Declining brain glucose metabolism in normal individuals with a maternal history of Alzheimer disease
Open accessAbstract
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.
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Maternal inheritance appears to determine several AD endophenotypes.
“Maternal inheritance appears to determine several AD endophenotypes.”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [133]
Cognitively intact children of AD mothers, relative to children of AD fathers, show greater age-associated brain atrophy, faster longitudinal brain atrophy, increased Aβ plaque deposition, elevated CSF oxidative stress markers, and AD-like CSF Aβ changes.
“Subsequent studies found that the cognitively intact children of AD mothers, relative to the cognitively intact children of AD fathers, show greater degrees of age-associated brain atrophy, faster rates of longitudinal brain atrophy, increased Aβ plaque deposition, elevated cerebrospinal fluid (CSF) oxidative stress markers, and AD-like CSF Aβ changes [130-137].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [133]
IN insulin may support impaired brain glucose turnover in patients with AD and at-risk individuals.
“In addition to improvements in insulin signalling, IN insulin may support impaired brain glucose turnover in patients with AD and at-risk individuals.143,144”
From Intranasal insulin (2021) · cites this paper as [144]
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- Authors
- Mosconi, L., Mistur, R., Switalski, R., Brys, M., Glodzik, L., Rich, K., Pirraglia, E., Tsui, W., De Santi, S., & de Leon, M. J.
- Affiliations
- Nathan Kline Institute for Psychiatric Research (US)
- 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.
- Venue
- Neurology
- Published
- 2009-02-10
- Volume
- 72
- Issue
- 6
- Pages
- 513-520
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- PMC
- PMC2677512
- OpenAlex
- W1964043919
- Cited by
- 188
- References
- 36
- Citations by year
- 2026: 4 · 2025: 2 · 2024: 5 · 2023: 5 · 2022: 12 · 2021: 8 · 2020: 8 · 2019: 5 · 2018: 8 · 2017: 10 · 2016: 7 · 2015: 11 · 2014: 15 · 2013: 18 · 2012: 21
- FWCI
- 11.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neurology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alzheimer's Association
- National Institutes of Health (MO1RR0096, AG12101, AG08051)
- National Institute on Aging (AG022374, R01AG022374, AG 12101, R01AG012101, P30AG008051, AG 08051, R01AG013616, AG 13616)
- National Center for Research Resources (MO1-RR-0096, M01RR000096)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Medical Imaging Techniques and Applications
- Keywords
- Alzheimer's disease, family history (medicine), maternal history, brain glucose metabolism, FDG-PET, cognitively normal individuals, longitudinal decline, temporoparietal cortex, posterior cingulate cortex, medial temporal cortex, familial risk, neurodegeneration
- MeSH terms
- Aged, Aged, 80 and over, Aging, Alzheimer Disease, Brain, Female, Glucose, Heterozygote, Humans, Male, Middle Aged, Mothers, Genetic Predisposition to Disease
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