SNCA_PIG SNCA ELISA tesk kit
- Known as:
- SNCA_PIG SNCA Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15681
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- SNCA_PIG SNCA ELISA tesk kit
Related genes to: SNCA_PIG SNCA ELISA tesk 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
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- Lewy body dementia (LBD) is a clinically and pathologically complex neurodegenerative disease. Its etiology remains poorly understood and, as such, it is likely underdiagnosed in clinical practice. Clinically, LBD is defined by fluctuations in cognition, visual hallucinations, rapid eye movement (REM) sleep behavior disorder (RBD), and motor dysfunction. The disease is pathologically defined by the presence of Lewy bodies in the brain, which are protein aggregates made up of misfolded α-synuclein; however, co-pathologies are often present and greatly complicate both symptom presentation and research interpretation. This heterogeneous pathology paired with overlapping clinical features of Alzheimer's disease and Parkinson's disease hinder diagnostic clarity. With no specific biological biomarkers currently identified, it is the hope that genetics can help with diagnosis and to clarify the pathomechanistic nature of this multifaceted disorder. Through rare familial studies, SNCA, the gene which encodes α-synuclein, was implicated in disease risk and development, underscoring its central role in α-synucleinopathies. Shortly after this discovery, a genome wide association study (GWAS) confirmed this risk, and identified two other major genes, APOE and GBA, to be associated with LBD. The APOE ε4 allele, which is a well-established risk factor for AD, is also associated with an increased risk for LBD. This common association demonstrates that APOE is implicated in a broader role in neurodegenerative disease pathogenesis. Meanwhile, GBA mutations, which are associated with lysosomal dysfunction and are also a known risk factor for PD, are linked to a more severe cognitive decline and earlier disease onset. However, even with these advances, our understanding of LBD's genetic architecture remains incomplete. Overcoming these limitations will require larger, more diverse study cohorts, comprehensive analyses, technological advances, and improved phenotyping upon clinical presentation of disease. Current clinical diagnostic strategies often struggle to capture the full spectrum of LBD symptoms and commonly lead to misdiagnosis/misclassification. By combining genetic data with improved phenotyping and the latest novel technologies, we can greatly improve our mechanistic understanding of LBD. These insights will not only improve diagnostic accuracy but will also lead to the development of disease modifying treatments specifically designed to best treat each individual patient. - Source: PubMed
Publication date: 2026/07/08
Watkins Molly MXhafkollari GiselaZhao NaRoss Owen A - Most insights into the genetics of Parkinson's disease (PD) arise from European cohorts, leaving the genomic diversity of India underexplored. To address this gap, we performed whole-genome sequencing of 197 Indian PD cases (106 with early-onset PD (EOPD) and 91 with late-onset PD (LOPD)), capturing SNVs, indels, splice, and structural variants. We identified pathogenic variants in 31 cases across seven PD-associated genes (GBA1, PRKN, PINK1, DJ1, SYNJ1, SNCA, and PLA2G6), giving a diagnostic rate of 27.6% in EOPD and 2.2% in LOPD. Seven of these variants were novel to Indian populations. GBA1 and PRKN were the most frequently mutated genes. Candidate genes with pathogenic variants were enriched in lysosomal pathways. Cases had significantly higher polygenic risk scores, supporting a polygenic contribution to PD risk. Our study establishes one of the first comprehensive sequencing-based resources for PD genetics in India, and underscores the need for large-scale genomic studies across diverse populations. - Source: PubMed
Publication date: 2026/07/06
Ali HibaMondal BanashreePinto AndieSarkar CamelliaPanda Bikram KumarRupanagudi Khader ValliHolla Vikram VNagaraj TarunyaBhat Shubha GsPrasad ShwetaBhardwaj MahimaMailankody PoojaMahale Rohan RKamble NitishYadav RaviPal Pramod KumarStezin AlbertDiwakar LathaRamdas Shweta - 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