Precuneus and Cingulate Cortex Atrophy and Hypometabolism in Patients with Alzheimer’s Disease and Mild Cognitive Impairment: MRI and¹⁸F-FDG PET Quantitative Analysis Using FreeSurfer

Abstract

Objective. The objective of this study was to compare glucose metabolism and atrophy, in the precuneus and cingulate cortex, in patients with Alzheimer's disease (AD) and mild cognitive impairment (MCI), using FreeSurfer. Methods. 47 individuals (17 patients with AD, 17 patients with amnestic MCI, and 13 healthy controls (HC)) were included. MRI and PET images using 18F-FDG (mean injected dose of 185 MBq) were acquired and analyzed using FreeSurfer to define regions of interest in the hippocampus, amygdala, precuneus, and anterior and posterior cingulate cortex. Regional volumes were generated. PET images were registered to the T1-weighted MRI images and regional uptake normalized by cerebellum uptake (SUVr) was measured. Results. Mean posterior cingulate volume was reduced in MCI and AD. SUVr were different between the three groups: mean precuneus SUVr was 1.02 for AD, 1.09 for MCI, and 1.26 for controls (p < 0.05); mean posterior cingulate SUVr was 0.96, 1.06, and 1.22 for AD, MCI, and controls, respectively (p < 0.05). Conclusion. We found graduated hypometabolism in the posterior cingulate cortex and the precuneus in prodromal AD (MCI) and AD, whereas atrophy was not significant. This suggests that the use of 18F-FDG in these two regions could be a neurodegenerative biomarker.

Blood–brain barrier breakdown in Alzheimer disease and other neurodegenerative disorders

“…Similarly, asymptomatic carriers of presenilin-1 ( PSEN1 ) mutations associated with early-onset autosomal dominant AD show AD-like reductions in FDG uptake in the absence of brain atrophy 116 . Diminished glucose uptake in the hippocampus, parieto-temporal cortex and/or posterior cingulate cortex has been repeatedly shown by FDG-PET in early AD 117,118 , in individuals at genetic risk of AD 119,120 , with a positive family history of AD 121 and/or MCI, as well as in individuals with no cognitive impairment who went on to develop AD 122,123 . The patterns of FDG brain uptake can also discriminate individuals with normal cognition from those with MCI and AD 117 .…”

Amyloid β deposition in subcortical stroke patients and effects of educational achievement: A pilot study

“…The PCu/PCC was spatially distinct from the subcortical stroke lesions, and the increase of PiB retention was unlikely to be due to free PiB leakage across the blood–brain barrier damaged by ischemia or reperfusion injury . The PCu/PCC exhibit marked neurodegeneration in the early stage of AD, and abnormalities of the PCu/PCC serve as useful markers of AD pathology . Aβ accumulation in this region in stroke patients may indicate the development of AD‐related pathology.…”

Brain imaging of neurovascular dysfunction in Alzheimer’s disease

“…Reductions in cerebral metabolic rate of glucose (CMRglc) have been reported in the AD literature for over three decades, consistently demonstrating that individuals with AD have decreased transport of glucose across the BBB and therefore decreased metabolism in AD-affected regions, such as posterior parietal and temporal cortices [13, 55]. Metabolic patterns of FDG-PET uptake have also been shown to discriminate between individuals with normal cognition, MCI, and clinical AD [100, 102].…”