Maternal family history of Alzheimer's disease predisposes to reduced brain glucose metabolism.
Publication Type | Academic Article |
Authors | Mosconi L, Brys M, Switalski R, Mistur R, Glodzik L, Pirraglia E, Tsui W, De Santi S, de Leon M |
Journal | Proc Natl Acad Sci U S A |
Volume | 104 |
Issue | 48 |
Pagination | 19067-72 |
Date Published | 11/14/2007 |
ISSN | 1091-6490 |
Keywords | Alzheimer Disease, Cerebral Cortex, Genomic Imprinting, Glucose, Positron-Emission Tomography |
Abstract | Having a parent affected with late-onset Alzheimer's disease (AD) is a risk factor for developing AD among cognitively normal subjects. We examined whether cognitively normal subjects with a parental family history of AD show cerebral metabolic rate of glucose (CMRglc) reductions consistent with AD as compared with those without a family history and whether there are parent gender effects. Forty-nine 50- to 80-year-old normal subjects were examined who received clinical, neuropsychological, and 2-[(18)F]fluoro-2-deoxy-d-glucose-positron emission tomography examinations, including 16 subjects with a maternal (FHm) and eight with a paternal (FHp) family history of AD and 25 with no family history (FH(-)). FH groups were comparable for demographic and neuropsychological measures. As compared with both FH(-) and FHp groups, FHm subjects showed CMRglc reductions in the same regions as clinically affected AD patients, involving the posterior cingulate cortex/precuneus, parietotemporal and frontal cortices, and medial temporal lobes (P < 0.05, corrected for multiple comparisons). These effects remained significant after accounting for possible risk factors for AD, including age, gender, education, apolipoprotein E genotype, and subjective memory complaints. No CMRglc differences were found between FHp and FH(-) subjects. This study shows a relationship between reduced CMRglc in AD-vulnerable brain regions and a maternal family history of AD in cognitively normal individuals. |
DOI | 10.1073/pnas.0705036104 |
PubMed ID | 18003925 |
PubMed Central ID | PMC2141909 |