Open AccessRelationship of fasting glucose and longitudinal Alzheimer's disease imaging markers
Author(s) -
Honea Robyn A.,
John Casey S.,
Green Zachary D.,
Kueck Paul J.,
Taylor Matthew K.,
Lepping Rebecca J.,
Townley Ryan,
Vidoni Eric D.,
Burns Jeffery M.,
Morris Jill K.
Publication year - 2022
Publication title -
alzheimer's and dementia: translational research and clinical interventions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.49
H-Index - 30
ISSN - 2352-8737
DOI - 10.1002/trc2.12239
Subject(s) - precuneus , dementia , medicine , cognitive decline , atrophy , endocrinology , neurodegeneration , neuroimaging , alzheimer's disease , glucose uptake , amyloid (mycology) , disease , insulin , cognition , pathology , psychiatry
Fasting glucose increases with age and is linked to modifiable Alzheimer's disease risk factors such as cardiovascular disease and Type 2 diabetes (T2D). Methods We leveraged available biospecimens and neuroimaging measures collected during the Alzheimer's Prevention Through Exercise (APEx) trial (n = 105) to examine the longitudinal relationship between change in blood glucose metabolism and change in regional cerebral amyloid deposition and gray and white matter (WM) neurodegeneration in older adults over 1 year of follow‐up. Results Individuals with improving fasting glucose (n = 61) exhibited less atrophy and regional amyloid accumulation compared to those whose fasting glucose worsened over 1 year (n = 44). Specifically, while individuals with increasing fasting glucose did not yet show cognitive decline, they did have regional atrophy in the hippocampus and inferior parietal cortex, and increased amyloid accumulation in the precuneus cortex. Signs of early dementia pathology occurred in the absence of significant group differences in insulin or body composition, and was not modified by apolipoprotein E ε4 carrier status. Discussion Dysregulation of glucose in late life may signal preclinical brain change prior to clinically relevant cognitive decline. Additional work is needed to determine whether treatments specifically targeting fasting glucose levels may impact change in brain structure or cerebral amyloid in older adults.