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Abstract Details

Cerebello-parietal Functional Connectivity in Amnestic Mild Cognitive Impairment Due to Alzheimer’s Disease
Aging, Dementia, and Behavioral Neurology
P7 - Poster Session 7 (11:45 AM-12:45 PM)
9-006
To characterize the cerebello-cerebral functional connectivity (FC) in amnestic mild cognitive impairment (aMCI).
The cerebellum has disease-specific volume change in Alzheimer’s disease (AD). However, as the brain region typically spared in early stage of AD, the characteristic of cerebello-cerebral functional circuits and its clinical correlates remains to be determined.
We recruited 15 controls and 16 aMCI participants. All participants received the Montreal Cognitive Assessment (MoCA), AD Assessment Scale-Cognitive subscale (ADAS-Cog), and resting state functional MRI, analyzed by the Conn Functional Connectivity Toolbox. Lobule-specific cerebello-cerebral connectivity was conducted using seed-to-voxel analysis with the cerebellar seeds/region of interests placed in the cognitive cerebellar lobules, specifically, lobule VI, VII, Crus I and II. We then compared the cerebello-cerebral FC between aMCI vs. controls (i.e., by diagnosis) and between people with higher (MoCA ≥ 25) vs. lower cognitive function (MoCA = 21-24). Clinico-imaging correlates between the ADAS-Cog and cerebellar FC was also studied.

Using the complete set of significance with peak voxel p < 0.001 and cluster threshold p-FDR < 0.05, we identified when compared to controls, aMCI demonstrated significantly weaker FC between left VIIb of the cerebellum and right supramarginal gyrus of the parietal lobe. Participants with lower cognitive function demonstrated significantly weaker FC between the cerebellar left Crus II and the right superior parietal lobe as well as right supramarginal gyrus of the parietal lobe. Interestingly, higher ADAS-Cog score (i.e., worse cognitive function) was correlated with stronger, instead of weaker FC between the cerebellar right VIIb and thalamus, suggesting the cerebellum might provide a compensatory effect on cognitive function in aMCI via the cerebello-thalamo-cortical pathway.

The alteration of cerebello-parietal functional network commences from aMCI, the early stages of AD. It is essential to explore whether augmenting cerebello-thalamo or cerebello-parietal FC through neuromodulation could provide insights into future symptomatic and disease-modifying therapeutic implication.
Authors/Disclosures
Chi-Ying (Roy) Lin, MD, FAAN (Baylor College of Medicine)
PRESENTER 		Dr. Lin has received research support from Texas Alzheimer's Research and Care Consortium (TARCC). Dr. Lin has received research support from CurePSP. Dr. Lin has received research support from Mike Hogg Fund. Dr. Lin has received research support from The Michael J. Fox Foundation Parkinson's Progression Markers Initiative (PPMI). Dr. Lin has a non-compensated relationship as a Secretary with Broadway for Ataxia Foundation (a 501 (c) (3) non-profit organization) that is relevant to AAN interests or activities.
Shayla Yonce (Baylor College of Medicine) Shayla Yonce has nothing to disclose.
Nat Pacini (Baylor College of Medicine) No disclosure on file
Melissa Yu, MD, FAAN An immediate family member of Dr. Yu has received personal compensation for serving as an employee of CVS/Aetna. The institution of Dr. Yu has received research support from Alzheimer's Association. The institution of Dr. Yu has received research support from Biogen. The institution of Dr. Yu has received research support from Eisai. The institution of Dr. Yu has received research support from Novo Nordisk. The institution of Dr. Yu has received research support from Suven. The institution of Dr. Yu has received research support from AriBio. Dr. Yu has received personal compensation in the range of $500-$4,999 for serving as a advisory board member with Eli Lilly.
Jeffrey S. Bishop, PA (Baylor College of Medicine) Mr. BISHOP has nothing to disclose.
Valory Pavlik, PhD (Baylor College of Medicine) The institution of Dr. Pavlik has received research support from Alzheimer's Association.
Ramiro Salas (Baylor College of Medicine) The institution of Ramiro Salas has received research support from VHA. The institution of Ramiro Salas has received research support from Wallace foundation.