity-associated metabolic disorders.
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6. Unraveling the regulatory nexus of aggrephagy in ALS: identification of novel candidate biomarkers and molecular triggers.
6. 揭示ALS中聚集自噬的调控网络：鉴定新型候选生物标志物和分子触发因素PMID:日期:2026-09-16Amyotrophic lateral sclerosis (ALS) is a progressive and ultimately fatal neurodegenerative disorder involving multiple systems, with motor neuron degeneration as its primary feature. This disease can be classified into sporadic and familial types. Genes such as SOD1, C9orf72, FUS, and TDP-43 have been identified as the main causative genes for familial ALS. Multiple bioinformatics tools combined with an experimental verification strategy have helped in understanding the association of a selective autophagy pathway called aggrephagy with the disease. The transcriptome data of spinal cord tissue from SOD1-G93A mice was obtained from the Gene Expression Omnibus (GEO) database. Based on the GSE281064 dataset, we investigated aggrephagy-related transcriptional alterations in the SOD1-G93A mouse model of ALS. After comparison with the aggrephagy-related genes (AGGRGs) set included in the GeneCards database, 49 candidate genes closely related to the autophagy process were obtained. Functional enrichment analysis showed these genes participate in extracellular matrix remodeling, hyaluronic acid and glycosaminoglycan metabolism, tumor necrosis factor regulation, and lysosomal function, indicating central roles in inflammation, apoptosis, and metabolic disorders. Based on feature selection algorithms, this study employed machine learning methods such as random forest (RF), extreme gradient boosting (XGBoost), and Boruta to conduct multi-angle screening of candidate genes. The intersection of the results ultimately identified three key genes: Ctsb, Kif11, and S100a6. In both the training data and external validation data, Ctsb and S100a6 showed significant upregulation and demonstrated excellent discriminatory capabilities. The nomogram constructed based on Ctsb and S100a6 expression showed potential for distinguishing SOD1-G93A model samples from nontransgenic controls. The predicted probability demonstrated the potential of these two as candidate biomarkers. Meanwhile, further validation is needed in larger independent population cohorts in the future. The SOD1-G93A mouse model and SOD1-G93A-expressing NSC34 cell model showed expression patterns of Ctsb and S100a6 consistent with the bioinformatics findings. Through S100a6 overexpression and knockdown experiments in an NSC34 motor neuron-like ALS model, we found that S100a6 impaired autophagy and promoted SOD1 aggregation. These findings further validate its potential as a biomarker and provide new insights into the pathogenesis of ALS.
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7. CRISPR-Enabled functional genomics in hPSCs-derived neural models for autism spectrum disorder.
7. 在hPSCs衍生的神经模型中利用CRISPR进行功能性基因组学研究以探究自闭症谱系障碍PMID:日期:2026-09-16Autism Spectrum Disorder (ASD) is a genetically heterogeneous neurodevelopmental condition in which hundreds of individually rare risk variants converge on a small number of shared biological pathways, including synaptic scaffolding, chromatin remodeling, excitation-inhibition balance, and cellular energy metabolism. Translating this genetic heterogeneity into mechanistic insight requires experimental systems capable of interrogating individual gene functions in human-relevant neural contexts at scale. CRISPR-enabled functional genomics in human pluripotent stem cell (hPSC)-derived neural models, spanning neural progenitors, cortical and inhibitory neurons, astrocytes, microglia, and brain organoids, provides precisely this capability. By integrating pooled perturbation screens with multimodal readouts including single-cell and spatial transcriptomics, chromatin accessibility profiling, proximity labeling proteomics, multi-electrode array electrophysiology, and metabolic flux analysis, these platforms enable systematic, causal mapping of ASD gene function at system resolution. Early applications have already revealed convergent mechanisms: BAF complex disruption expands the ventral progenitor pool and biases its fate toward oligodendrocyte and interneuron lineages; ADNP loss impairs microglial synaptic pruning through altered endocytic trafficking; and mTOR pathway dysregulation in PTEN- and TSC2-perturbed models links genetic risk directly to metabolic and mitochondrial dysfunction. Computational frameworks including MIMOSCA and SCEPTRE enable causal network reconstruction and pseudotime inference from these datasets, moving the field from gene lists toward pathway-level models of ASD pathobiology. Translational applications leverage isogenic iPSC panels and variant-level base and prime editing to stratify ASD variants by functional impact, informing gene therapy design for haploinsufficient targets such as CHD8 and SCN2A via AAV or antisense oligonucleotide delivery. Remaining challenges, including model developmental immaturity, batch variability, and the difficulty of modeling polygenic risk, are addressed by a roadmap integrating spatial perturbomics, AI-driven causal inference, and population-scale standardized biobanks. This review synthesizes the current state of CRISPR-based functional genomics in human stem cell neural models as a coherent experimental framework for converting ASD genetic associations into mechanistic understanding and therapeutic opportunity.
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8. Significance of NAD anabolism profiles in neurological diseases.
8. NAD合成代谢谱在神经系统疾病中的意义PMID:日期:2026-09-14Neurons are post-mitotic polarized cells with a higher energy budget which is required to maintain ion gradients, axonal trafficking, firing, and synaptic transmission. The increased cell surface area resulting from the extension of the neuronal membrane and the protrusion of axoplasm from the soma also significantly amplifies neuronal energy demands. To achieve bioenergetic homeostasis, neurons have a higher metabolic rate and engage in continuous NAD production. Biosynthesis of NAD occurs via the enzymatic conversion of tryptophan, and breakdown in NAD biosynthesis leads to neuronal deterioration and the accumulation of tryptophan metabolites in affected brain regions. There exists a good body of evidence linking associations between several neurological disorders and tryptophan metabolites, aberrant expression of NAD biosynthesis enzymes, and polymorphisms in genes encoding enzymes. This review describes the involvement of NAD biosynthetic enzymes in neuropathogenesis and disease. Further, it discusses the association of CNS disorders with various polymorphisms and altered levels of tryptophan metabolites in biofluids, as well as the prognostic value of NAD-associated biomolecules in neurological diseases. Together, the review suggests that quantifying tryptophan-catabolizing enzymes and tryptophan catabolites involved in NAD biosynthesis in biofluids provides a minimally invasive means to monitor neurodegenerative and neuropsychiatric processes. This approach offers a prognostic insight into disease progression, treatment efficacy, and individualized risk assessment.
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9. AMPK activation by Aldometanib from Bigujing improves metabolic and cognitive dysfunction in aging mice.
9. 比居精中的Aldometanib通过激活AMPK改善衰老小鼠的代谢和认知功能障碍PMID:日期:2026-09-12Aging-related cognitive decline is closely associated with disrupted energy metabolism and impaired autophagic clearance in the brain. Aldometanib, an active ingredient from the traditional formulation Bigujing, exerts systemic metabolic benefits, but its effects on brain aging and the underlying mechanisms remain unclear. This study aims to evaluate the efficacy of Aldometanib in mitigating cognitive decline in D-galactose-induced aging mice, and to elucidate its potential mechanisms involving AMPK-mediated energy metabolism and autophagy regulation. Male C57BL/6 J mice were treated with D-gal for 42 days, with or without 100 μg/mL Aldometanib in drinking water. Cognitive function was evaluated using the novel object recognition test, Y-maze test, and the Morris water maze test. Brain tissues were analyzed for neuronal morphology, the total antioxidant capacity (T-AOC) and the expressions of senescence, AMPK/ACC pathway and autophagy-related proteins (p-mTOR, LC3B-II, P62). In vitro assays validated Aldometanib's mechanistic effects in D-gal-treated C8-D1A astrocytes and Neuro-2a cells. Aldometanib significantly mitigated D-gal-induced weight loss and cognitive deficits and alleviated neuronal atrophy and loss in the hippocampus and cortex. Aldometanib downregulated the expression of senescence markers P53, P21 and P16 and increased T-AOC levels. Mechanistically, Aldometanib specifically activated the AMPK/ACC pathway in neurons and astrocytes, suppressed mTOR phosphorylation and P62 accumulation, and enhanced autophagy both in vivo and in vitro. Aldometanib can effectively ameliorate the cognitive and physiological decline in aged mice by activating AMPK, suppressing mTOR and promoting autophagy, and enhancing antioxidant capacity. It represents a promising therapeutic candidate for age-related neurodegenerative diseases.
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10. Dihydromyricetin ameliorates cognitive dysfunction in SAMP8 mice via autophagy-mediated degradation of the NLRP3 inflammasome.
10. 二氢杨梅素通过自噬介导的NLRP3炎症小体降解改善SAMP8小鼠的认知功能障碍PMID:日期:2026-09-12Alzheimer's disease (AD) is characterized by progressive cognitive decline and neuropathology, but its mechanisms remain incompletely understood. Impaired autophagy and overactivation of the NLRP3 inflammasome are thought to contribute to AD progression. Dihydromyricetin (DHM) is a natural flavonoid with known neuroprotective effects, yet it remains unclear whether DHM modulates the autophagy-lysosome pathway to suppress NLRP3 inflammasome activation and improve cognitive deficits. Here, we combined bioinformatics predictions with in vitro and in vivo experiments to investigate DHM's effects on autophagy and NLRP3 inflammasome signaling. Bioinformatic analysis of aging, AD, and cognition-related gene sets identified autophagy and immune regulation as key enriched pathways. Molecular docking predicted that DHM binds favorably to core autophagy and inflammasome proteins. In vitro, DHM (6.25-25 µg/mL) increased autophagy in BV2 microglia, as evidenced by an increased LC3-II/LC3-I ratio and ULK1 expression and reduced p62 accumulation, and markedly reduced LPS/ATP-induced upregulation of NLRP3, cleaved caspase-1, IL-1β, and IL-18. DHM also reduced LPS-induced intracellular ROS accumulation in BV2 cells and attenuated NF-κB p65 phosphorylation in SAMP8 hippocampus. In vivo, 8-week oral administration of DHM to senescence-accelerated mouse-prone 8 (SAMP8) mice, an accelerated aging model with AD-like cognitive and pathological features, enhanced hippocampal autophagy marker expression, reduced NLRP3 inflammasome-related proteins and AD-related pathological protein changes. Immunofluorescence and Western blot analyses showed that DHM increased the spatial association of NLRP3 with LC3- and LAMP1-positive structures, reduced ASC expression, and increased the lysosomal protease Cathepsin D. These molecular changes corresponded with improved spatial learning and memory in the Morris water maze. However, co-treatment with the autophagy inhibitor chloroquine (CQ) abolished the DHM's effects on autophagy markers, reversed its reduction of NLRP3-related inflammatory proteins, and negated its cognitive benefits. Taken together, these results suggest that DHM enhances autophagy-lysosome pathway activity and facilitates autophagy-associated suppression of NLRP3 inflammasome activation, thereby mitigating neuroinflammation and cognitive impairment in SAMP8 mice. This autophagy-dependent mechanism suggests that DHM, a well-tolerated natural compound, has potential as a multitarget therapeutic candidate for AD-like cognitive impairment.