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Relationship of fasting glucose and longitudinal Alzheimer's disease imaging markers.
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.
Afiliación
  • Honea RA; University of Kansas Alzheimer's Disease Research Center Kansas City Kansas USA.
  • John CS; Department of Neurology University of Kansas Medical Center Kansas City Kansas USA.
  • Green ZD; University of Kansas Alzheimer's Disease Research Center Kansas City Kansas USA.
  • Kueck PJ; Department of Neurology University of Kansas Medical Center Kansas City Kansas USA.
  • Taylor MK; University of Kansas Alzheimer's Disease Research Center Kansas City Kansas USA.
  • Lepping RJ; Department of Neurology University of Kansas Medical Center Kansas City Kansas USA.
  • Townley R; University of Kansas Alzheimer's Disease Research Center Kansas City Kansas USA.
  • Vidoni ED; Department of Neurology University of Kansas Medical Center Kansas City Kansas USA.
  • Burns JM; Department of Dietetics and Nutrition University of Kansas Medical Center Kansas City Kansas USA.
  • Morris JK; Hoglund Biomedical Imaging Center University of Kansas Medical Center Kansas City Kansas USA.
Alzheimers Dement (N Y) ; 8(1): e12239, 2022.
Article en En | MEDLINE | ID: mdl-35128029
INTRODUCTION: 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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Risk_factors_studies Idioma: En Revista: Alzheimers Dement (N Y) Año: 2022 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Tipo de estudio: Risk_factors_studies Idioma: En Revista: Alzheimers Dement (N Y) Año: 2022 Tipo del documento: Article Pais de publicación: Estados Unidos