Apolipoprotein E polymorphism influences not only cerebral senile plaque load but also Alzheimer-type neurofibrillary tangle formation
Abstract
Only recently, evidence was provided that apolipoprotein E allele epsilon 4 located on Chromosome 19 is associated with late onset (i.e. senile) sporadic Alzheimer's disease. Histologically, Alzheimer's disease is associated with intraneuronal neurofibrillary changes and extraneuronal A4/beta-amyloid deposition. We set out with a histological staging system which considers the gradual development of Alzheimer's disease-related histological changes over time and correlates highly with the cognitive decline ante mortem. Our analysis revealed that both the mean stage for A4/beta-amyloid deposits and the mean stage for neurofibrillary tangles get significantly shifted upwards in epsilon 4-carriers. This represents an earlier onset of the histopathological process of about one decade. The fact that both types of Alzheimer's disease-related changes correlate positively with the prevalence of the epsilon 4-allele suggests for a causal relationship between the apolipoprotein E polymorphism and the development of Alzheimer's disease.
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Some studies reported a positive relationship between neurofibrillary tangle density and apoE ε4 allele dosage.
“Although some studies reported a positive relationship between the neurofibrillary tangle density and apoE ε4 allele dosage (Ghebremedhin et al., 1998; Nagy et al., 1995; Ohm et al., 1995; Polvikoski et al., 1995)”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Ohm et al., 1995
ApoEε4 has reduced ability to suppress inflammatory stimuli and higher densities of NFTs have been reported in ApoEε4 carriers.
“Additionally, ApoEε4 has been found to have reduced ability to suppress inflammatory stimuli and higher densities of NFTs have been reported in ApoEε4 carriers [88].”
From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [88]
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References 21 · Cited by 157
- Authors
- Ohm, T. G., Kirca, M., Bohl, J., Scharnagl, H., Groβ, W., & März, W.
- Affiliations
- Goethe University Frankfurt (DE)
- Johannes Gutenberg University Mainz (DE)
- Corresponding author
- Ohm, T.G.
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 1995-06
- Volume
- 66
- Issue
- 3
- Pages
- 583-587
- ISSN
- 0306-4522 (ISSN-L)
- OpenAlex
- W2064552352
- Cited by
- 157
- References
- 21
- Citations by year
- 2024: 2 · 2023: 2 · 2021: 3 · 2020: 2 · 2019: 2 · 2018: 2 · 2017: 4 · 2016: 2 · 2015: 2 · 2014: 3 · 2013: 3 · 2012: 4
- FWCI
- 10.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- FreiDok plus (Universitätsbibliothek Freiburg) (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- apolipoprotein E, APOE ε4, Alzheimer's disease, neurofibrillary tangles, amyloid plaques, amyloid-beta deposition, genetic polymorphism, histological staging, disease onset, cognitive decline, sporadic Alzheimer's disease
- MeSH terms
- Age Factors, Aged, Aged, 80 and over, Alleles, Alzheimer Disease, Apolipoproteins E, Brain, Chromosomes, Human, Pair 19, Genotype, Humans, Middle Aged, Polymorphism, Genetic, Regression Analysis, Amyloid beta-Peptides, Neurofibrillary Tangles
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