Supporting evidence for using biomarkers in the diagnosis of MCI due to AD

Deutsche Zeitschrift für Nervenheilkunde - Tập 260 - Trang 640-650 - 2012
Samantha Galluzzi1, Cristina Geroldi2, Giovanni Amicucci3, Luisella Bocchio-Chiavetto4, Matteo Bonetti5, Cristian Bonvicini6, Maria Cotelli7, Roberta Ghidoni8, Barbara Paghera9, Orazio Zanetti2, Giovanni B. Frisoni1
1Laboratory of Epidemiology, Neuroimaging and Telemedicine (LENITEM), IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy
2Alzheimer’s Unit, IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy
3Service of Anesthesiology, Azienda Ospedaliera Mellino Mellini di Chiari, Brescia, Italy
4Neuropsychopharmacology Unit, IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy
5Neuroradiology Service, Istituto Clinico Città di Brescia, Brescia, Italy
6Genetics Unit, IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy
7Neuropsychology Unit, IRCCS Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy
8Proteomics Unit, IRCCS Istituto Centro San Giovanni di Dio, Fatebenefratelli, Brescia, Italy
9Nuclear Medicine Service, Spedali Civili of Brescia, Brescia, Italy

Tóm tắt

The aim of this study is to support the use of biomarkers in the diagnosis of mild cognitive impairment (MCI) due to Alzheimer’s disease (AD) according to the revised NIA-AA diagnostic criteria. We compared clinical features and conversion to AD and other dementias among groups of MCI patients with different abnormal biomarker profiles. In this study, we enrolled 58 patients with MCI, and for each of them AD biomarkers (CSF Abeta42 and tau, temporoparietal hypometabolism on 18F-FDG PET, and hippocampal volume) were collected. Patients were divided into three groups: (i) no abnormal biomarker, (ii) AD biomarker pattern (including three subgroups of early = only abnormal Abeta42, intermediate = abnormal Abeta42 and FDG PET or tau, and late = abnormal Abeta42, FDG PET or tau, and HV), and (iii) any other biomarker combination. MCI patients with AD biomarker pattern had lower behavioural disturbances than patients with any other biomarker combination (p < 0.0005). This group also showed lower performance on verbal and non-verbal memory than the other two groups (p = 0.07 and p = 0.004, respectively). Within the three subgroups with AD biomarker patterns we observed a significant trend toward a higher rate of conversion to dementia (p for trend = 0.006). With regard to dementia conversion, 100 % of patients with an AD biomarker pattern developed AD, but none of the patients with no abnormal biomarker and 27 % of patients with any other biomarker combination (p = 0.002) did so. We also described some clinical cases representative for each of these three groups. The results of this study provide evidence in favour of the use of biomarkers for the diagnosis of MCI due to AD, in line with recently published research criteria.

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