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Table 1 Summary of PET studies

From: Neuroimaging advances regarding subjective cognitive decline in preclinical Alzheimer’s disease

Authors Definition of SCD Modality Design Sample (mean age ± SD) Main findings
Amariglio et al. (2012) [29] E-Cog;
Composite of 7 questions
PiB-PET Cross-sectional SCC: n=131(73.5±6.0)
amyloid-: n=97(72.7±5.9)
amyloid+: n=34(75.5±6.9)
SCC score relate to cortical PiB binding
Amariglio et al. (2018) [39] Composite of 7 questions PiB-PET Cross-sectional All: n=279(73.4±6.1)
amyloid-: n=209(72.9±6.0)
amyloid+: n=70(70.0±5.7)
Amyloid positivity individuals have pronounced progression of SCD
Buckley et al. (2016) [41] MAC-Q scale PiB-PET
18F-florbetapir PET
Cross-sectional NC: n=288
amyloid-: n=230(69±5.9)
amyloid+: n=58(72±7.2)
High SMD related to greater rates of clinical progression, greater depressive symptom and smaller left hippocampal volume
Cacciamani et al. (2017) [31] Composite of 15 questions
18F-florbetapir PET
Cross-sectional High awareness:
Low awareness:
No relationship between SCD score and neuroimaging markers; higher amyloid burden and lower cortical metabolism in “high awareness” group
Chen et al. (2019) [27] Metamemory in Adulthood questionnaire 18F-florbetapir PET
Cross-sectional Total: n=85(66.97±15.11)
Negative: n=53(61.25±14.86)
Positive: n=32(76.46±9.96)
Poor memory performance mediates the relationship between amyloid and SCD
Hollands et al. (2015) [37] MAC-Q
Composite of 16 questions
PiB-PET Cross-sectional Low Aß: n=224(68.37±5.88)
High Aß: n=65(73.46±7.33)
High Aß group show moderate decline in learning and working memory over 18 months. al. (2018) [32] MAC-Q
1 binary question
18F-florbetaben PET Cross-sectional All: n=112(69.2, 2.5) Self-reported confusion predicted higher global amyloid burden and regional amyloid in the prefrontal, posterior cingulate, precuneus and the lateral temporal.
Moreno–Grau et al. (2018) [42] Cognitive complaints 18F-florbetaben PET
18F-florbetapir PET
Cross-sectional ADNI_NC: n=182(73.4±6.3)
ADNI_SMC: n=103(72.2±5.6)
ADNI_EMCI: n=303(71.3±7.4)
ADNI_LMCI: n=157(72.2±7.5)
ADNI_AD: n=144(74.4±8.1)
FACEHBI_SCD: n=200(65.8±7.1)
ADNI_NC: n=182(73.4±6.3)
Higher ApoE ɛ4 carrier in SCD and ApoE ɛ4 dosage explained 9% and 11% cerebral amyloid variation.
Perrotin et al. (2017) [23] Composite of 26 questions 18F-florbetapir PET
Cross-sectional Controls: n=35(65.6±8.6)
SCDcommunity: n=35(70.8±7.5)
Both groups with high self-reported difficulties has higher amyloid deposition
Perrotin et al. (2012) [25] 2 questions PiB-PET
Cross-sectional High PiB uptake: n=11(75.73±6.05)
Low PiB uptake: n=28(71.89±5.45)
Correlation between memory self-reports and regional PiB uptake in right medial prefrontal, anterior cingulate, right precuneus and posterior cingulate.
Risacher et al. (2015) [43] CCI
18F-florbetapir PET
Cross-sectional NC ApoE ɛ4-: n=132(73.7±6.1)
NC ApoE ɛ4+: n=53(71.8±6.4)
SMC ApoE ɛ4-: n=71(72.5±5.7)
SMC ApoE ɛ4+: n=33(70.3±5.2)
EMCI ApoE ɛ4-: n=174(71.6±7.3)
EMCI ApoE ɛ4+: n=131(70.0±7.5)
SMC ApoE ɛ4+ show greater amyloid deposition than SMC ApoE ɛ4-
Rodda et al. (2010) [30] Memory complain PiB-PET Cross-sectional No presented No difference in amyloid load between SCI and controls
Rowe et al. (2010) [28] 1 binary question PiB-PET
  HC: n=177(71.6±7.4)
MCI: n=57(75.5±7.5)
AD: n=53(72.6±8.9)
HC nMC: n=81(72.0±7.5)
HC SMC: n=96(71.2±7.4)
SMC related to elevated PiB in ApoE ɛ4 carriers
Snitz et al. (2015) [24, 26] MFQ
PiB-PET Cross-sectional SCD: n=14(68.1±4.0)
NC: n=84(73.6±5.8)
57% of SCD and 31% of NC were PiB-positive. SCD had higher PiB retention in frontal cortex, lateral temporal cortex, and parietal cortex.
Snitz et al. (2015) [24, 26] MFQ
PiB-PET Cross-sectional Total: n=92(81.2±8.4) MFQ score relate to global PiB retention
Timmers et al. (2019) [38] Memory clinic consultation
Intact cognition
18F-florbetapir PET Cross-sectional Total: n=107(64±8) Higher 18F-florbetapir BPND relates to steeper rate of decline on memory, attention/executive and language
Verfaillie et al. (2019) [33] CCI
Composite of 4 questions
18F-florbetapir PET Cross-sectional Total: n=106(63.83±7.65) Higher cortical amyloid deposition relates to SCD-related worries and higher memory deficit awareness but not to SCD questionnaires
Zwan et al. (2016) [44] MAC-Q
18F-flutematamol PET
Cross-sectional Low amyloid burden: n=229(71.9±6.5)
High amyloid burden: n=78(75.0±7.2)
SMC with younger age and ApoE ɛ4 carriers had higher amyloid burden.
Swinford et al. (2018) [50] E-Cog 18F-flortaucipir PET Cross-sectional CN: n=40(76.48±7.211)
SMC: n=11(71.55±5.11)
EMCI: n=31(75.32±7.29)
Memory concern and the self-perception relate to tau aggregation.
Cavedo et al. (2018) [60] Memory complaints 18F-flortaucipir -PET
Cross-sectional Women: n=201(76.02±3.24)
Men had higher amyloid load glucose hypometabolism and lower RSFC.
Gardener et al. (2016) [58] 1 binary question FDG-PET Cross-sectional All: n=43(66±10.1)
n=20 (68±11.4)
Positive association between memory immediate recall and FDG-PET SUVR in the right amygdala in SMC individuals.
Matias-Guiu et al. (2017) [61] Memory complaint FDG-PET Cross-sectional HC: n=20(65.0±10.6)
SMC: n=9(72.4±10.6)
FCSRT positively correlate with metabolism in the medial and anterior temporal region bilaterally, the left precuneus, and posterior cingulate; BNT results correlate with metabolism in the middle temporal, superior, fusiform, and frontal medial gyri bilaterally; VOSP results relate to the occipital and parietotemporal regions bilaterally; ToL scores correlate to metabolism in the right temporoparietal and frontal regions
Mosconi et al. (2008) [55] Structured interview FDG-PET Cross-sectional SMC- ApoE ɛ4-: n=7(63±5)
SMC+ ApoE ɛ4-: n=8(60±9)
SMC- ApoE ɛ4+: n=7(54±9)
SMC+ ApoE ɛ4+: n=6(59±7)
ApoE ɛ4+ carriers had decreased CMRglc and higher CSF IP, P-Tau, T-Tau, and P-Tau/Amyloid42 levels. SMC had reduced CMRglc. ApoE genotype and SMC interacted on lowest PHG CMRglc and the highest CSF IP, P-Tau, and P-Tau/Amyloid42 levels.
Scheef et al. (2012) [59] Memory clinic consultation
1 binary question
Cross-sectional NC: n=56(66.4±7.2)
SMI: n=31(67.6±6.2)
SMI had hypometabolism in the right precuneus and hypermetabolism in the right medial temporal lobe and gray matter atrophy in the right hippocampus. Association between longitudinal memory decline and reduced glucose metabolism in the right precuneus at baseline.
Song et al. (2016) [56] Memory complaint FDG-PET
Cross-sectional HC: n=42(68.02±5.44)
SMI: n=31(69.94±6.44)
MCI: n=47(69.55±6.65)
SMI had hypometabolism in the periventricular regions. SMI had hypometabolism in the parietal, precentral frontal, and periventricular regions.
Vannini et al. (2017) [57] MFQ PiB-PET
Cross-sectional All: n=251(73.3±6.2)
amyloid-: n=190(72.8±6.1)
amyloid+: n=61(74.9±6.2)
Correlation between SMCs and FDG metabolism. SMCs interacted with amyloid burden on FDG metabolism in the bilateral medial temporal lobes.
  1. SCC Subjective cognitive complaints, ND Neurodegeneration, FDG 18F-Fluorodeoxyglucose, MAC-Q Memory assessment clinics questionnaire, SMD Subjective memory decline, FTP Flortaucipir, SCD Subjective cognitive decline, CDR Clinical dementia rating, AD Alzheimer’s disease, SMI Subjective memory impairment, CMRglc Cerebral metabolic rates for glucose, ApoE Apolipoprotein E, FCSRT Free and cued selective reminding test, BNT Boston naming test, VOSP Visual object and space perception battery, ToL Tower of London test, CSF Cerebrospinal fluid, IP Isoprostane, SUVR Standardized uptake value ratio, SCI Subjective cognitive impairment, MCI Mild cognitive impairment, NC Normal control, PET Positron emission tomography, PiB Pittsburgh compound B. ADNI: Alzheimer’s Disease Neuroimaging Initiative, MRI Magnetic resonance imaging, MFQ Mood and Feelings Questionnaire, E-Cog Everyday Cognition Scale, RSFC Resting-state functional connectivity