Liara Rizzi1, Marcelle Maria Portal2, Carlos Eduardo Alves Batista3, Luciane Missiaggia4, Matheus Roriz-Cruz5. 1. Division of Geriatric Neurology, Service of Neurology, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street 2.350, 90035-903 Porto Alegre, RS, Brazil. Electronic address: lirizzi@hcpa.edu.br. 2. Division of Geriatric Neurology, Service of Neurology, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street 2.350, 90035-903 Porto Alegre, RS, Brazil. Electronic address: marcelleportal@gmail.com. 3. Division of Geriatric Neurology, Service of Neurology, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street 2.350, 90035-903 Porto Alegre, RS, Brazil. Electronic address: cebatista@hcpa.edu.br. 4. Division of Geriatric Neurology, Service of Neurology, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street 2.350, 90035-903 Porto Alegre, RS, Brazil. Electronic address: lumissiaggia@gmail.com. 5. Division of Geriatric Neurology, Service of Neurology, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street 2.350, 90035-903 Porto Alegre, RS, Brazil. Electronic address: mcruz@hcpa.edu.br.
Abstract
AIM: Individuals with amnestic mild cognitive impairment (aMCI) are at a high risk to develop Alzheimer's disease (AD). We compared CSF levels of biomarkers of amyloidosis (Aβ1-42) and neurodegeneration (p-Tau181) in individuals with aMCI and with subjective cognitive impairment (SCI) in order to ascertain diagnostic accuracy and predict the odds ratio associated with aMCI. METHODS: We collected CSF of individuals clinically diagnosed with aMCI (33) and SCI (12) of a memory clinic of Southern Brazil. Levels of Aβ1-42 and p-Tau181 were measured by immunoenzymatic assay. Participants also underwent neuropsychological testing including the verbal memory test subscore of the Consortium to Establish a Registry for Alzheimer's Disease (VM-CERAD). RESULTS: CSF concentration of Aβ1-42 was significantly lower (p: .007) and p-Tau181/Aβ1-42 ratio higher (p: .014) in aMCI individuals than in SCI. However, isolate p-Tau181 levels were not associated with aMCI (p: .166). There was a statistically significant association between Aβ1-42 and p-Tau181 (R2: 0.177; β: -4.43; p: .017). ROC AUC of CSF Aβ1-42 was 0.768 and of the p-Tau181/Aβ1-42 ratio equals 0.742. Individuals with Aβ1-42 < 823 pg/mL levels were 6.0 times more likely to be diagnosed with aMCI (p: .019), with a 68.9% accuracy. Those with p-Tau181/Aβ1-42 ratio > 0.071 were at 4.6 increased odds to have aMCI (p: .043), with a 64.5% accuracy. VM-CERAD was significantly lower in aMCI than among SCI (p: .041). CONCLUSION: CSF Aβ1-42, but not p-Tau181, level was significantly associated with aMCI.
AIM: Individuals with amnestic mild cognitive impairment (aMCI) are at a high risk to develop Alzheimer's disease (AD). We compared CSF levels of biomarkers of amyloidosis (Aβ1-42) and neurodegeneration (p-Tau181) in individuals with aMCI and with subjective cognitive impairment (SCI) in order to ascertain diagnostic accuracy and predict the odds ratio associated with aMCI. METHODS: We collected CSF of individuals clinically diagnosed with aMCI (33) and SCI (12) of a memory clinic of Southern Brazil. Levels of Aβ1-42 and p-Tau181 were measured by immunoenzymatic assay. Participants also underwent neuropsychological testing including the verbal memory test subscore of the Consortium to Establish a Registry for Alzheimer's Disease (VM-CERAD). RESULTS: CSF concentration of Aβ1-42 was significantly lower (p: .007) and p-Tau181/Aβ1-42 ratio higher (p: .014) in aMCI individuals than in SCI. However, isolate p-Tau181 levels were not associated with aMCI (p: .166). There was a statistically significant association between Aβ1-42 and p-Tau181 (R2: 0.177; β: -4.43; p: .017). ROC AUC of CSF Aβ1-42 was 0.768 and of the p-Tau181/Aβ1-42 ratio equals 0.742. Individuals with Aβ1-42 < 823 pg/mL levels were 6.0 times more likely to be diagnosed with aMCI (p: .019), with a 68.9% accuracy. Those with p-Tau181/Aβ1-42 ratio > 0.071 were at 4.6 increased odds to have aMCI (p: .043), with a 64.5% accuracy. VM-CERAD was significantly lower in aMCI than among SCI (p: .041). CONCLUSION: CSF Aβ1-42, but not p-Tau181, level was significantly associated with aMCI.