ArticleToxicological sciences : an official journal of the Society of Toxicology2020
The Effects of Gene-Environment Interactions Between Cadmium Exposure and Apolipoprotein E4 on Memory in a Mouse Model of Alzheimer's Disease.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 49 citations in OpenAlex.
- Cadmium-induced gut dysbiosis precedes the onset of hippocampus-dependent learning and memory deficits in mice.Toxicology · 2025Article
- Influence of TPH2 DNA methylation and family functioning, parenting styles on OCD severity.BMC psychiatry · 2025Article
- Heavy metal-induced disruption of the autophagy-lysosomal pathway: implications for aging and neurodegenerative disorders.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025Review
- Associations of Environmental Exposure to Arsenic, Manganese, Lead, and Cadmium with Alzheimer's Disease: A Review of Recent Evidence from Mechanistic Studies.Journal of xenobiotics · 2025Review
- Effect of Interaction of ATG7 and Plasma Metal Concentrations on Cognitive Impairment in Rural China.Journal of molecular neuroscience : MN · 2025Article
- Air Pollution as an Environmental Risk Factor for Alzheimer's Disease and Related Dementias.Medical research archives · 2024Article
- Cadmium inhibits calcium activity in hippocampal CA1 neurons of freely moving mice.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Environmental Toxins and Alzheimer's Disease: a Comprehensive Analysis of Pathogenic Mechanisms and Therapeutic Modulation.Molecular neurobiology · 2024Review
- Article
- JAK2/STAT3 Signaling Pathway and Klotho Gene in Cadmium-induced Neurotoxicity In Vitro and In Vivo.Biological trace element research · 2023Article
- Inducible and Conditional Activation of Adult Neurogenesis Rescues Cadmium-Induced Hippocampus-Dependent Memory Deficits in ApoE4-KI Mice.International journal of molecular sciences · 2023Article
- Gene-environment interactions in Alzheimer disease: the emerging role of epigenetics.Nature reviews. Neurology · 2022Review
- Effect of Chronic Cadmium Exposure on Brain and Liver Transporters and Drug-Metabolizing Enzymes in Male and Female Mice Genetically Predisposed to Alzheimer's Disease.Drug metabolism and disposition: the biological fate of chemicals · 2022Article
- Lead-exposure associated miRNAs in humans and Alzheimer's disease as potential biomarkers of the disease and disease processes.Scientific reports · 2022Article
- Toxic Metals Exposure and APOE4 Gene Variant in Cognitive Decline Disorders.Archives of Razi Institute · 2022Review
- Cadmium exposure modulates the gut-liver axis in an Alzheimer's disease mouse model.Communications biology · 2021Article
- Article
- Sex-specific neurotoxic effects of heavy metal pollutants: Epidemiological, experimental evidence and candidate mechanisms.Environmental research · 2021Review
- Heavy metals and adult neurogenesis.Current opinion in toxicology · 2021Article
- A mechanistic view on the neurotoxic effects of air pollution on central nervous system: risk for autism and neurodegenerative diseases.Environmental science and pollution research international · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cadmium (Cd) is a heavy metal of great public health concern. Recent studies suggested a link between Cd exposure and cognitive decline in humans. The ε4 allele, compared with the common ε3 allele, of the human apolipoprotein E gene (ApoE) is associated with accelerated cognitive decline and increased risks for Alzheimer's disease (AD). To investigate the gene-environment interactions (GxE) between ApoE-ε4 and Cd exposure on cognition, we used a mouse model of AD that expresses human ApoE-ε3 (ApoE3-KI [knock-in]) or ApoE-ε4 (ApoE4-KI). Mice were exposed to 0.6 mg/l CdCl2 through drinking water for 14 weeks and assessed for hippocampus-dependent memory. A separate cohort was sacrificed immediately after exposure and used for Cd measurements and immunostaining. The peak blood Cd was 0.3-0.4 µg/l, within levels found in the U.S. general population. All Cd-treated animals exhibited spatial working memory deficits in the novel object location test. This deficit manifested earlier in ApoE4-KI mice than in ApoE3-KI within the same sex and earlier in males than females within the same genotype. ApoE4-KI but not ApoE3-KI mice exhibited reduced spontaneous alternation later in life in the T-maze test. Finally, Cd exposure impaired neuronal differentiation of adult-born neurons in the hippocampus of male ApoE4-KI mice. These data suggest that a GxE between ApoE4 and Cd exposure leads to accelerated cognitive impairment and that impaired adult hippocampal neurogenesis may be one of the underlying mechanisms. Furthermore, male mice were more susceptible than female mice to this GxE effect when animals were young.
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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.