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Impact of the APOE genotype, early-life infection, and sex in Alzheimer’s disease pathology

Sundgren, Anna (2024) MOBM02 20232
Degree Projects in Molecular Biology
Popular Abstract
Anna Sundgren, MOBM02 September 23 - January 24, Department of Biology, Lund University

Baby infection as Alzheimer´s disease protection?

The characteristic pathology of Alzheimer’s disease (AD) includes accumulation of amyloid-beta protein as plaques, and tau-protein as tangles in the brain. Another important feature of the disease is neuroinflammation. One important risk gene for AD is the apolipoprotein E (APOE) gene, that in humans can be classified into six major genotypes, whereof APOE4 is the strongest risk factor. Apolipoprotein E4 is strongly related to neuroinflammation. One of the key players in the innate immune system of the brain and in regulating neuroinflammation, is the microglial cells. These cells can switch... (More)
Anna Sundgren, MOBM02 September 23 - January 24, Department of Biology, Lund University

Baby infection as Alzheimer´s disease protection?

The characteristic pathology of Alzheimer’s disease (AD) includes accumulation of amyloid-beta protein as plaques, and tau-protein as tangles in the brain. Another important feature of the disease is neuroinflammation. One important risk gene for AD is the apolipoprotein E (APOE) gene, that in humans can be classified into six major genotypes, whereof APOE4 is the strongest risk factor. Apolipoprotein E4 is strongly related to neuroinflammation. One of the key players in the innate immune system of the brain and in regulating neuroinflammation, is the microglial cells. These cells can switch appearance between “the good” (balancing and protective) to “the bad” (neurodegenerative). Influences on the immune system from brain injury, disease or other environmental factors contributes to the shape and function of the microglial cells, and thereby how the brain will be affected. Outcomes from AD will include cognitive decline, memory loss and cell death in the brain.
Not only our genes will affect the risk of developing AD, but also our biological sex. These factors are not so easily changed, but how is it with other environmental factors? Like to have an infection that activates our immune system? One bacterial toxin, lipopolysaccharide (LPS), has been shown to affect how brain immune cells will react on other insults later, beneficially as well as detrimentally. One such “later insult” could be the development of AD pathology.
One endogenous molecule that act as a modulator of neuroinflammation is galectin-3 (Gal3). Our project aimed to investigate the impact of early-life infection and biological sex on the hallmarks of AD, in the context of the APOE genotype. For this, we examined mice with different genotypes, sex and that was given a LPS or saline stimuli in early life. By labelling the mice brain tissue with fluorescence, we could get a picture of how the brain was affected regarding the microglial immune cells, amyloid-beta protein plaques and the occurrence of Gal3.
Just like previous research, we found an influence of the genotype, and there were sometimes differences between the sexes. Most important, was an insight that could be further explored, that this early-life infection stimuli could lower the Gal3 levels, and in the context of neuroinflammation thereby mitigate AD pathology. (Less)
Please use this url to cite or link to this publication:
author
Sundgren, Anna
supervisor
organization
course
MOBM02 20232
year
type
H2 - Master's Degree (Two Years)
subject
language
English
id
9149214
date added to LUP
2024-02-28 15:14:23
date last changed
2024-02-28 15:14:23
@misc{9149214,
  author       = {{Sundgren, Anna}},
  language     = {{eng}},
  note         = {{Student Paper}},
  title        = {{Impact of the APOE genotype, early-life infection, and sex in Alzheimer’s disease pathology}},
  year         = {{2024}},
}