SOD1
- Known as:
- SOD1
- Catalog number:
- 000495A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- SOD1
Related genes to: SOD1
- Gene:
- SOD1 NIH gene
- Name:
- superoxide dismutase 1
- Previous symbol:
- ALS, ALS1
- Synonyms:
- IPOA
- Chromosome:
- 21q22.11
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: SOD1
Related articles to: SOD1
- Diabetes mellitus is frequently associated with cognitive dysfunction, primarily attributed to impaired hippocampal neurogenesis, oxidative stress, inflammation, and pyroptosis. Caffeic acid (CA), a dietary polyphenol, has demonstrated antioxidant and neuroprotective effects. This study evaluated the protective role of CA under diabetic-like conditions using an in vitro glucolipotoxicity model in HT-22 hippocampal neurons exposed to high glucose and oleic acid (HG + OA). CA was administered at low (5 µM) and high (25 µM) concentrations prior to HG + OA treatment. CA significantly enhanced neuronal viability and restored the expression of neurogenesis markers (Nestin, DCX, NeuN) and synaptic proteins (PSD-95, Synaptophysin). Furthermore, CA elevated antioxidant enzyme levels (Nrf2, catalase, SOD-1), regulated apoptosis through increased Bcl-2 and decreased BAX expression, and attenuated inflammatory responses. Pyroptosis was also suppressed, as evidenced by reduced gasdermin D (GSDMD) expression. These findings suggest that CA confers multifactorial neuroprotection against glucolipotoxic injury, and may serve as a dietary modulator for mitigating diabetes-associated cognitive decline in vitro. - Source: PubMed
Publication date: 2026/05/28
Tsai I-NingXie Xiang-NingKo Ping-EnTsai Yung-CheChen Ching-ChunHsu Li-SungWang Chau-Jong - Amyotrophic lateral sclerosis is a progressive multifocal neurodegenerative condition involving motor neurons and other cell types. To analyze spatiotemporal cellular dynamics in amyotrophic lateral sclerosis, we performed single-nucleus ribonucleic acid sequencing and spatial transcriptomics analysis of cervical spinal cords from wild-type control mice and SOD1-G93A transgenic mice in the pre-symptomatic (d50), early symptomatic (d90), and late-stage (d130) phases of disease. Single-nucleus ribonucleic acid sequencing identified 17 cell clusters and showed that progressive neuronal loss occurred over time, paralleled by glial expansion. Spatial transcriptomics mapped these clusters anatomically onto oligodendrocytes in white matter, neurons in horns, and diffuse astrocytes/microglia. Subcluster analysis demonstrated neuronal heterogeneity, with early mitochondrial stress in ventral motor neurons evolving into synaptic dysfunction, transient maturation peaks in interneurons, and amplified age-related decline in amyotrophic lateral sclerosis. Astrocyte and oligodendrocyte subclusters, which were originally misclustered due to spot-level contamination, were reinterpreted to highlight A1-reactive states and progenitor expansions, validated by immunohistochemistry detection of serum/glucocorticoid regulated kinase 1. Temporal profiles tracked the transition from compensatory to inflammatory gliosis, while gene signatures were linked to human amyotrophic lateral sclerosis cohorts, including complement activation and mitochondrial dysfunction. This study provides a high-resolution spatiotemporal cellular map of amyotrophic lateral sclerosis pathogenesis through the integration of single-nucleus and spatial transcriptomics, uncovering early mitochondrial impairment in neurons, delineating the trajectory of neurotoxic glial states, and identifying compensatory progenitor responses, to highlight the highly intricate interaction between glial reactivity and neuronal susceptibility that drives the pathogenesis of ALS. - Source: PubMed
Publication date: 2026/05/14
Zhou QiGong TianLiu JiahaoMa JunpengZheng MinxiuZhong ZiweiDeng HaitaoLin HaiyanFeng NanLei XiaoZhang Chengsheng - Weight loss and hypermetabolism are negative prognostic factors in amyotrophic lateral sclerosis (ALS). Ketone bodies (β-hydroxybutyrate, βHB) as high-energy substrates may compensate for this energy deficit, since a ketogenic diet (KD) has been shown to increase survival and stabilize body weight in the mouse model. In this case series, we tested exogenous ketone salts (KS), ketone esters (KE), and a KD, in patients with ALS and in healthy subjects to identify novel therapeutic interventions for subsequent clinical studies. KS (KetoForce (KetoSports, Frisco, TX, USA)) were tested in healthy subjects (11.7 g and 15.6 g βHB) and patients (15.6 g βHB 3×/day over 3 days). KE (KE4 (KetoneAid, Falls Church, VA, USA)) containing 10.0 g βHB were applied in healthy subjects (once) and in patients (3×/day over 2 days). For the KD, KetoCal 2.5:1 LQ MCT MF Vanilla (Nutricia, Frankfurt, Germany) was applied via percutaneous endoscopic gastrostomy over four weeks. Regular capillary βHB measurements were conducted, and adverse events were recorded. Between January 2021 and March 2025, we treated nine patients with ALS and two healthy subjects at the Department of Neurology of Ulm University, Germany. KE and KS increased βHB temporarily. However, the elevation was more pronounced following KE (maximum 2.2-2.7 mmol/L vs. 0.8-1.2 mmol/L). The KD increased βHB levels continuously with nighttime fluctuations. No adverse events occurred under KE. KS caused diarrhea in 3/5 patients and 1/2 healthy subjects. The KD was well tolerated, with mild gastrointestinal symptoms occurring in all patients. All ketogenic approaches increased βHB blood levels. While the KD and KE provided good tolerability, KS caused significant gastrointestinal side effects. KD seems to be an interesting candidate for future clinical studies, as it prompted a long-term increase in βHB while providing satisfying tolerability. Since maintaining a KD long-term is difficult for oral-feeding patients, KE may constitute a feasible alternative. - Source: PubMed
Publication date: 2026/05/21
Herrmann ChristineSatari SamanthaWeber AndreaRuschitzka TanjaJagodzinski LuisaElmas ZeynepBecker FelicitasRichter LarsWiesenfarth MaximilianMichels SebastianWeishaupt Jochen HSchuster JoachimDorst Johannes - The resurrection plant is a rare species endemic to Greece and Bulgaria, renowned for its exceptional desiccation tolerance and rich phytochemical composition. This study investigated the antioxidant, cytoprotective, and wound-healing-associated effects of ethanolic extract (HEE) in human keratinocytes (HaCaT cells) under oxidative and cytotoxic stress conditions. Antioxidant capacity was initially evaluated using a plasmid DNA protection assay, in which HEE attenuated oxidative DNA damage induced by a Fenton reaction system and preserved the native supercoiled structure of pUC19 plasmid DNA. Cytotoxicity screening using the sulforhodamine B (SRB) assay and real-time proliferation monitoring (HoloMonitor M4) identified 20 μg/mL as a non-toxic pre-treatment concentration (EC). Under hydrogen peroxide (HO)-induced oxidative stress, HEE pre-treatment maintained cell viability and significantly reduced intracellular reactive oxygen species (ROS) levels, indicating a protective effect. In vitro wound-healing assays demonstrated enhanced scratch closure in keratinocyte monolayers. RT-qPCR analysis revealed modulation of antioxidant-related genes (, , , , , ), while mRNA sequencing suggested selective stress-adaptive responses, involving extracellular matrix (ECM)-, metabolic-, and tissue-repair/aging-associated pathways. Overall, HEE exhibits antioxidant and cytoprotective effects in keratinocytes and is associated with transcriptional changes linked to cellular stress responses and wound closure. These findings support its potential relevance for dermatological, pharmaceutical, and cosmeceutical applications, while further studies are required to establish the underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/05/11
Ermogenous AntreasSarigiannidou EleniPsomiadou MariaPanagiotidou AfroditiVoulgaridou Georgia PersephoniKiousi Despoina EugeniaMoyankova DanielaDjilianov DimitarGalanis AlexPappa Aglaia - Tofersen is a gene-targeted therapy for superoxide dismutase 1 ()-associated amyotrophic lateral sclerosis (ALS), but neurofilament light chain (NfL) may not fully capture the biological response to treatment. We performed a multicentre retrospective longitudinal study including 24 patients with -ALS treated with intrathecal tofersen at four Italian referral centres between 2022 and 2025. Cerebrospinal fluid (CSF) and serum biomarkers were assessed at baseline, month 3, month 6, and last available administration using single-molecule array assays to quantify NfL, glial fibrillary acidic protein (GFAP), ubiquitin C-terminal hydrolase L1 (UCHL-1), and total Tau. NfL decreased after treatment initiation in both CSF and serum, providing the clearest pharmacodynamic signal. In contrast, CSF GFAP increased progressively over follow-up, while CSF total Tau and UCHL-1 rose mainly at later timepoints; serum GFAP, total Tau, and UCHL-1 also showed increases during follow-up. ALS Functional Rating Scale-Revised trajectories were broadly stable, whereas disease progression rate was lower at last follow-up than at baseline. Greater reductions in CSF NfL were observed in pathogenic versus uncertain variants, and early serum NfL and UCHL-1 changes were associated with longer-term changes in disease progression. These findings suggest that longitudinal multi-analyte profiling may refine biological response stratification beyond NfL alone in tofersen-treated -ALS. - Source: PubMed
Publication date: 2026/05/09
Giordano AndreaMandrioli JessicaCerri FedericaLunetta ChristianSaebfar HamidrezaCatania MarcellaBattipaglia ClaudiaLeone LauraTrojsi FrancescaVizziello MariaGerardi FrancescaFarè MatteoZulueta AidaPiras RacheleGiacchino MatteoGianferrari GiuliaDalla Bella EleonoraDomi TeutaBonanomi DarioGanci GiuseppeLombardi RaffaellaLauria GiuseppeRiva Nilo