TABLE 3.

PET studies showing lower cerebral metabolic rate for glucose (CMRg) in carriers of apolipoprotein E4.

Reference	n in each group	CMRg
Reiman et al (1996)138	n = 11 E4+ homozygous n = 22 E4−	↓ in posterior cingulate, parietal, temporal, & prefrontal regions of E4+
Reiman et al (1998)140	n = 11 E4+ homozygous n = 22 E4−	↓ in posterior cingulate, parietal, temporal, & prefrontal regions of E4+
De Leon et al (2001)229	n = 48 HC of whom n = 12 → MCI, and n = 1 → AD	↓ in entorhinal cortex predicted conversion of HC to MCI ↓ in hippocampus and temporal cortex in MCI compared with HC at follow-up ↓ in temporal cortex of E4+
Mosconi et al (2004)230	n = 37 MCI n = 16 E4+ n = 21 E4−, of whom n = 8 → AD	↓ in inferior parietal cortex for converters to AD ↓ in temporoparietal & posterior cingulate cortex for E4+ further ↓ in anterior cingulate & inferior frontal cortex for E4+ MCI converters
Reiman (2004)139	n = 12 E4+ heterozygous n = 15 E4−	↓ in posterior cingulate, parietal, temporal, & prefrontal cortex for E4+ compared to HC
Reiman (2005)62	n = 78 E4− n = 26 E4+ homozygous n = 46 E4+ heterozygous	↓ in posterior cingulate, precuneaus, parietotemporal, & frontal regions; negative correlations between CMRg & gene dose of E4+ allele
Rimajova et al (2008)231	n = 30 E4+	↓ in anterior & posterior cingulate cortex, temporal association cortex for E4+
Langbaum et al (2009)232	n = 82 HC n = 142 aMCI n = 74 pAD	↓ in posterior cingulate, precuneaus, parietotemporal, frontal cortex ↓ in precuneaus and frontal cortex for HC who were E4+ ↓ in lateral temporal cortex for aMCI who were E4+

AD – Alzheimer’s disease

aMCI – amnestic mild cognitive impairment

E4− – no apolipoprotein E4 allele

HC – healthy controls

pAD – probable Alzheimer’s disease

→ progressed to