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Basic Science and Pathogenesis
Joice Coutinho de Alvarenga1,2,3,4, Ivonne Carolina Bolaños Burgos5, Gabriela Tomé Oliveira Engelmann1,4,6,7
1Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Background:
Previous evidence suggests that eotaxin-1 could suppress neurogenesis in the hippocampus in mice and has been associated with left temporal medial reduction in humans with mild cognitive impairment (MCI) and dementia.
Objectives:
To evaluate the relationship between eotaxin-1 (CCL11) and cognitive decline in a sample of Brazilian older adults METHOD: This is a cross-sectional study that included 108 older adults participants from the Cog-Aging Cohort Study, evaluated from 2023 to 2024. All participants underwent cognition assessment and cerebrospinal fluid collection (CSF). Cytokines were measured using the Luminex xMAP technique. The participants were classified into three groups: cognitive unimpaired (CU), MCI, and dementia, according to CDR score, and clinical evaluation. Mini-Mental State Examination (MMSE) cut-off scores were 19/20 for illiterate and 23/24 for literate participants. We used the Spearman's test; Mann-Whitney test; Kruskal-Wallis with Dunn's Post-Hoc analyses; and the logistic regression (LR) with age, years of schooling, sex, APOE carrier status and eotaxin levels. All tests used a significance level of 5%.
Result:
The mean age was 74.85 years (SD±6.77); median 4 years (IQR7) of formal education, 63.8% were female and 39.04% were APOEε4 carriers. The MMSE median score was 23 points (IQR6); 19.4% of the participants were in the CU group, 30.6% had MCI and 50% had dementia. There was significant direct correlation between eotaxin with CDR (rho=0.195, p = 0.04) and inverse correlation with MMSE score (rho=-0.267, p = 0.005). The post-hoc analyses showed a difference of eotaxin levels between CU group and MCI (p = 0.004), and between CU and dementia group (p = 0.006). There was also a difference between eotaxin levels between impaired and unimpaired MMSE groups (p = 0.027). The LR model with age, years of schooling, sex and APOE could predict 68.57% CU participants from cognitively impaired ones. The inclusion of eotaxin levels to the model improved it, raising the performance to 86.6% with an AUC of 0.834. In the final model, only age (OR= 1.17, p = 0.002) and eotaxin levels (OR= 11.07, p = 0.029) were significant.
Conclusion:
CSF eotaxin levels were lower in cognitively unimpaired participants, as assessed by both CDR and MMSE. These results point to the association of eotaxin and cognitive impairment in MCI and Dementia.
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