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Abstract Details

Correlates between functional connectivity and amyloid deposition in healthy controls
Aging, Dementia, and Behavioral Neurology
P5 - Poster Session 5 (5:30 PM-6:30 PM)
9-027

The aim of this study is to explore the effects of amyloid-β deposition in brain function, from the prism of functional connectivity. In this work, we study 50 healthy control subjects from the Human Connectome Project database in order to find the effects of amyloid deposition on functional connectivity.

Amyloid-β deposition starts even decades before cognitive symptoms onset. While considered one of the main signs of AD, very little is known on the effect of amyloid plaques in the normal function of the brain. MEG and fMRI techniques are known to be able to measure pre-clinical changes in brain function. It is not known, at the moment, if amyloid deposition in healthy elders affects functional connectivity, indicating the beginning of a neurodegenerative disease.

50 healthy elderly controls from the Human Connectome Database were analyzed in this study. All subjects underwent: one MEG session, where 5 minutes of resting state data with eyes open were acquired; one MRI session, including an anatomical T1 and a resting-state fMRI; one PET session, measuring Amyloid-β deposition by means of Pittsbugh compound B.

We calculated functional connectivity matrices both from fMRI (using time-series correlations) and MEG (using Phase Locking Value) between cortical regions. These connectivity matrices were used to extract network-based characteristics for each area. Then, we correlated the functional connectivity markers with the amyloid-β deposition in the area.

MEG and fMRI showed brain clusters of hipo- and hyper-synchronization in relation to amyloid deposition in regions typically related with AD progression such as DMN areas. These changes may represent the earliest alterations in completely clinically normal population.

Non-invasive functional neuroimaging techniques like fMRI and MEG are useful tools to evaluate the brain function. We think these techniques can also be used as biomarkers to identify neuronal damage in healthy elders at risk of developing AD.

Authors/Disclosures
Ricardo Bruña (Complutense University of Madrid)
PRESENTER
No disclosure on file
No disclosure on file
No disclosure on file
No disclosure on file
No disclosure on file
Yu D. Cheng, MD, PhD (Sharp Health System) No disclosure on file
Fernando Maestu Fernando Maestu has nothing to disclose.
James T. Becker, PhD (University of Pittsburgh) No disclosure on file