Lower Plasma β-Amyloid 1-42 Levels in Amnestic Mild Cognitive Impairment Compared to Healthy Individuals

Cynthia Cynthia (Doctoral Program of Medical Science, Faculty of Medicine, Universitas Airlangga, Jl. Prof. Dr. Moestopo No.47, Surabaya 60132)
Jusak Nugraha (Department of Clinical Pathology, Dr. Soetomo General Academic Hospital, Jl. Prof. Dr. Moestopo No.6-8, Surabaya 60286)
Muhammad Hamdan (Department of Neurology, Dr. Soetomo General Academic Hospital, Jl. Prof. Dr. Moestopo No.6-8, Surabaya 60286)
Hari Basuki Notobroto (Department of Epidemiology, Biostatistics, Population Studies and Health Promotion, Faculty of Public Health, Universitas Airlangga, Kampus C UNAIR, Mulyorejo, Surabaya 60115)
Silvia Francina Lumempouw (Department of Neurobehaviour, Movement Disorder, and Neurogeriatry, Prof Dr dr Mahar Mardjono National Brain Center Hospital, Jl. MT Haryono Kav.11, Jakarta 13630)
Rahajuningsih Dharma (Division of Clinical Pathology, Faculty of Medicine, Universitas Tarumanagara, Jl. Taman S. Parman No.1, Jakarta 11440)

The Indonesian Biomedical Journal
Vol 16, No 6 (2024)

BACKGROUND: Amnestic mild cognitive impairment (aMCI) is strongly associated with an increased risk of progression to Alzheimer’s disease (AD). In AD, cerebrospinal fluid (CSF) β-Amyloid 1-42 levels are known to decrease, a pattern which is also observed in aMCI. While in AD, apolipoprotein E (ApoE) ε4 allele is known to be a genetic risk factor, the role of ApoE ε4 allele in modulating plasma β-Amyloid 1-42 levels in aMCI remains unclear. Therefore, this study was performed to evaluate plasma β-Amyloid 1-42 levels in aMCI patients compared to cognitively healthy individuals and investigate its association with ApoE ε4 allele.METHODS: A cross-sectional study involving 57 aMCI and 54 cognitively healthy control (HC) subjects was performed. Blood samples were taken from subjects from both groups for measurement of the plasma β-Amyloid 1-42 and ApoE ε4 allele. The plasma levels of β-Amyloid 1-42 were measured using an enzyme-linked immunosorbent assay (ELISA) methods, while the ApoE ε4 allele genotyping was conducted using polymerase chain reaction (PCR) techniques.RESULTS: Plasma β-Amyloid 1-42 in individuals with aMCI (23.9 pg/mL) was significantly lower than that in HC (25.3 pg/mL) with cut-off value of 24.6 pg/mL (AUC: 70.8%; 95% CI: 61.1–80.5%; p<0.001) sensitivity of 64.8%, and specificity of 71.9%. There was no significant association between plasma β-Amyloid 1-42 and the ApoE ε4 allele. However, plasma β-Amyloid 1-42 in ε4 carriers were lower than in ε4 non-carriers.CONCLUSION: Lower plasma β-Amyloid 1-42 levels were observed in aMCI patients compared to cognitively healthy individuals, suggesting its potential as a biomarker for identifying aMCI.KEYWORDS: blood biomarkers, amyloid beta peptides, amnestic mild cognitive impairment (aMCI)