Ask about this productRelated genes to: NTF3 antibody
- Gene:
- NTF3 NIH gene
- Name:
- neurotrophin 3
- Previous symbol:
- -
- Synonyms:
- NGF2
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1991-01-15
- Date modifiied:
- 2016-10-05
Related products to: NTF3 antibody
Related articles to: NTF3 antibody
- Dietary patterns can modulate the expression of proteins involved in inflammatory and metabolic pathways in people living with HIV. The aim of this study was to examine whether adherence to the Mediterranean diet is associated with distinct plasma proteomic signatures in PWH on stable antiretroviral therapy. Chronic inflammation persists despite virological suppression, making diet a potential modifiable factor in this setting. - Source: PubMed
Publication date: 2026/04/22
Manzano MónicaMoreno ElenaMartín-Pedraza LauraDíaz-García ClaudioMoreno SantiagoNavia BeatrizSerrano-Villar Sergio - Hospitalization in older adults often leads to disability in daily living activities, thereby increasing the risk of functional and cognitive impairments. This randomized controlled trial analyzed the serum protein profile of patients admitted to an acute geriatric unit who engaged in supervised multicomponent functional exercises compared with a control group. Potential protein biomarkers were assessed using Olink® serum proteomics platform employing two predefined panels: Cardiometabolic and Inflammation. Notably, short-term exercise intervention was associated with moderate but consistent changes in the serum proteome. Nominal differences (p < 0.05, unadjusted) were observed for amyloid beta precursor-like protein 1 (APLP1), complement C1q tumor necrosis factor-related protein 1 (C1QTNF1), interleukin-8 (CXCL8), interleukin-7 (IL-7), M-phase phosphoprotein 8 (MPHOSPH8), neurotrophin 3 (NTF3), tissue-type plasminogen activator (PLAT), SFRS1-interacting protein (PSIP1), pleiotrophin (PTN), cardiac-type troponin I (TNNI3), von Willebrand factor (vWF), and while levels of CD40 ligand (CD40LG) were reduced. These findings suggest that short-term multicomponent functional exercises during acute hospitalization can induce changes in the serum proteome. These molecular alterations provide exploratory insight into the biological processes associated with the functional benefits observed following the intervention in hospitalized older adult patients. - Source: PubMed
Publication date: 2026/04/30
Izco-Cubero MaiteLachén-Montes MercedesChenhuichen ChenhuiVeloz Ba CedeñoEcheverría-Beistegui IcíarZambom-Ferraresi FabricioZambom-Ferraresi Fabiolade la Riva María Luisa Fernández-GonzálezÁlvarez-Rodríguez PatriciaSantamaría EnriqueMartínez-Velilla Nicolás - Adenylosuccinate synthase 1 (ADSS1)-deficient myopathy is an ultra-rare disease characterized by progressive muscle dysfunction. The objective of this investigation was to employ a noninvasive biomarker approach to phenotype (fine-)motor skills, communication and cognition in adults with ADSS1-deficient myopathy. Five individuals with ADSS1-deficient myopathy and five age-sex-matched healthy controls (HCs) underwent a multimodal evaluation. Assessments included, (i) evaluation of motor performance, (ii) speech and voice production and cognitive test batteries, (iii) patient-reported outcomes, (iv) electrical impedance myography (EIM), (v) musculoskeletal magnetic resonance imaging (MRI), and (vi) plasma proteomics. ADSS1-deficient myopathy participants vs. HCs demonstrated reduced performance on the 9-Hole Peg and grip strength tests as well as lower self-reported mobility. Analysis of speech and voice performance revealed asthenia (vocal weakness) (p = 0.02), lower intelligibility (p = 0.008), and worse voice quality during the sustained vowel task (p = 0.03) in the ADSS1-deficient myopathy cohort. Cognitive functioning remained unaffected in patients with ADSS1-deficient myopathy. On EIM, ADSS1-deficient myopathy participants vs. HCs, demonstrated a pattern of higher resistance and lower reactance and phase across upper- and lower-extremity measurements, indicative of poorer muscle health, with large effect sizes (Cliff's δ = 0.5-0.9). MRI revealed intramuscular fat infiltration, particularly in posterior compartments of the upper leg (e.g., biceps femoris). Proteomics indicated reduced (p = 0.04) Neurotrophin-3 (NTF3; implicated in neuronal development, survival, and differentiation) levels in the ADSS1-deficient myopathy cohort relative to HCs. Lower NTF3 levels associated with poorer performance on hand-motor tasks as well as higher resistance and lower reactance and phase on EIM. This study highlighted the value of multimodal phenotyping for quantifying disease expression and advancing monitoring strategies in ADSS1-deficient myopathy. This multimodal investigation demonstrates that integrating electrical impedance myography with quantitative motor, speech, musculoskeletal imaging, and proteomic assessments provides a sensitive and noninvasive research framework for capturing neuromuscular dysfunction and functional disease burden in patients with ADSS1-deficient myopathy, thereby supporting the current biomarker strategy for refined phenotyping and longitudinal disease monitoring in this ultra-rare condition. - Source: PubMed
Yekedüz Merve Koçvan Gool Raquelvan der Heijden HanneCobb Buket SonbasShah NehalJohnson GeorginaTimpani Cara AShulman JulieRameh VanessaHsu Evan ELeSon CourtneyLee Pui YVogel Adam PAl-Hertani WallaPark Hyung JunRybalka EmmaRutkove Seward BUpadhyay Jaymin - Huntington's disease (HD) is a progressive neurodegenerative disorder characterized by motor, cognitive, and psychiatric impairments, partly due to disruptions in neurotrophin signaling. Brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and neurotrophin-3 (NT-3) play critical roles in neuronal survival, synaptic plasticity, and neuroprotection, yet their alterations across biofluids and brain regions in HD remain unclear. This study systematically reviewed and meta-analyzed human and rodent studies to quantify neurotrophin changes and explore moderating factors. Comprehensive searches of PubMed, Scopus, Web of Science, Embase, Google Scholar, and clinical trial registries were conducted up to December 2025. Studies reporting measurable BDNF, NGF, or NT-3 levels in HD patients or animal models were included. Data were extracted on neurotrophin type, sample source, subject characteristics, and measurement methods. Standardized mean differences were calculated using random-effects models, and meta-regression was applied to evaluate the effects of species, sex, sampling region, and analytical techniques. The results showed a significant decrease in neurotrophin levels in both peripheral biofluids and central brain regions in HD. The results for moderator analyses showed that species and sex significantly affected the magnitude of changes in ELISA-based studies, whereas molecular methods consistently detected reductions irrespective of these factors. No significant publication bias was identified. These findings highlight significant neurotrophic deficits in HD, highlight the importance of biological and methodological considerations in interpreting neurotrophin data, and suggest that peripheral neurotrophin measurements may serve as accessible biomarkers for disease progression. - Source: PubMed
Publication date: 2026/03/24
Pour Homa ValiMotamedi ShayesteMirzaei BitaFernandes Carolina Beatriz LopesMourtaja Hamdy - (1) Background: Bioactive peptides from marine and plant sources show neuroprotective potential, yet how their combination ratios affect memory regulation via the gut-brain axis remains unclear. This study investigated the effects of different ratios of marine peptide QMDDQ (Glutamine-Methionine-Aspartate-Aspartate-Glutamine) and plant peptide AGLPM (Alanine-Glycine-Leucine-Proline-Methionine) on scopolamine-induced memory impairment in mice. (2) Methods: Cognitive function was assessed using the Morris water maze and novel object recognition tests. Nissl staining, microplate-based assays for acetylcholine (ACh) content and acetylcholinesterase (AChE) activity, Western blotting for neurotrophic factors, LC-MS/MS-based intestinal peptide profiling, and HPLC-based brain amino acid analysis were performed. (3) Results: The 1:1 ratio most effectively restored learning and memory, regulated hippocampal cholinergic function, mitigated neuronal damage, and elevated BDNF, NGF, and NTF-3 expression. In the gut, peptides were hydrolyzed into glutamate- and proline-rich fragments, which influenced brain amino acid balance by elevating glutamate and proline levels while reducing NH-related signaling. (4) Conclusions: These results highlight the ratio-dependent efficacy of QMDDQ-AGLPM combinations and provide evidence for a gut peptide remodeling-brain metabolic link relevant to cognitive impairment. - Source: PubMed
Publication date: 2026/03/02
Xu XiaomengLiu RuowenMa EnhuiZhong LiminLin Songyi