bACE1 ELISA kit
- Known as:
- bACE1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-bACE1-Mu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- bACE1 ELISA kit
Related genes to: bACE1 ELISA kit
- Gene:
- BACE1 NIH gene
- Name:
- beta-secretase 1
- Previous symbol:
- BACE
- Synonyms:
- -
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-29
- Date modifiied:
- 2016-10-05
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- Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory loss, and neuronal death. Approved therapies, including acetylcholinesterase inhibitors and NMDA receptor antagonists, provide only symptomatic relief without halting progression. AD involves multifaceted pathologies: amyloid-β (Aβ) accumulation, tau hyperphosphorylation, oxidative stress, neuroinflammation, mitochondrial dysfunction, and apoptosis. Multi-target natural compounds like ginsenosides from Panax ginseng show promise in preclinical models by modulating these pathways. Key ginsenosides (Rg1, Rb1, Rc, Rd, Re, Rg3) inhibit Aβ production (via BACE1 suppression and α-secretase enhancement), promote Aβ clearance (via IDE/NEP upregulation), reduce tau phosphorylation (via GSK-3β/CDK5 modulation), and exert antioxidant, anti-inflammatory, and anti-apoptotic effects. Limited clinical evidence from small open-label trials of Korean Red Ginseng suggests cognitive improvements (e.g., in ADAS-cog and MMSE scores), with good tolerability. However, poor oral bioavailability and limited blood-brain barrier (BBB) penetration remain challenges, addressable via intranasal or nanoparticle delivery. While preclinical data are robust, clinical translation is limited by study heterogeneity and small samples. Ginsenosides warrant further investigation as adjunctive multi-target agents for AD. - Source: PubMed
Publication date: 2026/05/15
Oriquat GhalebAli Afaq MahdiH MalathiAhmad Israa AbdulhameedMaharana LaxmidharChauhan Ashish SinghArora VimalPurohit BilakshanKumar-Mishra Manoj - Poly(ADP-ribose) (PAR) polymerase 1 (PARP1) has been implicated in DNA damage responses and neuroinflammation in Alzheimer's disease (AD), yet its role in amyloid-beta (Aβ) pathology remains unclear. Here, we show that PARP1 activation drives Aβ pathology and neurodegeneration. Using a sensitive enzyme-linked immunosorbent assay, we observed significantly elevated PAR levels in the cerebrospinal fluid (CSF) of patients with mild cognitive impairment (MCI) and AD compared to controls. In vitro, oligomeric Aβ activated PARP1 and induced DNA damage, while genetic or pharmacological inhibition of PARP1 conferred neuroprotection. In vivo, PARP1 knockout in the 5XFAD mouse model of amyloidosis led to reduced amyloid plaque burden, preserved synaptic and neuronal integrity, attenuated glial activation and neuroinflammation, and rescued cognitive deficits. Mechanistically, PARP1 deficiency decreased amyloid precursor protein and BACE1 levels, altered γ-secretase complex composition, and enhanced Aβ degradation via neprilysin. These findings position PARP1 as a critical mediator of Aβ toxicity and neurodegeneration, suggesting its inhibition as a promising therapeutic strategy for AD. - Source: PubMed
Publication date: 2026/05/15
Jhaldiyal AanishaaKumari ManishaGuttman Lauren CTripathi TruptiKhan Mohammed ReponWang JustinBiswas DevanikPasupuleti AbhishekAggarwal AkanshaPandya ShraddhaChou Shih-ChingPanicker NikhilMonghekar AbhayAlbert MarilynBekris Lynn MLeverenz James BKam Tae-InDawson Ted MDawson Valina L - Diet quality, beyond total fat, may shape the immune tone of the brain in Alzheimer's-relevant contexts. We examined whether the fatty acid profile and food matrix of high-fat diets (HFD) modulate hippocampal neuroinflammation and explored target-level mechanisms with molecular docking. Male B6129SF2/J mice received a standard diet (SD) or HFD enriched with extra-virgin olive oil (EVOO), refined olive oil (ROO), refined palm oil (RPO), or ω3 long-chain polyunsaturated fatty acids (ω3-LCPUFA). During the final week, scopolamine induced acute cholinergic dysfunction. Neuroinflammation was assessed in the dentate gyrus by IHC (Iba-1, COX-2, and TNF-α) and by IF of astrocytes (GFAP intensity and morphology). Docking was employed to evaluate interactions of oleic and palmitic acids, EPA, and DHA with AChE, COX-2, BACE1, and TREM2. All HFD groups attenuated scopolamine-induced increases in Iba-1, COX-2 and TNF-α compared with the SD-scopolamine group, with limited separation among lipid classes under this acute stressor. By contrast, astroglial readouts showed a clear hierarchy: EVOO-HFD produced the lowest GFAP signal and the most ramified morphology, followed closely by ω3-LCPUFA, with ROO being intermediate and SFA being the least favourable. Docking supported a mechanistic framework: EPA/DHA displayed stronger predicted engagement than oleate/palmitate at COX-2 and BACE1, while long-chain fatty acids occupied the AChE peripheral site and a lipid/apoE-responsive surface on TREM2. In conclusion, PUFA-rich feeding, and notably that with the EVOO matrix, preferentially buffers hippocampal neuroinflammation in a scopolamine-induced Alzheimer's-like model. These findings support a composition, binding, and function framework and strengthen the translational rationale for precision nutrition strategies prioritizing ω3-LCPUFA and high-quality olive oils. - Source: PubMed
Publication date: 2026/05/14
Albertuni MarluaTorrecillas-Lopez MariaGonzalez-de la Rosa TeresaBarrera-Chamorro LunaMarquez-Paradas ElviraDel Rio-Vazquez Jose LNavarro-Hortal Maria DClaro-Cala Carmen MMontserrat-de la Paz Sergio - Alzheimer's disease (AD) is characterized by extracellular β-amyloid (Aβ) deposition and intracellular Tau hyperphosphorylation, yet upstream factors that coordinately regulate both pathologies remain poorly understood. Here, we identify proline-rich transmembrane protein 3 (PRRT3) as a previously unrecognized, neuron-enriched upstream regulator of AD dual pathology. PRRT3 expression is elevated in brain tissues from AD patients and exhibits abnormal persistence in / mice. knockdown markedly reduces , , and mRNA expressions, thereby decreasing Aβ generation in neuronal cells. Mechanistically, PRRT3 promotes the expressions of these amyloidogenic genes via activation of the activator protein-1 (AP-1) complex, as evidenced by reduced phosphorylation of c-Fos and c-Jun after knockdown. Transcriptomic profiling further reveals broad downregulation of calcium signaling-related receptors and intracellular calcium-handling proteins, accompanied by attenuated calcium signaling and ERK activity. Artificially elevating intracellular calcium with thapsigargin completely reverses the neuroprotective effects of knockdown, restoring both the Ras-ERK-AP-1-dependent amyloidogenic machinery and CaMKII/PP2A-mediated Tau hyperphosphorylation. In parallel, knockdown shifts the balance between the Ca -dependent Tau kinase CaMKII and the phosphatase PP2A, leading to reduced Tau hyperphosphorylation at multiple AD-relevant sites. Collectively, these findings establish PRRT3 as a neuron-enriched upstream regulator linking calcium dysregulation to both amyloidogenic processing and Tau phosphorylation. Targeting PRRT3 may therefore represent a promising strategy to simultaneously modulate the two core pathological processes in AD. - Source: PubMed
Publication date: 2026/05/25
Chen FeiZhang HaohanHuang YaruZhu JieCui FangLiang ShiyuLi YangjieWang YujiongXie XixiuLiu Ruitian - : Long-term diabetes mellitus may precipitate severe complications, including cognitive dysfunction. Existing research has shown that diabetic cognitive impairment (DCI) in rats is characterized by memory deterioration and a disordered arrangement of hippocampal cells. The Shichangpu-Xiyangshen herb pair (SX) effectively improved the pathological changes induced by DCI. However, the role of SX in regulating the physiological and behavioral responses to DCI remains unclear. : We sought to determine the small-molecule metabolites of cerebrospinal fluid (CSF) and delineate the pathways to elucidate the potential mechanism of the effect of SX in the treatment of DCI by metabolomics strategies, focusing on key mechanisms. Behavioral assessments were conducted on DCI rats and the rats treated with SX, as well as an evaluation of neuronal morphology in the hippocampal region. Metabolomics was used to analyze biomarkers in cerebrospinal fluid at different time points during the development of DCI, to uncover the underlying core mechanisms of DCI, and to investigate the regulatory effects of SX on these core mechanisms. The mechanisms of SX on DCI were investigated using quantitative reverse transcription polymerase chain reaction, immunohistochemistry, Western blot, and ELISA. : The Morris water maze (MWM) and social interaction test results revealed that SX administration effectively counteracted cognitive impairments in rats with DCI while simultaneously diminishing pathological damage in the CA1, CA3, and DG hippocampal regions. Further analysis showed that SX restored the significantly reduced levels of IL-8, ROX, and TNF-α, and reduced Aβ plaque formation (as indicated by APP and BACE1 protein expression). Simultaneously, SX markedly ameliorated arachidonic acid metabolic disorders in DCI, including significant reductions in arachidonic acid (AA), PGE2, and LTB4 and reduced expression of COX-2 (PTGS2) and 5-LOX (ALOX-5). : Our findings indicate that SX effectively counteracted cognitive impairment in rats with DCI by inhibiting AA metabolism through both cyclooxygenase and lipoxygenase pathways, thereby minimizing neuronal damage. - Source: PubMed
Publication date: 2026/04/27
Wang JialinWang DongxueYang YangJing ChangyuanLi XinruiXin YixuanWang YingXie Hailong