ArticleBMC medicine2012
Evidence that an APOE ε4 'double whammy' increases risk for Alzheimer's disease.
Article in BMC medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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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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
10 citing papers in PubMed, 20 citations in OpenAlex.
- Histone Deacetylation in Alzheimer's Diseases (AD); Hope or Hype.Cell biochemistry and biophysics · 2025Review
- Epigenetic mechanisms of neurodegenerative diseases and acute brain injury.Neurochemistry international · 2020Review
- Pharmacoepigenomic Interventions as Novel Potential Treatments for Alzheimer's and Parkinson's Diseases.International journal of molecular sciences · 2018Review
- Epigenetics in Alzheimer's Disease: Perspective of DNA Methylation.Molecular neurobiology · 2018Review
- Milk's Role as an Epigenetic Regulator in Health and Disease.Diseases (Basel, Switzerland) · 2017Review
- Epigenetics of Aging and Alzheimer's Disease: Implications for Pharmacogenomics and Drug Response.International journal of molecular sciences · 2015Review
- The epigenetics of aging and neurodegeneration.Progress in neurobiology · 2015Review
- Aging, Alzheimer's, and APOE genotype influence the expression and neuronal distribution patterns of microtubule motor protein dynactin-P50.Frontiers in cellular neuroscience · 2015Article
- Epilepsy: neuroinflammation, neurodegeneration, and APOE genotype.Acta neuropathologica communications · 2013Article
- Preclinical Alzheimer disease: identification of cases at risk among cognitively intact older individuals.BMC medicine · 2012Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Temporal lobe epilepsy (TLE) is associated with some of the same neuropathological features as those reported for early stages of typical Alzheimer's disease (AD). The APOE ε4 allele is associated with a gene-dose-dependent increase in AD risk and in the severity of amyloid-β (Aβ) pathology. In a study published in the current BMC Medicine, Sue Griffin and colleagues studied markers of brain resilience in the amputated temporal lobes of TLE patients. They discovered compelling evidence that the APOE ε3 isoform in TLE patients is apparently more neuroprotective from Aβ toxicity than is the APOE ε4 isoform, as shown by the reduced levels of neuronal damage, glial activation, and expression of IL-1α in the APOE ε3/ε3 brains. This result points to a new property of APOE isoforms: not only are APOE ε4 alleles associated with increased brain amyloid plaque burden, but these alleles are also apparently inferior to APOE ε3 alleles in conveying resistance to Aβ neurotoxicity. This 'double whammy' result opens up a new direction for studies aimed at elucidating the relevant neurobiological activities of APOE isoforms in the pathogenesis of AD.
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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.