Functional connectivity changes differ in early and late-onset Alzheimer's disease
Natalina Gour1, Olivier Felician, Mira Didic
1Aix-Marseille Université, CNRS, CRMBM UMR 7339, 13385, Marseille, France; Aix-Marseille Université, INSERM, Institut des Neurosciences des Systèmes (INS) UMR 1106, 13385, Marseille, France; APHM, Hôpitaux de la Timone, Service de Neurologie et Neuropsychologie, 13385, Marseille, France; APHM, Hôpitaux de la Timone, CEMEREM, 13385, Marseille, France.
Early-onset Alzheimer's disease (EOAD) and late-onset Alzheimer's disease (LOAD) show distinct brain network alterations. While both exhibit default mode network (DMN) dysfunction, EOAD has reduced dorso-lateral prefrontal network (DLPFN) connectivity, and LOAD shows the opposite pattern.
Area of Science:
- Neuroscience
- Neurology
- Medical Imaging
Background:
- Early-onset Alzheimer's disease (EOAD) and late-onset Alzheimer's disease (LOAD) present with differing patterns of brain atrophy and dysfunction.
- The distinct organization of neural networks in EOAD versus LOAD remains largely uninvestigated.
Purpose of the Study:
- To characterize and compare basal functional connectivity (FC) patterns in the default mode network (DMN), anterior temporal network (ATN), and dorso-lateral prefrontal network (DLPFN) between EOAD and LOAD patients.
- To investigate the relationship between FC patterns and cognitive performance in these patient groups.
Main Methods:
- Magnetic resonance imaging (MRI) was used to assess brain atrophy and resting-state functional connectivity (FC).
- Neuropsychological assessments were conducted on 14 EOAD patients, 14 LOAD patients (matched for disease duration and severity), and age-matched controls.
Main Results:
- Both EOAD and LOAD showed decreased FC within the DMN compared to controls.
- A double-dissociation was observed in other networks: EOAD exhibited decreased FC in the DLPFN and increased FC in the ATN, while LOAD showed the reverse pattern.
- FC in the ATN and DLPFN correlated with memory and executive functions, respectively, suggesting compensatory mechanisms.
Conclusions:
- Alzheimer's disease presents with both common and distinct large-scale neural network alterations in its early-onset and late-onset forms.
- These differences in network organization likely stem from variations in the distribution of pathological changes.
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