Clinical and neurochemical correlates of the APOE genotype in early-stage Parkinson’s disease

Emerging evidence indicates that apolipoprotein E (APOE) genotype may influence Parkinson's disease (PD) course, although clinical and neurochemical correlates have not been completely established. This study aimed to determine the associations of APOE genotypes (ε4 vs. non-ε4) with cerebrospin...

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Veröffentlicht in:Neurobiology of aging 2023-11, Vol.131, p.24-28
Hauptverfasser: Zenuni, Henri, Bovenzi, Roberta, Bissacco, Jacopo, Grillo, Piergiorgio, Simonetta, Clara, Mascioli, Davide, Pieri, Massimo, Bernardini, Segio, Sancesario, Giulia Maria, Stefani, Alessandro, Mercuri, Nicola Biagio, Schirinzi, Tommaso
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Sprache:eng
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Zusammenfassung:Emerging evidence indicates that apolipoprotein E (APOE) genotype may influence Parkinson's disease (PD) course, although clinical and neurochemical correlates have not been completely established. This study aimed to determine the associations of APOE genotypes (ε4 vs. non-ε4) with cerebrospinal fluid (CSF) neurodegeneration biomarkers and clinical parameters in early-stage PD patients. One hundred and seventy-five PD patients and 89 non-neurodegenerative controls grouped in APOE-ε4 carriers (28 PD; 12 controls) and non-APOE-ε4 carriers (147 PD; 78 controls) were enrolled. CSF levels of amyloid-β-42, amyloid-β-40, total and 181-phosphorylated tau, and clinical scores were compared among groups adjusting for main covariates. APOE genotypes prevalence was similar in PD and controls. PD APOE-ε4 carriers had lower amyloid-β-42 CSF levels than PD non-APOE-ε4 carriers and controls, independently from age. PD APOE-ε4 carriers also had higher total and “item 5” (attention and memory) non-motor symptoms scale scores than PD non-APOE-ε4 carriers, independently from confounding factors. APOE-ε4 genotype might thus account for a more vulnerable PD subtype characterized by prominent amyloidopathy and a greater burden of non-motor symptoms in the early disease stages. Data are available upon reasonable request.
ISSN:0197-4580
1558-1497
DOI:10.1016/j.neurobiolaging.2023.07.011