TY  - JOUR
AU  - Abdelmoity, Omar
AU  - Wisch, Julie K
AU  - Kennedy, James T
AU  - Goyal, Manu
AU  - Vlassenko, Andrei
AU  - Flores, Shaney
AU  - Handen, Benjamin L
AU  - Head, Elizabeth
AU  - Keator, David
AU  - Rafii, Michael S
AU  - Lao, Patrick
AU  - Lai, Florence
AU  - Rosas, H Diana
AU  - Hartley, Sigan L
AU  - Zaman, Shahid
AU  - Brickman, Adam M
AU  - Tudorascu, Dana
AU  - Lee, Joseph H
AU  - Allegri, Ricardo Francisco
AU  - Keefe, Sarah
AU  - la Fougère, Christian
AU  - Llibre-Guerra, Jorge
AU  - Ikeuchi, Takeshi
AU  - Morris, John C
AU  - Roh, Jee Hoon
AU  - Day, Gregory S
AU  - Levin, Johannes
AU  - Schofield, Peter R
AU  - Gordon, Brian A
AU  - Benzinger, Tammie L S
AU  - Ances, Beau M
AU  - Syndrome, Alzheimer's Biomarker Consortium-Down
TI  - Cross-Sectional FDG in Down Syndrome and Autosomal Dominant Alzheimer's Disease.
JO  - Annals of neurology
VL  - 98
IS  - 6
SN  - 0364-5134
CY  - Hoboken, NJ
PB  - Wiley-Blackwell
M1  - DZNE-2025-01348
SP  - 1237 - 1248
PY  - 2025
AB  - Directly compare the brain glucose patterns seen with [F-18] fluorodeoxyglucose (FDG) positron emission tomography (PET) between 2 genetically determined forms of Alzheimer's disease: Down syndrome (DS) and autosomal dominant Alzheimer's disease (ADAD).Cross-sectional analyses of FDG were performed in individuals with DS (n = 76) from the Alzheimer Biomarker Consortium-Down Syndrome (ABC-DS), ADAD (n = 297), and neurotypical familial controls (n = 188) from the Dominantly Inherited Alzheimer Network (DIAN). Within-group linear regression models and generalized additive models were performed for select regional FDG uptake measures (isthmus cingulate and inferior parietal, precuneus, middle temporal gyrus, and precentral gyrus). Age, sex, apolipoprotein (APOE) ε4 carrier status, and cortical amyloid burden were included within these analyses.Even 20 years before expected onset of clinical symptoms, FDG uptake was lower for DS compared to neurotypical familial controls (p < 0.01). ADAD baseline FDG was similar to neurotypical familial controls until 7 years before expected symptom onset. Both symptomatic individuals with DS and ADAD had lower FDG compared to neurotypical familial controls (p < 0.01). A higher amyloid burden was associated with lower FDG for both genetic forms, with similar rates of decline in FDG uptake for DS and ADAD who were amyloid positive.Brain glucose metabolism is substantially lower for people with DS, even in individuals who are cognitively stable. The patterns of FDG decline are distinct in these 2 genetically determined forms of AD. The diagnostic utility of FDG-PET is specific to the genetic form of AD. ANN NEUROL 2025;98:1237-1248.
KW  - Humans
KW  - Alzheimer Disease: diagnostic imaging
KW  - Alzheimer Disease: genetics
KW  - Alzheimer Disease: metabolism
KW  - Male
KW  - Female
KW  - Fluorodeoxyglucose F18: metabolism
KW  - Cross-Sectional Studies
KW  - Down Syndrome: diagnostic imaging
KW  - Down Syndrome: metabolism
KW  - Down Syndrome: genetics
KW  - Positron-Emission Tomography
KW  - Middle Aged
KW  - Adult
KW  - Aged
KW  - Brain: diagnostic imaging
KW  - Brain: metabolism
KW  - Radiopharmaceuticals
KW  - Glucose: metabolism
KW  - Fluorodeoxyglucose F18 (NLM Chemicals)
KW  - Radiopharmaceuticals (NLM Chemicals)
KW  - Glucose (NLM Chemicals)
LB  - PUB:(DE-HGF)16
C6  - pmid:40977577
DO  - DOI:10.1002/ana.78002
UR  - https://pub.dzne.de/record/282588
ER  -