ArticleFrontiers in psychiatry2020
Genetic Burden for Late-Life Neurodegenerative Disease and Its Association With Early-Life Lipids, Brain, Behavior, and Cognition.
Article in Frontiers in psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Insights into AlphaFold's breakthrough in neurodegenerative diseases.Irish journal of medical science · 2024Review
- Family history of dementia and brain health in childhood and middle age: a prospective community-based study.European journal of epidemiology · 2024Article
- Impact of genetic predisposition to late-onset neurodegenerative diseases on early life outcomes and brain structure.Translational psychiatry · 2024Review
- Article
- Association between polygenic risk for Alzheimer's disease and brain structure in children and adults.Alzheimer's research & therapy · 2023Article
- Integration of multiple-omics data to reveal the shared genetic architecture of educational attainment, intelligence, cognitive performance, and Alzheimer's disease.Frontiers in genetics · 2023Article
- The neuroprotective effect of betanin in trimethyltin-induced neurodegeneration in mice.Metabolic brain disease · 2020Article
- Genetic risk for Alzheimer disease in children: Evidence from early-life IQ and brain white-matter microstructure.Genes, brain, and behavior · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGenetics play a significant role in the etiology of late-life neurodegenerative diseases like Alzheimer's disease, Parkinson's disease, and frontotemporal dementia. Part of the individual differences in risk for these diseases can be traced back decades before the onset of disease symptoms. Previous studies have shown evidence for plausible links of apolipoprotein E (APOE), the most important genetic marker for Alzheimer's disease, with early-life cognition and neuroimaging markers. We aimed to assess whether genome-wide genetic burden for the aforementioned neurodegenerative diseases plays a role in early-life processes.
methodsWe studied children from the Generation R Study, a prospective birth cohort. APOE genotypes and polygenic genetic burdens for Alzheimer's disease, Parkinson's disease, and frontotemporal dementia were obtained through genome-wide genotyping. Non-verbal intelligence was assessed through cognitive tests at the research center around the age of 6 years, and educational attainment through a national school performance test around the age of 11 years. The Child Behavior Checklist was administered around the age of 10 years, and data from the anxious/depressed, withdrawn/depressed, and the internalizing behavior problems scales were used. Children participated in a neuroimaging study when they were 10 years old, in which structural brain metrics were obtained. Lipid serum profiles, which may be influenced by APOE genotype, were assessed from venal blood obtained around the age of 6 years. The sample size per analysis varied between 1,641 and 3,650 children due to completeness of data.
resultsWe did not find evidence that APOE genotype or the polygenic scores impact on childhood nonverbal intelligence, educational attainment, internalizing behavior, and global brain structural measures including total brain volume and whole brain fractional anisotropy (all p > 0.05). Carriership of the APOE ε2 allele was associated with lower and APOE ε4 with higher low-density lipoprotein cholesterol concentrations when compared to APOE ε3/ε3 carriers.
conclusionWe found no evidence that genetic burden for late-life neurodegenerative diseases associates with early-life cognition, internalizing behavior, or global brain structure.
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