ArticleBrain : a journal of neurology2006
Familial risk for Alzheimer's disease alters fMRI activation patterns.
Article in Brain : a journal of neurology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 2 of them syntheses that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
98 citing papers in PubMed, 2 syntheses or guidelines pooled it, 173 citations in OpenAlex.
- Cognitive Functioning of Unaffected First-degree Relatives of Individuals With Late-onset Alzheimer's Disease: A Systematic Literature Review and Meta-analysis.Neuropsychology review · 2023Pooled it
- Alzheimer Disease and Epilepsy: A Mendelian Randomization Study.Neurology · 2023Pooled it
- Proximal improvement and higher-order resting state network change after multidomain cognitive training intervention in healthy older adults.GeroScience · 2022Trial
- Trial
- Cortical correlates of self-generation in verbal paired associate learning.Brain research · 2012Trial
- mTORC2-NaChannels (Austin, Tex.) · 2026Article
- Functional and morphological alterations of light detection circuits in postmortem retina from donors with different stages of Alzheimer's-like pathology.Communications biology · 2026Article
- The rise and deceleration of neuronal excitability in aging and Alzheimer's disease: Mechanisms, implications, and therapeutic targets.Ageing research reviews · 2026Review
- Astrocytes as Therapeutic Targets in Neurodegenerative Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- Chronic optogenetic activation of hippocampal CA1 neurons triggers Alzheimer's disease-like proteomic remodeling.iScience · 2025Article
- Chaperone-mediated autophagy regulates neuronal activity by sex-specific remodelling of the synaptic proteome.Nature cell biology · 2025Article
- Adiponectin Receptor Agonist Ameliorates Synaptic Dysfunction in 3xTg Alzheimer's Disease Mouse Model by Activation of AMPK.CNS neuroscience & therapeutics · 2025Article
- Abnormal calcium activity and CREB phosphorylation are associated with motor memory impairment in presenilin-1 mutant knock-in mice.Cell calcium · 2025Article
- Longitudinal excitation-inhibition balance altered by sex and APOE-ε4.Communications biology · 2025Article
- Article
- Excessive Alcohol Use as a Risk Factor for Alzheimer's Disease: Epidemiological and Preclinical Evidence.Advances in experimental medicine and biology · 2025Review
- Xanthohumol Protects Against Neuronal Excitotoxicity and Mitochondrial Dysfunction in APP/PS1 Mice: An Omics-Based Study.Nutrients · 2024Article
- Chronic Neuronal Hyperexcitation Exacerbates Tau Propagation in a Mouse Model of Tauopathy.International journal of molecular sciences · 2024Article
- Adenosine deficiency facilitates CA1 synaptic hyperexcitability in the presymptomatic phase of a knock in mouse model of Alzheimer's disease.bioRxiv : the preprint server for biology · 2024Article
- Structural lesions and transcriptomic specializations shape gradient perturbations in Wilson disease.Brain communications · 2024Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease poses a looming crisis for the health care system as well as society in general. The low efficacy of current treatments for those already affected with this disease has prompted the suggestion that interventions might be more successful if they were applied before the development of significant pathology, that is, when individuals are clinically asymptomatic. Currently, the field requires a sensitive and specific diagnostic tool for identifying those individuals destined to develop this disease. As a first step, we present here an analysis of cross-sectional data for 95 asymptomatic offspring (50-75 years of age) of autopsy-confirmed late-onset familial Alzheimer's disease cases and 90 age-matched controls, studied with functional magnetic resonance imaging (fMRI) to investigate brain activation patterns. Analysis of activation in response to a paired-associates memory paradigm found significantly different patterns in these groups. At-risk individuals showed more intense and extensive activation in the frontal and temporal lobes including the hippocampus during memory encoding, an increase unrelated to the APOE epsilon4 allele. They also showed decreased activation particularly in the cingulum and thalamus during both the encoding and recall phases of the task. These results demonstrate that asymptomatic individuals, at genetic risk for development of late-onset Alzheimer's disease by virtue of familial clustering, show functional activation patterns distinct from those without such risk more than a decade before their parent's onset age. While longitudinal study is needed to determine whether these patterns, or a subset of them, are predictive of disease onset, these findings suggest that functional neuroimaging holds promise as a method of identifying pre-clinical Alzheimer's disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.