Microglial activation, but not tau pathology, is independently associated with amyloid positivity and memory impairment. Academic Article uri icon

Overview

abstract

  • We sought to determine if upstream amyloid accumulation and downstream cognitive impairment have independent relationships with microglial activation and tau pathology. Fifty-eight older adults were stratified by amyloid and cognitive status based on 18F-florbetaben PET, history, and neuropsychological testing. Of these, 57 had 11C-PBR28 PET to measure microglial activation and 43 had 18F-MK-6240 PET to measure tau pathology. Amyloid and cognitive status were associated with increased overall binding for both 11C-PBR28 and 18F-MK-6240 (p's < 0.01). While there was no interaction between amyloid and cognitive status in their association with 11C-PBR28 binding (p = 0.6722), there was an interaction in their association with 18F-MK-6240 binding (p = 0.0115). Binding of both radioligands was greater in amyloid-positive controls than in amyloid-negative controls; however, this difference was seen in neocortical regions for 11C-PBR28 and only in medial temporal cortex for 18F-MK-6240. We conclude that, in the absence of cognitive symptoms, amyloid deposition has a greater association with microglial activation than with tau pathology.

publication date

  • September 29, 2019

Research

keywords

  • Alzheimer Disease
  • Amyloid
  • Memory Disorders
  • Microglia

Identity

PubMed Central ID

  • PMC6919274

Scopus Document Identifier

  • 85074224201

Digital Object Identifier (DOI)

  • 10.1016/j.neurobiolaging.2019.09.019

PubMed ID

  • 31698286

Additional Document Info

volume

  • 85