Bovine Alpha-Synuclein,SNCA ELISA Kit
- Known as:
- Bovine Alpha-Synuclein,SNCA Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- YHB0009BO
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- yehua
- Gene target:
- Bovine Alpha-Synuclein SNCA ELISA Kit
Related genes to: Bovine Alpha-Synuclein,SNCA ELISA Kit
- Gene:
- SNCA NIH gene
- Name:
- synuclein alpha
- Previous symbol:
- PARK1, PARK4
- Synonyms:
- NACP, PD1
- Chromosome:
- 4q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-01-24
- Date modifiied:
- 2018-04-18
Related products to: Bovine Alpha-Synuclein,SNCA ELISA Kit
Related articles to: Bovine Alpha-Synuclein,SNCA ELISA Kit
- To investigate how visceral adiposity and insulin resistance, defined respectively by visceral adiposity index (VAI) and triglyceride-glucose (TyG) index, jointly influence gut microbiota composition and immune transcriptomes in metabolic dysfunction-associated steatotic liver disease (MASLD), and to explore potential mechanistic pathways. - Source: PubMed
Publication date: 2026/07/02
Tung Chien-YiLin Yi-HsuanChang Ya-YuanRuan Jhen-WeiChen Pei-ChenChen Chian-FengYeh Hsiao-YunShen Hsiao-ChinTsai Hung-ChengLi Tzu-HaoSu Chien-WeiYang Ying-YingHou Ming-Chih - The pathological characteristics of Parkinson's Disease (PD) are multifactorial, encompassing the aggregation of α-synuclein, mitochondrial dysfunction, and oxidative stress, necessitating the adoption of multitarget therapeutic strategies. In this study, a borneol-modified carboxymethyl chitosan nanoparticle system (BC/P/HCR NPs) was developed, aiming to codeliver curcumin, rosmarinic acid, and plasmid DNA (pDNA) targeting the SNCA gene for synergistic therapeutic intervention in PD. Borneol is capable of enhancing the permeability of the blood-brain barrier (BBB), while carboxymethyl chitosan contributes to improving the solubility of curcumin and preventing premature drug release. In a C57BL/6 mouse model of PD, BC/P/HCR NPs demonstrated enhanced penetration through the BBB, effectively alleviating motor dysfunction and reducing neuronal damage by downregulating the expression of α-synuclein, restoring mitochondrial function, and mitigating oxidative stress. These findings underscore the potential of BC/P/HCR NPs as a multifunctional nanotherapeutic platform for addressing the complex pathological features of PD. - Source: PubMed
Publication date: 2026/07/02
Cheng YuxueZhai LiminWang HaoyuanLiao BeiningChe JingfengMa KuoHuang GuoweiPan ShengjunYang HaoGuan Yan-Qing - Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are primary tauopathies defined by aggregation of four-repeat (4R) tau, yet early diagnosis remains limited by the dissociation between clinical phenotype and molecular pathology. Clinical presentations are heterogeneous, evolve over time, and frequently overlap with Alzheimer's disease, synucleinopathies, and mixed pathologies, particularly in corticobasal syndrome. As a result, clinical criteria provide structured phenotypic classification but have constrained specificity in early disease. This review synthesizes current evidence relevant to early diagnostic stratification in 4R tauopathies, integrating clinical criteria, supportive biomarkers of neurodegeneration, and emerging tau-directed molecular tools. The probabilistic value and limitations of contemporary criteria frameworks are discussed alongside the role of structural and functional imaging, dopaminergic imaging, and fluid markers as indicators of disease intensity and progression rather than molecular specificity. Advances in tau positron emission tomography and tau seed amplification assays are reviewed as biologically grounded approaches that directly interrogate aggregated and seed-competent tau species, with growing evidence for their potential contribution to individual-level stratification. Collectively, the literature supports a layered diagnostic approach in which clinical phenotype, supportive biomarkers, and tau-directed molecular measures are integrated to refine attribution of 4R tau pathology , a prerequisite for mechanism-based therapeutic development. - Source: PubMed
Publication date: 2026/06/16
Bernhardt Alexander MHöglinger Günter UPalleis Carla - Distant metastasis, predominantly to the liver, remains the leading cause of death in colorectal cancer (CRC), yet biomarkers that capture metastatic competence remain limited. Ferroptosis is an iron-dependent, lipid peroxidation-driven form of regulated cell death that can restrain tumor progression, but whether primary CRC from patients with liver metastasis shows ferroptosis-resistance-related features remains incompletely understood. In a small exploratory set of T-stage-matched primary CRC tumors with or without liver metastasis, we quantified glutathione redox and lipid peroxidation-related readouts and assessed SLC7A11 and GPX4 expression. We integrated GSE62321 transcriptomic profiles with a FerrDb ferroptosis gene set, evaluated prognosis in TCGA-COAD/READ, and performed genetic knockdown, MDA assays, C11-BODIPY lipid ROS staining, ferrostatin-1 rescue assays, and Transwell assays in CRC cell models. Primary tumors from patients with liver metastasis showed a more reduced redox profile and increased expression of core ferroptosis-suppressive proteins, consistent with enhanced ferroptosis resistance potential but not direct evidence of lower in vivo ferroptotic cell death. Integrative discovery highlighted fatty acid binding protein 4 (FABP4), α-synuclein (SNCA), and discoidin domain receptor 2 (DDR2) as CRC-LM-associated ferroptosis-related candidates. High expression of each gene was associated with unfavorable disease-free survival. In CRC cell models, including the lymph-node-metastasis-derived SW620 line and additional validation lines, silencing FABP4, SNCA, or DDR2 increased bulk MDA and/or C11-BODIPY-detected lipid ROS, altered ferroptosis susceptibility, and suppressed migratory and/or invasive phenotypes. Ferrostatin-1 partially rescued knockdown-induced viability loss, lipid ROS accumulation, and migratory/invasive defects, supporting involvement of ferroptosis-associated lipid peroxidation while not excluding broader stress-response mechanisms. FABP4, SNCA, and DDR2 are CRC-LM-associated ferroptosis-related candidates that modulate lipid peroxidation, ferroptosis susceptibility, and migratory/invasive phenotypes in CRC cell models, warranting further validation in viability-controlled and liver metastasis-specific models. - Source: PubMed
Publication date: 2026/06/30
Ge ZhengGuo WeiLi JingxinWang YanqingWang Kexin - Understanding the genetic foundations of dementia is critical to unraveling its complex molecular basis. Given that a clinical diagnosis of Alzheimer's disease (AD) dementia often results from interplay between multiple underlying neuropathologic co-morbidities, previous genome-wide association studies (GWAS) of clinically diagnosed AD are restricted in their ability to translate genetic associations to potential targeted therapeutics. The current study seeks to address these limitations by presenting the largest GWAS to date (n = 12,509) of neuropathologic hallmarks of AD and AD related dementias (ADRDs). We further performed a candidate-variant analysis using loci previously identified in GWAS of clinically diagnosed AD dementia and Parkinson's disease (PD). Finally, we conducted heritability and genetic correlation analyses using linkage disequilibrium (LD) score regression. We found broad genome-wide significant associations with APOE across AD and ADRDs but not cerebrovascular disease and vascular brain injury. We further identified 12 significant loci across 10 neuropathologic phenotypes, including 5 loci previously implicated in GWAS of clinical AD and ADRDs (variants on BIN1, PICALM/ EED, TMEM106B, GRN, and SNCA/ SNCA-AS1) and 7 novel genome-wide associations (variants on EPHA5, PSMG1, LINC00276, VAPA, LINC00290, DOCK4 and SLAIN2/ SLC10A4). Our analysis of AD and PD clinical candidate variants demonstrated several that were associated with AD neuropathologic change and Lewy body disease, as well as substantial overlap with neuropathologic lesions other than the primary neuropathologic hallmarks of these diseases. Heritability analyses demonstrated heritability that was high for amyloid plaques (78%) relative to prior clinical AD heritability analyses, intermediate for TDP-43 inclusions (41%), and low for remaining AD and ADRD pathologic features. This study underscores the importance of investigating the underlying neuropathologic hallmarks of AD and ADRDs as a step toward refining the translation of genetic associations to biomarker interpretation and development of targeted therapeutics. - Source: PubMed
Publication date: 2026/06/29
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