Hyperphosphorylated tau is an important pathological agent in Alzheimer's disease (AD). Tau effluxes from the brain to the blood could potentially stimulate the production of naturally occurring antibodies (NAbs). We aimed to investigate whether NAbs to tau (NAbs-tau) was generated in human blood and to figure out the alteration of plasma NAbs-tau level in AD patients. About 192 AD patients and 192 age-matched and non-demented controls (NC) were enrolled in the present study. Immunofluorescence staining and western blot assays were used to confirm the existence of NAbs-tau in human blood. The plasma level of NAbs-tau in NC and AD group was analyzed by ELISA. Immunofluorescence staining and western blot assays confirmed the existence of NAbs-tau in human blood. However, no significant difference in the plasma level of NAbs-tau was observed between NC and AD group. Furthermore, the plasma level of NAbs-tau had no significant correlation with MMSE scores. The present study confirmed that NAbs-tau exists in human blood but does not differ in level between the NC and AD group. Plasma NAbs-tau is not a reliable biomarker for AD.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s12640-020-00161-9DOI Listing

Publication Analysis

Top Keywords

human blood
20
plasma level
12
level nabs-tau
12
nabs-tau
9
naturally occurring
8
occurring antibodies
8
exists human
8
alzheimer's disease
8
plasma nabs-tau
8
immunofluorescence staining
8

Similar Publications

This study examined internal, external training loads, internal:external ratios, and aerobic adaptations for acute and short-term chronic repeated-sprint training (RST) with blood flow restriction (BFR). Using randomised crossover (Experiment A) and between-subject (Experiment B) designs, 15 and 24 semi-professional Australian footballers completed two and nine RST sessions, respectively. Sessions comprised three sets of 5-7 × 5-second sprints and 25 seconds recovery, with continuous BFR (45% arterial occlusion pressure) or without (Non-BFR).

View Article and Find Full Text PDF

Introduction: Infants and young children typically have the highest age-related risk of invasive meningococcal disease. The immunogenicity and safety of a single primary dose and a booster of a meningococcal A/C/W/Y tetanus toxoid conjugate vaccine (MenACWY-TT; Nimenrix) in infants were evaluated.

Methods: In this phase 3b, open-label, single-arm study, healthy 3-month-old infants received a single Nimenrix dose followed by a booster at age 12 months (1 + 1 series).

View Article and Find Full Text PDF

Antiretroviral therapy (ART) adherence is crucial for HIV viral suppression. Tenofovir diphosphate (TFV-DP) concentrations in dried blood spots (DBS) offer a potential tool for monitoring and supporting adherence. We assessed acceptability and preferences of fingerstick-based DBS collection and drug-level feedback among 224 people living with HIV (PLWH) in South Africa.

View Article and Find Full Text PDF

Therapeutic gene correction of HBB frameshift CD41-42 (-TCTT) deletion in human hematopoietic stem cells.

Adv Biotechnol (Singap)

January 2025

MOE Key Laboratory of Gene Function and Regulation, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-Sen University, Guangzhou, 510275, Guangdong, China.

Β-thalassemia is one of the global health burdens. The CD41-42 (-TCTT) mutation at HBB is the most prevalent pathogenic mutation of β-thalassemia in both China and Southeast Asia. Previous studies focused on repairing the HBB CD41-42 (-TCTT) mutation in β-thalassemia patient-specific induced pluripotent stem cells, which were subsequently differentiated into hematopoietic stem and progenitor cells (HSPCs) for transplantation.

View Article and Find Full Text PDF

Adenine base editor corrected ADPKD point mutations in hiPSCs and kidney organoids.

Adv Biotechnol (Singap)

June 2024

MOE Key Laboratory of Gene Function and Regulation, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-Sen University, Guangzhou, Guangdong, 510275, China.

Autosomal dominant polycystic kidney disease (ADPKD) is a dominant genetic disorder caused primarily by mutations in the PKD1 gene, resulting in the formation of numerous cysts and eventually kidney failure. However, there are currently no gene therapy studies aimed at correcting PKD1 gene mutations. In this study, we identified two mutation sites associated with ADPKD, c.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!