ArticleCerebral cortex (New York, N.Y. : 1991)2011
Effects of risk genes on BOLD activation in presymptomatic carriers of familial Alzheimer's disease mutations during a novelty encoding task.
Article in Cerebral cortex (New York, N.Y. : 1991), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Cerebral microvascular changes in healthy carriers of the APOE-ɛ4 Alzheimer's disease risk gene.PNAS nexus · 2024Article
- Article
- Neural Networks in Autosomal Dominant Alzheimer's Disease: Insights From Functional Magnetic Resonance Imaging Studies.Frontiers in aging neuroscience · 2022Review
- Abnormal retinal capillary blood flow in autosomal dominant Alzheimer's disease.Alzheimer's & dementia (Amsterdam, Netherlands) · 2021Article
- Neuroimaging in aging and neurologic diseases.Handbook of clinical neurology · 2019Review
- Different Hippocampus Functional Connectivity Patterns in Healthy Young Adults with Mutations of APP/Presenilin-1/2 and APOEε4.Molecular neurobiology · 2018Article
- Memory performance and fMRI signal in presymptomatic familial Alzheimer's disease.Human brain mapping · 2013Article
- Interaction of age and APOE genotype on cerebral blood flow at rest.Journal of Alzheimer's disease : JAD · 2013Article
- Characterization of Mexican Americans with mild cognitive impairment and Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2013Article
- Family history and APOE-4 genetic risk in Alzheimer's disease.Neuropsychology review · 2012Review
- Effect of mild cognitive impairment and APOE genotype on resting cerebral blood flow and its association with cognition.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2012Article
- Plasma signaling proteins in persons at genetic risk for Alzheimer disease: influence of APOE genotype.Archives of neurology · 2012Article
- Brain imaging in Alzheimer disease.Cold Spring Harbor perspectives in medicine · 2012Review
- Increased fMRI signal with age in familial Alzheimer's disease mutation carriers.Neurobiology of aging · 2012Article
- Assessment of Alzheimer's disease risk with functional magnetic resonance imaging: an arterial spin labeling study.Journal of Alzheimer's disease : JAD · 2012Article
- Increased hippocampal default mode synchronization during rest in middle-aged and elderly APOE ε4 carriers: relationships with memory performance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Autosomal-dominant Alzheimer's disease: a review and proposal for the prevention of Alzheimer's disease.Alzheimer's research & therapy · 2011Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Prior functional magnetic resonance imaging (fMRI) studies have found increased activity-related blood oxygen level-dependent (BOLD) signal in cognitively normal persons at genetic risk for Alzheimer's disease (AD). This has been interpreted as a compensatory response to incipient AD pathology. We studied the effects of fully penetrant familial Alzheimer's disease (FAD) mutations and apolipoprotein E (APOE) genotype on BOLD fMRI during a novelty encoding task in presymptomatic subjects. Twenty-three Mexican or Mexican-American persons at-risk for inheriting FAD mutations performed a block design novelty encoding task, and activation exhibited by FAD mutation carriers (MCs) was contrasted with that of noncarriers (NCs) and among APOE genotype groups. FAD MCs (n = 14) showed decreased BOLD activation in the anterior cingulate gyrus relative to 9 NCs. No increased activation was seen in MCs relative to NCs. Four APOE ε3/4 carriers demonstrated increased BOLD signal compared with 14 ε3/3 carriers in the occipital and perisylvian cortices bilaterally. There were no areas where ε3/3 carriers activated more than ε3/4 carriers. Our findings of increased fMRI activation associated with APOE genotype but not with FAD mutations suggest that APOE exerts an effect on the BOLD signal that is not readily explained as a compensatory phenomenon.
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