Positron emission tomography in familial Alzheimer disease.
There is increasing evidence for genetic heterogeneity in Alzheimer disease. A longitudinal clinical and imaging study had been established in order to determine whether specific phenotypic profiles are present in aetiologically distinct familial Alzheimer disease (FAD) pedigrees. [18F]fluorodeoxyglucose positron emission tomography has been used in conjunction with statistical parametric mapping to determine the relative distribution of hypometabolism. A parietotemporal deficit has been observed in individuals from both amyloid precursor protein mutation and chromosome 14 linked FAD families. Preliminary data from asymptomatic individuals at risk of FAD shows similar, although a less extensive pattern of deficit.
Kennedy
A M
AM
Department of Neurology, St. Mary's Hospital Medical School, Imperial College, London, England.
Rossor
M N
MN
Frackowiak
R S
RS
D000368:Aged; D000544:Alzheimer Disease / Q000000981:diagnostic imaging / Q000235:genetics*; D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D001786:Blood Glucose / Q000378:metabolism*; D001921:Brain / Q000000981:diagnostic imaging / Q000503:physiopathology; D002883:Chromosomes, Human, Pair 14; D003847:Deoxyglucose / Q000031:analogs & derivatives / Q000378:metabolism; D004734:Energy Metabolism / Q000235:genetics / Q000502:physiology; D019788:Fluorodeoxyglucose F18; D008040:Genetic Linkage / Q000235:genetics; D006801:Humans; D008137:Longitudinal Studies; D010641:Phenotype; D012307:Risk Factors; D014055:Tomography, Emission-Computed
D016564:Amyloid beta-Protein Precursor; D001786:Blood Glucose; D019788:Fluorodeoxyglucose F18; D003847:Deoxyglucose