Blood levels of cytokines highlight the role of inflammation in Alzheimer’s disease.
Heliyon. 2025-01-01; 11(2): e41725
DOI: 10.1016/j.heliyon.2025.e41725
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https://www.bordeaux-neurocampus.fr/12138
Campanelli L(1), Galeano P(1), Prestia FA(1), Cuesta C(2), Dalmasso MC(3),
Flores-López M(4)(5), Gona C(6), Irureta N(3)(6), Kairiyama C(2), Lisso J(3)(6),
López-Gambero AJ(4)(5), Mintz I(3)(6), Medel N(3)(6), Campuzano KS(1), Muchnik
C(7), Novack GV(1), Olivar N(7), Quiroga I(6), Requena-Ocaña N(4)(5),
Reyes-Bueno JA(8)(9), Serrano-Castro P(8)(9), Sevillano Z(3)(6), Solis P(3)(6),
Suárez J(4)(9)(10), Villella I(3)(6), Wukitsevits N(6), Castaño EM(1), Taragano
F(11), Kochen S(3), Politis DG(2), Brusco LI(7), Rodríguez de Fonseca
F(4)(5)(8)(9), Morelli L(1).
Author information:
(1)Laboratory of Brain Aging and Neurodegeneration, Fundación Instituto Leloir,
IIBBA-CONICET, Av. Patricias Argentinas 435, Ciudad Autónoma de Buenos Aires,
Argentina.
(2)Hospital Interzonal General de Agudos (HIGA) Eva Perón, Av. 101 Dr. Ricardo
Balbín 3200, Provincia de Buenos Aires, Buenos Aires, B1650NBN, Argentina.
(3)Studies in Neuroscience and Complex Systems Unit (CONICET-HEC-UNAJ), Av.
Calchaquí 5402, Florencio Varela, Argentina.
(4)Grupo de Neuropsicofarmacología, IBIMA-Plataforma BIONAND, Hospital Regional
Universitario de Málaga, Puerto de la Torre, 29010, Málaga, Spain.
(5)Unidad de Gestión Clínica de Salud Mental, IBIMA-Plataforma BIONAND, Hospital
Regional Universitario de Málaga, Málaga, Spain, Puerto de la Torre, 29010,
Málaga, Spain.
(6)Asistencia Medica Integral, Hospital El Cruce, Av. Calchaquí 5401, Provincia
de Buenos Aires, Florencio Varela, Argentina.
(7)Center of Neuropsychiatry and Behavior Neurology, School of Medicine,
University of Buenos Aires, Paraguay 2155, Ciudad Autónoma de Buenos Aires,
Argentina.
(8)Unidad de Neurología, IBIMA-Plataforma BIONAND, Hospital Regional
Universitario de Málaga, Malaga, Puerto de la Torre, 29010, Málaga, Spain.
(9)Andalusian Network for Clinical and Translational Research in Neurology
[NEURO-RECA], Av. Carlos Haya, 88, Pabellon B, 4 planta, 29010, Málaga, Spain.
(10)Departamento of Anatomía Humana, Medicina Legal e Historia de la Ciencia,
Facultad de Medicina, Universidad de Málaga, Av. Cervantes, 2, 2907, Málaga,
Spain.
(11)Neuropsychiatric Clinic Nuestra Señora de Las Nieves, Av. Álvarez Thomas
268, C1427CCP, Ciudad Autónoma de Buenos Aires, Argentina.
Inflammation and angiogenesis have been defined as potential mechanisms
associated with clinical progression from a cognitively normal state to
Alzheimer’s disease (AD). In this observational case-control study, we aimed to
determine plasma levels of cytokines as indicators of inflammation involved in
cognitive decline. We measured 30 plasma proteins in 49 controls (CTL), 36
individuals with mild cognitive impairment (MCI) and 52 patients diagnosed with
probable AD. After applying strict filters for quantification limits, only 13
analytes were included in the analysis. Kruskal-Wallis tests showed significant
differences between diagnostic groups for nine cytokines (IL-16, IL-7, VEGF,
IL-8, eotaxin, MCP-1, MCP-4, MDC and TARC). Non-parametric MANCOVA showed that
sex and diagnosis affected cytokine levels in the blood. To determine the
sensitivity and specificity of the markers, we performed receiver operating
characteristic (ROC) curve analysis. Only those analytes that showed an area
under the curve (AUC) ≥ 0.70 were included in the multivariate logistic
regression models to better understand the contribution of cytokines to clinical
status. Three models: 1) CTL vs. AD; 2) CTL vs. MCI, and 3) MCI vs. AD were
developed, with sex and age as covariates. In each model, two cytokines remained
significantly different (model 1: IL-16 and MDC; model 2: eotaxin and MDC and
model 3: IL-7 and VEGF). Taken together, this report identifies a set of plasma
markers of inflammation and strengthens the role of glial biology in different
clinical stages of AD.
© 2025 Published by Elsevier Ltd.
DOI: 10.1016/j.heliyon.2025.e41725
PMCID: PMC11770505
PMID: 39872450
Conflict of interest statement: The authors declare that they have no known
competing financial interests or personal relationships that could have appeared
to influence the work reported in this paper.