Cerebral Amyloidosis in Individuals with Subjective Cognitive Decline: From Genetic Predisposition to Actual Cerebrospinal Fluid Measurements
Stefanos N. Sampatakakis,
Niki Mourtzi,
Sokratis Charisis,
Faidra Kalligerou,
Eirini Mamalaki,
Eva Ntanasi,
Alex Hatzimanolis,
Georgios Koutsis,
Alfredo Ramirez,
Jean-Charles Lambert,
Mary Yannakoulia,
Mary H. Kosmidis,
Efthimios Dardiotis,
Georgios Hadjigeorgiou,
Paraskevi Sakka,
Konstantinos Rouskas,
Kostas Patas,
Nikolaos Scarmeas
Affiliations
Stefanos N. Sampatakakis
1st Department of Neurology, Aiginition Hospital, Athens Medical School, National and Kapodistrian University, 11528 Athens, Greece
Niki Mourtzi
1st Department of Neurology, Aiginition Hospital, Athens Medical School, National and Kapodistrian University, 11528 Athens, Greece
Sokratis Charisis
Department of Neurology, UT Health San Antonio, San Antonio, TX 78229, USA
Faidra Kalligerou
1st Department of Neurology, Aiginition Hospital, Athens Medical School, National and Kapodistrian University, 11528 Athens, Greece
Eirini Mamalaki
1st Department of Neurology, Aiginition Hospital, Athens Medical School, National and Kapodistrian University, 11528 Athens, Greece
Eva Ntanasi
1st Department of Neurology, Aiginition Hospital, Athens Medical School, National and Kapodistrian University, 11528 Athens, Greece
Alex Hatzimanolis
Department of Psychiatry, Aiginition Hospital, Athens Medical School, National and Kapodistrian University, 11528 Athens, Greece
Georgios Koutsis
Neurogenetics Unit, 1st Department of Neurology, Aiginition Hospital, Athens Medical School, National and Kapodistrian University, 11528 Athens, Greece
Alfredo Ramirez
Division of Neurogenetics and Molecular Psychiatry, Department of Psychiatry and Psychotherapy, Medical Faculty, University of Cologne, 50923 Cologne, Germany
Jean-Charles Lambert
Inserm, CHU Lille, Institut Pasteur de Lille, U1167-RID-AGE Facteurs de Risque et Déterminants Moléculaires des Maladies Liés au Vieillissement, University of Lille, 59000 Lille, France
Mary Yannakoulia
Department of Nutrition and Dietetics, Harokopio University, 17676 Athens, Greece
Mary H. Kosmidis
Lab of Neuropsychology and Behavioral Neuroscience, School of Psychology, Aristotle University of Thessaloniki, 54124 Thessaloniki, Greece
Efthimios Dardiotis
Department of Neurology, University Hospital of Larissa, Faculty of Medicine, School of Health Sciences, University of Thessaly, 41334 Larissa, Greece
Georgios Hadjigeorgiou
Department of Neurology, Medical School, University of Cyprus, Nicosia 1678, Cyprus
Paraskevi Sakka
Athens Association of Alzheimer’s Disease and Related Disorders, 11636 Marousi, Greece
Konstantinos Rouskas
Institute of Applied Biosciences, Centre for Research & Technology Hellas, 54124 Thessaloniki, Greece
Kostas Patas
Department of Medical Biopathology and Clinical Microbiology, Aiginition Hospital, Athens Medical School, National and Kapodistrian University, 11528 Athens, Greece
Nikolaos Scarmeas
1st Department of Neurology, Aiginition Hospital, Athens Medical School, National and Kapodistrian University, 11528 Athens, Greece
The possible relationship between Subjective Cognitive Decline (SCD) and dementia needs further investigation. In the present study, we explored the association between specific biomarkers of Alzheimer’s Disease (AD), amyloid-beta 42 (Aβ42) and Tau with the odds of SCD using data from two ongoing studies. In total, 849 cognitively normal (CN) individuals were included in our analyses. Among the participants, 107 had available results regarding cerebrospinal fluid (CSF) Aβ42 and Tau, while 742 had available genetic data to construct polygenic risk scores (PRSs) reflecting their genetic predisposition for CSF Aβ42 and plasma total Tau levels. The associations between AD biomarkers and SCD were tested using logistic regression models adjusted for possible confounders such as age, sex, education, depression, and baseline cognitive test scores. Abnormal values of CSF Aβ42 were related to 2.5-fold higher odds of SCD, while higher polygenic loading for Aβ42 was associated with 1.6-fold higher odds of SCD. CSF Tau, as well as polygenic loading for total Tau, were not associated with SCD. Thus, only cerebral amyloidosis appears to be related to SCD status, either in the form of polygenic risk or actual CSF measurements. The temporal sequence of amyloidosis being followed by tauopathy may partially explain our findings.
