Deletion of Robo4 worsens neuroinflammation and motor coordination in a mouse model of Alzheimer's disease
Cullen, A. E.; Winder, N.; Lee, B.; Krishna Kumaran, S.; Arora, N.; Wolf, J.; Woltjer, R.; Walker, A.
Show abstract
Declines in vascular integrity are potential contributors to Alzheimers disease (AD) as these result in increased blood-brain barrier permeability and, as a consequence, accelerate neuroinflammation and cognitive impairment. Roundabout guidance receptor 4 (Robo4) is primarily expressed in endothelial cells and stabilizes the vasculature, and thus, has the potential to protect the brain in AD. To study the effect of Robo4 on neuroinflammation and cognitive function in the context of AD, we compared Robo4 knockout and wildtype mice crossed with mice with and without AD mutations (APP/tau). We found that the knockout of Robo4 led to greater astrocyte activation, as demonstrated by GFAP content, but this was dependent on the brain region studied. The knockout of Robo4 also led to greater activated microglia, as assessed by Iba1 content, but only in the presence of AD-related mutations. We found that AD mutations, but not Robo4, were associated with cognitive dysfunction measured by a nest-building test. In contrast, Robo4 deletion, but not AD mutations, was associated with impaired motor coordination. Lastly, Robo4 deletion was associated with greater arterial stiffness, but this trend did not reach statistical significance. In summary, these results demonstrate that Robo4 impacts neuroinflammation, motor coordination, and arterial stiffness, however, the impact on neuroinflammation is dependent on the presence/absence of AD-related mutations and the brain region examined.
Matching journals
The top 2 journals account for 50% of the predicted probability mass.
Similar papers in this journal
Similar papers in this journal
Similar papers in this journal
- Leveraging large multi-center cohorts of Alzheimer Disease endophenotypes to understand the role of Klotho heterozygosity on disease risk 95%
- Voluntary running does not increase capillary blood flow but promotes neurogenesis and short-term memory in the APP/PS1 mouse model of Alzheimers disease 95%
- Protective mutation A673T as a potential gene therapy for most forms of APP Familial Alzheimer's Disease 94%
Similar papers in this journal
- Differences between plasma and CSF p-tau181 and p-tau231 in early Alzheimer’s disease 95%
- The Association of Alzheimer’s Disease-related Blood-based Biomarkers with Cognitive Screening Test Performance in the Congolese Population in Kinshasa 95%
- Exenatide reverts the high-fat-diet-induced impairment of BDNF signaling and inflammatory response in an animal model of Alzheimer’s disease 95%
Similar papers in this journal
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.