Molecular biomarkers quantified using the Single Molecule Array in Brazilian patients with mild Alzheimer’s disease and mild cognitive impairment

• Published in: Alzheimer's & dementia Vol. 19; no. S14
• Main Authors: Magalhaes, Thamires Naela Cardoso, Teixeira, Camila Vieira de Ligo, Moraes, Adriel Santos, Cassani, Ana Flavia M K C, Joaquim, Helena Passarelli Giroud, Talib, Leda Leme, Forlenza, Orestes Vicente, Balthazar, Marcio Luiz Figueredo, Teunissen, Charlotte E.
• Format: Journal Article
• Language: English
• Published: 01-12-2023
• ISSN: 1552-5260; 1552-5279
• DOI: 10.1002/alz.076986

Background
The clinically diagnosed late‐onset Alzheimer’s disease (AD) cases has the most heterogeneous pathology. The development of more sensitive biomarkers is essential to perform an early diagnosis, especially in the prodromal phase, mild cognitive impairment (MCI). Biomarkers such as glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) have emerged as potential markers of the pathophysiological process of AD. The objective of this study was to evaluate the concentrations of GFAP and NfL in blood serum and CSF of patients with MCI and mild AD in a Brazilian sample, never quantified using the Single Molecule Array technology (Simoa).
Method
We used samples (blood serum and cerebrospinal fluid (CSF)) from 91 participants to perform molecular analyzes. These participants were recruited in the outpatient service of the UNICAMP Clinic Hospital. All participants underwent blood collection and only the patients, lumbar puncture, to analyze GFAP and NfL levels. All patients had pathophysiological evidence of AD (low Aβ1‐42 concentrations < 540pg/mL) and was considered Tau alteration: p‐Tau > 36.7 pg/mL and t‐Tau > 76.7 pg/mL.
Result
Statistical analyzes were performed using SPSS software (version 25). We performed a multivariate analysis of covariance (MANCOVA) to compare the biomarkers levels between the groups. To compare CSF levels (Aβ42, t‐Tau, p‐Tau, GFAP and NfL) we used T‐test analyses and to correlate GFAP and NfL with CSF proteins we use partial correlations. We did not find statistical differences between the groups regarding GFAP and NfL levels, but we did find differences between Aβ1‐42 protein between MCI and mild AD (p = 0.003). We also found moderate correlations between t‐Tau, GFAP and NfL CSF levels (r = .625, p = 0.0; r = .508, p = 0.005, respectively), and p‐Tau with GFAP CSF levels (r = .373, p = 0.046).
Conclusion
GFAP and NfL reflect neuro‐axonal damage and recent studies have demonstrated its effectiveness in tracking disease progression (5). Although we did not find differences between individuals in relation to GFAP and NfL markers, we were able to observe correlations between these markers at the CSF level and the proteins classically related to the pathological process of the disease.