ArticleNeuropsychologia2014
A gene-brain-cognition pathway for the effect of an Alzheimer׳s risk gene on working memory in young adults.
Article in Neuropsychologia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Comorbidity Genes of Alzheimer's Disease and Type 2 Diabetes Associated with Memory and Cognitive Function.International journal of molecular sciences · 2024Review
- A cognitive neurogenetic approach to uncovering the structure of executive functions.Nature communications · 2022Article
- Sex-dependent calcium hyperactivity due to lysosomal-related dysfunction in astrocytes from APOE4 versus APOE3 gene targeted replacement mice.Molecular neurodegeneration · 2020Article
- Autophagy and Alzheimer's Disease: From Molecular Mechanisms to Therapeutic Implications.Frontiers in aging neuroscience · 2018Review
- The role of APOE on lipid homeostasis and inflammation in normal brains.Journal of lipid research · 2017Review
- Identification and modification of amyloid-independent phenotypes of APOE4 mice.Experimental neurology · 2016Article
- Neuroimaging genetic risk for Alzheimer's disease in preclinical individuals: From candidate genes to polygenic approaches.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2016Article
- Two Alzheimer's disease risk genes increase entorhinal cortex volume in young adults.Frontiers in human neuroscience · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Identifying pathways by which genetic Alzheimer׳s disease (AD) risk factors exert neurocognitive effects in young adults are essential for the effort to develop early interventions to forestall or prevent AD onset. Here, in a brain-imaging cohort of 59 young adults, we investigated effects of a variant within the clusterin (CLU) gene on working memory function and gray matter volume in cortical areas that support working memory. In addition, we investigated the extent to which effects of CLU genotype on working memory were independent of variation in the strongest AD risk factor gene apolipoprotein E (APOE). CLU is among the strongest genetic AD risk factors and, though it appears to share AD pathogenesis-related features with, APOE, it has been far less well studied. CLU genotype was associated with working memory performance in our study cohort. Notably, we found that variation in gray matter volume in a parietal region, previously implicated in maintenance of information for working memory, mediated the effect of CLU on working memory performance. APOE genotype did not affect working memory within our sample, and did not interact with CLU genotype. To our knowledge, this work represents the first evidence of a behavioral effect of CLU genotype in young people. In addition, this work identifies the first gene-brain-cognition mediation effect pathway for the transmission of the effect of an AD risk factor. Relative to conventional pairwise associations in cognitive neurogenetic research, gene-brain-cognition mediation modeling provides a more integrated understanding of how genetic effects transmit from gene to brain to cognitive function.
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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.