Ask about this productRelated genes to: SV2A antibody
- Gene:
- SV2A NIH gene
- Name:
- synaptic vesicle glycoprotein 2A
- Previous symbol:
- -
- Synonyms:
- SV2, KIAA0736
- Chromosome:
- 1q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-02-24
- Date modifiied:
- 2014-11-19
Related products to: SV2A antibody
Related articles to: SV2A antibody
- Deficits in the synaptic vesicle protein 2A (SV2A) have been reported in various neurodegenerative diseases including Alzheimer's and Huntington's disease (HD). SV2A levels can be investigated using positron emission tomography (PET) radioligands such as [C]UCB-J, [F]UCB-J, and [F]SynVesT-1. To compare the performance of the PET radioligands [F]UCB-J and [F]SynVesT-1 in terms of brain penetration, binding profile, and SV2A quantification, we here report a head-to-head study in a mouse model of HD. Dynamic µPET/CT scans (60 min) were acquired in 17-month-old heterozygous (HET, = 20) zQ175DN and wild-type (WT, = 19) mice. Brain time-activity curves and image-derived input function were extracted and kinetic modeling was performed using Logan and the two-tissue compartmental model (2TCM). Intra-animal comparison between both radioligands revealed significantly higher ( < 0.01) but equal for [F]SynVesT-1 compared to [F]UCB-J. (Logan) quantification found significantly higher values for [F]SynVesT-1 compared to [F]UCB-J regardless of genotype (e.g. striatum WT: 22.4 ± 2.7 vs 18.6 ± 1.8 mL/cm). Regional analyses comparing the average between genotypes showed no significant differences; however, voxel-based analyses revealed significant SV2A alterations in several subregions of the brain for both radioligands. Overall, [F]SynVesT-1 and [F]UCB-J showed agreement across analyses, demonstrating the equal applicability of both radioligands for SV2A PET imaging. - Source: PubMed
Publication date: 2026/04/19
Everix LiesbethMiranda AlanAkkermans JordyKhetarpal VinodLiu LongbinBard JonathanStaelens StevenBertoglio Daniele - - Source: PubMed
Publication date: 2026/04/17
Panichnantakul PantilaShaw Robert CBurianova Valeria KMcErlain HollySutherland AndrewWilliams Anna CWaldman Adam DTavares Adriana A S - In tauopathies, tau accumulation and neuroinflammation are associated with progressive synaptic and network alterations that contribute to neurodegeneration. We used 8 PS19 and 12 C57Bl/6 (WT) mice undergoing consecutive [F]UCB-H PET scans between 5.7 and 11.0 months of age to longitudinally evaluate SV2A expression levels, with terminal validation via immunohistochemistry. A desynchronization index (DI) quantified deviation from a reference-derived inter-regional SV2A expression pattern from whole-brain SV2A-PET data, and principal component analysis (PCA) further summarized these regional deviation profiles. Baseline translocator protein (TSPO, [F]GE-180) and monoamine oxidase B (MAO-B, [F]F-DED) imaging for activated microglia and reactive astrogliosis were performed to detect early neuroinflammation, which was subsequently correlated with serial SV2A expression, evaluated by the area under the curve (AUC) of [F]UCB-H z-scores (PS19 vs. WT). We observed phased SV2A expression alterations in PS19 mice in the neocortex, hippocampus CA1, brainstem, thalamus, hypothalamus, and cerebellum, showing an increasing trend from 8.4 to 10.0 months of age (+8.1% ± 3.0%), followed by a rapid decline towards 11.0 months of age (-18.4% ± 4.7%), together with greater later-stage inter-regional SV2A expression pattern deviation. Tau burden tended to show a broadly negative association with SV2A expression levels across primary and exploratory regions. Associations of SV2A-PET signal variation with early microglial activation and reactive astrogliosis differed between PS19 and WT mice. In summary, these findings suggest that longitudinal [F]UCB-H PET may provide a feasible approach for tracking stage-dependent regional SV2A expression alterations and inter-regional deviation in this mouse model of primary tauopathy. - Source: PubMed
Publication date: 2026/04/15
Li YunleiZatcepin ArtemPalumbo GiovannaOos RoselWind-Mark KarinLindner SimonGildehaus Franz-JosefGnörich JohannesWerner Rudolf ABrendel MatthiasKunze Lea H - Synaptic dysfunction is implicated in the pathophysiology of schizophrenia, and positron emission tomography (PET) studies demonstrate in vivo reductions in synaptic density across illness stages. Stress is a key modifiable risk factor, and while animal studies show it disrupts synaptic function, its effects on humans remain unclear. We examined the relationship between stress and synaptic density in individuals with first-episode psychosis (FEP) and those at clinical high risk (CHR). Seventy-eight participants, including 25 FEP, 32 CHR, and 21 healthy controls (HC), underwent 90-min [F]SynVesT-1 PET scans to quantify synaptic density measured as SV2A binding across prioritized brain regions. Stress-related measures included the Hassles and Uplifts Scale and the Trier Inventory for Chronic Stress (TICS). Depressive symptoms were evaluated using the Hamilton Depression Rating Scale (HDRS). Across all participants, greater acute stress was associated with lower [F]SynVesT-1 binding (F = 12.0, p < 0.001), with no significant group interaction (F = 2.44, p = 0.09). Group differences emerged for chronic stress and depressive symptoms (TICS × Group: F = 3.87, p = 0.02; sqHDRS × Group: F = 4.47, p = 0.01). Post hoc analyses revealed that higher chronic stress was associated with lower synaptic density in HC (F = 7.07, p = 0.009) but not in clinical groups. Lower mood symptoms were associated with lower synaptic density in FEP (F = 5.19, p = 0.02) only. These findings indicate that the relationship between stress and synaptic density differs between clinical and healthy groups. The changes in the relationship between stress and synaptic density in FEP may reflect impaired adaptive neuroplasticity, providing a potential mechanism by which stress contributes to psychosis vulnerability. - Source: PubMed
Publication date: 2026/04/15
Blasco M BelenNisha Aji KankanaRamos-Jiménez ChristianChartrand DanielHsiao Chris Hung-HsinHopewell RobertMassarweh GassanCohen JohanRusjan Pablo MMizrahi Romina - The purpose of our study was to assess if spinacetin (SPC), a flavonoid found in spinach, can alleviate the cyclophosphamide (CYP)-induced changes in cystometric and inflammatory parameters indicative of the development of hemorrhagic cystitis. The animal experiments were conducted in female Wistar rats. The cohort of 60 animals was grouped as follows: I-control, II-CYP group, III-SPC group, and IV-CYP + SPC group. The cystometry and biochemical analyses were performed after a fortnight of SPC administration. SPC was found to restore normal cystometric parameters in CYP-induced cystitis and, similarly, it normalized c-Fos expression changes in the central micturition regions. SPC further prevented a massive increase in the bladder wall thickness/permeability due to exposition to CYP administration. CYP instillation resulted in the elevation of biomarkers found in urine (brain-derived neurotrophic factor, BDNF, and nerve growth factor, NGF), and in the bladder detrusor muscle (Rho kinase and vesicular acetylcholine transporter, VAChT), which were successfully restored after administration of SPC. As for the biomarkers in the bladder urothelium, the CYP-induced increases in TNF-α, IL-1β, IL-6, calcitonin gene-related peptide (CGRP), malondialdehyde, 3-nitrotyrosine, insulin-like growth factor-binding protein 3 (IGFBP-3), occludin, organic cation transporter 3 (OCT-3), orosomucoid-1 (ORM1), pituitary adenylate cyclase receptor 1 (PAC1), synaptosomal-associated protein 23 (SNAP23), SNAP25, and synaptic vesicle glycoprotein (SV2A) levels were attenuated by SPC. Finally, CYP administration resulted in a decrease in the heparin-binding EGF-like growth factor (HB-EGF), hemopexin (HPX), T-H protein, and tight junction protein (Z01), and we noted the successful restoration of all these changes in concentrations after application of SPC. In summary, SPC robustly mitigated cyclophosphamide (CYP)-induced cystometric dysfunction and biochemical alterations characteristic of iatrogenic hemorrhagic cystitis. These findings position SPC as a compelling therapeutic candidate and warrant further translational investigation for the management of CYP-induced bladder injury. - Source: PubMed
Publication date: 2026/03/27
Wróbel JanZapała ŁukaszNiemczyk GrzegorzBogaczyk AnnaKluz TomaszWdowiak ArturMisiek AleksandraBojar IwonaPoleszak EwaMisiek MarcinGaweł KingaWróbel Andrzej