Partial volume effect-corrected FDG PET and grey matter volume loss in patients with mild Alzheimer’s disease

Abstract

FDG uptake in PCG and PTL is reduced in AD regardless of whether or not PVE correction is applied, supporting the notion that the reduced FDG uptake in these areas is not the result of atrophy. Furthermore, FDG uptake by grey matter tissue in the MTL, including hippocampal areas, is relatively preserved, suggesting that compensatory mechanisms may play a role in patients with mild AD.

Animal model of posterior cingulate cortex hypometabolism implicated in amnestic MCI and AD

“…Although the cingulum carries reciprocal fibers between the PCC and parahippocampal areas (Schmahmann & Pandya, 2006), two facts argue against the possibility that hippocampal atrophy causes PCC hypometabolism in AD. First, PCC hypometabolism precedes hippocampal atrophy and is not the result of tissue atrophy (Chetelat et al, 2008;Minoshima et al, 1997;Mosconi et al, 2006;Samuraki et al, 2007). Second, the degree of hypometabolism is significantly greater than the degree of atrophy in the PCC (Chetelat et al, 2008).…”

Age-Related Metabolic Profiles in Cognitively Healthy Elders: Results from a Voxel-Based [18F]Fluorodeoxyglucose–Positron-Emission Tomography Study with Partial Volume Effects Correction: Fig 1.

“…This is mainly due to recent propositions regarding the potential of PVE correction to accurately differentiate normal and pathologic age-related processes through the dissociation between metabolic changes and brain atrophy. 12,44 It has been shown that regional hypometabolism exceeds brain atrophy in patients with MCI, 20,21 AD, 22,45 and other types of dementia, 46 but not in normal aging. 12,15,47 Most interesting, the study of Kalpouzos et al 8 was the only investigation on normal brain aging that reported areas of metabolic decline or preservation through the analysis of PVEcorrected PET images.…”

“…6,12,[15][16][17] According to this view, CMRglc decre-ments that persist after correction of PET images for PVE, representing hypometabolism that exceeds brain atrophy, should be interpreted as indicative of pathologic brain aging, 18,19 thus placing PVE correction as a critical methodologic tool to differentiate normal and pathologic brain aging in PET studies. Accordingly, recent PET studies of glucose metabolism using PVE correction have suggested that regional hypometabolism exceeds brain atrophy in patients with MCI or AD, [20][21][22] but not in normal aging. 15,16 Nevertheless, to the best of our knowledge, no PET study has confirmed these findings in a representative sample of cognitively healthy elderly individuals.…”

Age-associated physiological and pathological changes at the blood–brain barrier: A review

“…118 Protein expression of the glucose transporter GLUT1 is reduced in brain capillaries in Alzheimer's disease, without changes in GLUT1 mRNA structure 119 or levels of GLUT1 mRNA transcripts. 120 Furthermore, a reduction in CNS energy metabolites has been seen in several Positron Emission Tomography (PET) scanning studies of Alzheimer's patients using fluoro-deoxy-glucose (FDG), [121][122][123] likely because the surface area at the BBB available for glucose transport is substantially reduced in Alzheimer's disease. 120,124 Furthermore, GLUT1 deficiency in mice overexpressing amyloid b-peptide precursor protein leads to early cerebral microvascular degeneration, blood flow reductions and dysregulation and BBB breakdown, and to accelerated amyloid b-peptide pathology, reduced amyloid b clearance, diminished neuronal activity, behavioural deficits and progressive neuronal loss and neurodegeneration that develop after initial cerebrovascular degenerative changes.…”