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From New York University School of Medicine (L.M., R.M., R.S., M.B., L.G., K.R., E.P., W.T., S.D.S., M.J.d.L.), New York; and Nathan S. Kline Institute for Psychiatric Research (W.T., M.J.d.L.), Orangeburg, NY.
Address correspondence and reprint requests to Dr. Lisa Mosconi, Department of Psychiatry, NYU School of Medicine, 550 First Avenue, New York, NY 10016 lisa.mosconi{at}med.nyu.edu; or Dr. Mony de Leon, Department of Psychiatry, NYU School of Medicine, 560 First Avenue, New York, NY 10016 mony.deleon{at}med.nyu.edu
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.
Abbreviations: AD = Alzheimer disease; ApoE-4 = apolipoprotein E-4 genotype; CMRglc = cerebral metabolic rate for glucose; FDG-PET = 2-[18F]fluoro-2-deoxy-d-glucose positron emission tomography; FH = family history; FH– = negative family history of AD; FHm = maternal history of AD; FHp = paternal history of AD; FWHM = full-width at half maximum; GDS = Global Deterioration Scale; GLM = General Linear Model; MCI = mild cognitive impairment; MMSE = Mini-Mental State Examination; MNI = McGill Neurologic Institute; mtDNA = mitochondrial DNA; NL = normal individuals; PCC = posterior cingulate cortex; PHG = parahippocampal gyrus; SMC = subjective memory complaints.
Supplemental data at www.neurology.org
Editorial, page 486
e-Pub ahead of print on November 12, 2008, at www.neurology.org.
Supported by NIH-NIA AG13616, AG12101, AG08051, AG022374, NIH-NCRR MO1RR0096, and the Alzheimer’s Association.
Disclosure: The authors report no disclosures.
Received April 30, 2008. Accepted in final form July 24, 2008.
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