Jul 2026· International Journal of Nutrology· 0 citations
TL;DR
Increased serum p-tau217 and decreased ApoE levels were significantly associated with greater AD severity, suggesting that both biomarkers may serve as complementary noninvasive indicators of disease severity in Alzheimer’s disease.
Abstract
Introduction: Alzheimer's disease (AD) is a chronic neurodegenerative illness characterised by aberrant protein accumulation and progressive cognitive decline. One of the most researched blood indicators of tau pathology is phosphorylated tau 217 (p-tau217), and apolipoprotein E (ApoE) is essential for lipid metabolism, amyloid removal, and neuronal maintenance. The severity of AD may be correlated with changes in these biomarkers. Objective: To compare serum levels of p-tau217 and ApoE in individuals with different severities of Alzheimer's Disease. Methods: The present case–control study consisted of 156 subjects aged between 55 and 85 years:106 patients with ad (and balanced frequency matched to healthy controls on age, international classification of diseases t63 diagnosis). The DSM-5 criteria classified the patients as mild (n = 12), moderate (n = 50), or severe (n = 44). Using the sandwich enzyme-linked immunosorbent assay (ELISA), the levels of circulating ApoE and p-tau217 were determined. The receiver operating characteristics (ROC) curve examination, Spearman's correlation, and the Kruskal-Wallis test were used in the statistical studies. Results: The mean serum p-tau217 and ApoE level were 165 ± 84.2 pg/mL and 75.5 ± 55.6 ng/mL, respectively. While serum p-tau217 significantly increased with severity of disease, ApoE levels decreased. We found a significant positive association of p-tau217 (p<0.001) and a negative association of ApoE (p<0.001) with disease severity by DSM-5 criteria. ROC analysis showed high diagnostic accuracy of CSF p-tau217 (AUC=0.916, sensitivity: 87.18%, specificity: 90.00%) and ApoE (AUC=0.992, sensitivity: 100.00%, specificity:98.00%). Conclusion: Increased serum p-tau217 and decreased ApoE levels were significantly associated with greater AD severity. Both biomarkers may serve as complementary noninvasive indicators of disease severity in Alzheimer’s disease.
Objectives: The study objective is to reveal biochemical way to diagnose and know Alzheimer's patients biochemically instead of using traditional
Methods that used to diagnosis as an example using: Electroencephalography (EEG), computed tomography (CT), magnetic resonance imaging (MRI) and brain biopsy.
Methods: A case control research design was applied to current study, 156 individuals and thy were as follows: 12 with mild symptoms ,50 with moderate,44 with sever progression and 50 apparently as healthy control with an age range of 55 to 85 years were included. Samples were collected in accordance with the consultant's diagnosis; disease severity was categorized according to DSM-5(Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition) staging, which was then demonstrated by laboratory tests. A Human p-tau217 (Phospho Tau 217) Catalogue No.: EH5067 Revision: V4.0 Size: 48T/96T ELISA Kit was used and rang test was (7.813-500pg/ml) which tested by instrument (human reader).
Results: The baseline serum biomarkers analysis of whole Study Participants showed that the mean tau level was 165 ± 84.2 pg/mL, Tau levels increased markedly with disease severity, rising from 86.33 ± 34.40 pg/mL in the control group to 265.72 ± 50.91 pg/mL in the severe group. DSM-5 score also showed a strong positive correlation with Tau concentration, suggesting that higher clinical severity was associated with increased Tau levels. Tau showed very strong negative correlations with ApoE, the correlations' findings indicated that this effect size is substantial up to assay. ApoE demonstrated a mean value of 75.5 ± 55.6 ng/mL. of whole Study Participants. ApoE levels showed a pronounced and significant reduction across disease stages, with the lowest mean value observed in the severe group. While DSM-5 score also showed a negative association with ApoE was strong and significant.
Conclusion: Serum Tau levels increased markedly with disease severity, indicating that Tau may serve as a reliable marker of progressive neuronal injury and neurodegeneration in Alzheimer’s disease. ApoE levels declined substantially with increasing disease severity and showed the highest diagnostic accuracy among the studied biomarkers, indicating its strong potential as a predictive biomarker for Alzheimer’s disease progression.
This study provides Class II evidence that plasma NfL/p-tau217 discriminates patients with CJD from those with AD and Diagnosing AD with a single abnormal p-tau plasma biomarker risks misdiagnosing prion diseases as AD.
Thomas Coysh, Rhiannon Laban, Elena Veleva et al.· Neurology· 0 citations
This systematic review sought to assess the function of the blood biomarker phosphorylated tau 217 (p-tau217) in the early identification of Alzheimer's disease. A systematic review was carried out adhering to the PRISMA 2020 protocols. Literature searches were executed in PubMed, ScienceDirect, and Scopus to locate original studies published between 2023 and 2026. Eligible studies assessed blood p-tau217 in individuals with mild cognitive impairment, suspected Alzheimer's disease, Alzheimer's disease, or at-risk populations and reported diagnostic performance or correlations with established Alzheimer's biomarkers. Study quality was evaluated utilizing QUADAS-2 for diagnostic accuracy studies and the Study Quality Assessment Tools for observational and longitudinal studies. A total of 328 records were retrieved, of which 18 studies met the inclusion criteria. Research consistently demonstrates that plasma p-tau217 serves as a highly accurate biomarker for identifying the biological pathology of Alzheimer's disease, specifically regarding amyloid and tau status. Numerous studies have reported impressive area under the curve (AUC) scores between 0.92 and 0.97. When p-tau217 is paired with Aβ42 or the Aβ42/40 ratio, its diagnostic precision improves significantly, particularly in patients who are cognitively normal or in the preclinical stages of the disease.
Mangde Anata Sindhu· Health & Medical Science...· 0 citations
Phosphorylated-tau (p-tau217) is a promising blood-based biomarker for Alzheimer’s dementia (AD) in clinical settings. However, research from prospective cohort studies is sparse. We measured plasma p-tau217 levels in baseline blood samples of 779 participants in a population-based cohort of older adults followed over 17 years. Associations with AD were assessed and compared to those with previous measurements of p-tau181, neurofilament light chain (NfL), and glial fibrillary acidic protein (GFAP). Comparisons to the amyloid beta (Aβ) misfolding biomarker were performed in a subgroup analysis. P-tau217, NfL and GFAP showed strong associations with AD risk, especially within the first 9 years of follow-up, outperforming p-tau181. Over the later years of follow-up, the predictive accuracy of p-tau217 was significantly reduced. In contrast, the Aβ misfolding biomarker demonstrated superior performance especially as a preclinical indicator of the risk of AD many years before diagnosis. The combination of p-tau217 with NfL, GFAP, basic demographic and genetic information, as well as the misfolding biomarker yielded an AUC 0.86 for AD diagnoses over the entire 17-year follow-up period. P-tau217 is a promising blood-based biomarker for Alzheimer’s dementia (AD) in the clinical stage. In this prospective cohort study, it showed better performance in the prodromal than in the preclinical stage up to 17 years before diagnosis. In a subgroup analysis, the Aß misfolding biomarker showed higher discriminative ability in the preclinical stage compared to p-tau217. A prediction model including p-tau217, NfL, GFAP, Aß misfolding as well as basic demographic and genetic information reached an AUC of 0.86 for AD over the entire follow-up period. In a subgroup analysis, the Aß misfolding biomarker showed higher discriminative ability in the preclinical stage compared to p-tau217. A prediction model including p-tau217, NfL, GFAP, Aß misfolding as well as basic demographic and genetic information reached an AUC of 0.86 for AD over the entire follow-up period. P-tau217 is a promising blood-based biomarker for Alzheimer’s dementia (AD) in the clinical stage. In this prospective cohort study, it showed better performance in the prodromal than in the preclinical stage up to 17 years before diagnosis.
K. Trares, D. Duman, L. Beyer et al.· EMBO Molecular Medicine· 0 citations
BackgroundThe prominent pathological features of Alzheimer's disease (AD) are amyloid-β (Aβ) plaques and tau pathology. The complement cascade is closely related to AD-associated pathological processes; however, the precise mechanisms underlying its contributions remain incompletely elucidated.ObjectiveWe aim to investigate the changes in complement protein expression during AD progression.MethodsThis study enrolled 285 participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database. Participants were classified into biomarker-defined groups based on predefined cutoff values for Aβ42 and phosphorylated tau (P-tau). We compared cerebrospinal fluid (CSF) levels of complement proteins (C1q, C2, C3, C4a, C5, C6, C8b, and factor B) across these subgroups. Furthermore, we explored their associations with core AD biomarkers (Aβ42, P-tau, and T-tau) and clinical characteristics. Additionally, we investigated age-related changes in complement gene expression within the cerebral cortex of 3xTg mice using single-nucleus RNA sequencing.ResultsComplement protein levels in the CSF of A + subjects were significantly lower than those in A- subjects, and complement protein levels were positively correlated with Aβ pathology. Complement protein levels were influenced by factors such as age, gender, body mass index, APOE genotype, and hypertension. Compared with control mice, the complement gene C1qa in microglia was upregulated throughout the entire pathological cycle in 3xTg AD mice.ConclusionsComplement proteins undergo significant changes during the pathogenesis of AD, and alterations in their levels may reflect early pathological changes in AD and warrant further investigation. Notably, our findings suggest that microglia may contribute to complement-mediated pathological processes associated with AD.
Ying-Tong Lu, Zi Guo, Meng-Yuan Liu et al.· Journal of Alzheimer's Disea...· 0 citations