Abstract
Neuroinflammation is increasingly recognized as playing a key pathogenetic role in Alzheimer's disease (AD). We examined the relationship between in vivo neuroinflammation and gray matter (GM) changes. Twenty-eight subjects with clinically probable AD (n = 14) and amyloid-positive mild cognitive impairment (n = 14) (age 71.9 ± 8.4 years, 46% female) and 24 healthy controls underwent structural 3T brain MRI. AD/mild cognitive impairment participants exhibited GM atrophy and cortical thinning in AD-related temporoparietal regions (false discovery rate–corrected p < 0.05). Patients also showed increased microglial activation in temporal cortices. Higher 11C-PK11195 binding in these regions was associated with reduced volume and cortical thickness in parietal, occipital, and cingulate areas (false discovery rate p < 0.05). Hippocampal GM atrophy and parahippocampal cortical thinning were related to worse cognition (p < 0.05), but these effects were not mediated by microglial activation. This study demonstrates an association between in vivo microglial activation and markers of GM damage in AD, positioning neuroinflammation as a potential target for immunotherapeutic strategies.
Highlights
Alzheimer's disease (AD) causes structural brain abnormalities in the gray matter (GM) volume and cortical thickness, especially in temporoparietal regions (Du et al, 2007; Karas et al, 2003; Richards et al, 2009)
We included 14 participants with probable AD according to McKhann's criteria (McKhann et al, 2011) and 14 patients with mild cognitive impairment (MCI) defined by National Institute of AgingeAlzheimer's Association criteria (Petersen et al, 2013): a memory impairment at least 1.5 standard deviation below that expected for age and education, the absence of dementia. and a Mini-Mental State Examination (MMSE) score >24/30
MMSE and ACE-R scores were significantly lower in the AD/MCI group relative to the healthy controls (p < 0.0001, Mann-Whitney U test)
Summary
Alzheimer's disease (AD) causes structural brain abnormalities in the gray matter (GM) volume and cortical thickness, especially in temporoparietal regions (Du et al, 2007; Karas et al, 2003; Richards et al, 2009). One aspect of neuroinflammation is microglial activation, which can be measured in vivo with PET ligands such as 11C-
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