|Title||Declining brain glucose metabolism in normal individuals with a maternal history of Alzheimer disease.|
|Publication Type||Journal Article|
|Year of Publication||2009|
|Authors||Mosconi L, Mistur R, Switalski R, Brys M, Glodzik L, Rich K, Pirraglia E, Tsui W, De Santi S, de Leon MJ|
|Date Published||2009 Feb 10|
|Keywords||Aged, Aged, 80 and over, Aging, Alzheimer Disease, Brain, Female, Genetic Predisposition to Disease, Glucose, Heterozygote, Humans, Male, Middle Aged, Mothers|
BACKGROUND: At cross-section, cognitively normal individuals (NL) with a maternal history of late-onset Alzheimer disease (AD) have reduced glucose metabolism (CMRglc) on FDG-PET in the same brain regions as patients with clinical AD as compared to those with a paternal and a negative family history (FH) of AD. This longitudinal FDG-PET study examines whether CMRglc reductions in NL subjects with a maternal history of AD are progressive.
METHODS: Seventy-five 50- to 82-year-old NL received 2-year follow-up clinical, neuropsychological, and FDG-PET examinations. These included 37 subjects with negative family history of AD (FH-), 9 with paternal (FHp), and 20 with maternal AD (FHm). Two subjects had parents with postmortem confirmed AD. Statistical parametric mapping was used to compare CMRglc across FH groups at baseline, follow-up, and longitudinally.
RESULTS: At both time points, the FH groups were comparable for demographic and neuropsychological characteristics. At baseline and at follow-up, FHm subjects showed CMRglc reductions in the parieto-temporal, posterior cingulate, and medial temporal cortices as compared to FH- and FHp (p < 0.001). Longitudinally, FHm had significant CMRglc declines in these regions, which were significantly greater than those in FH- and FHp (p < 0.05).
CONCLUSIONS: A maternal history of Alzheimer disease (AD) predisposes normal individuals to progressive CMRglc reductions in AD-vulnerable brain regions, which may be related to a higher risk for developing AD.
|PubMed Central ID||PMC2677512|
|Grant List||R01 AG022374 / AG / NIA NIH HHS / United States |
M01 RR000096 / RR / NCRR NIH HHS / United States
MO1RR0096 / RR / NCRR NIH HHS / United States
R01 AG013616 / AG / NIA NIH HHS / United States
P30 AG008051 / AG / NIA NIH HHS / United States
R01 AG012101 / AG / NIA NIH HHS / United States
AG022374 / AG / NIA NIH HHS / United States
AG13616 / AG / NIA NIH HHS / United States
AG08051 / AG / NIA NIH HHS / United States
AG12101 / AG / NIA NIH HHS / United States