No observed effect on brain vasculature of Alzheimer's disease-related mutations in the zebrafish presenilin 1 gene.
Karissa BarthelsonMorgan NewmanCameron J NowellMichael LardelliPublished in: Molecular brain (2021)
Previously, we found that brains of adult zebrafish heterozygous for Alzheimer's disease-related mutations in their presenilin 1 gene (psen1, orthologous to human PSEN1) show greater basal expression levels of hypoxia responsive genes relative to their wild type siblings under normoxia, suggesting hypoxic stress. In this study, we investigated whether this might be due to changes in brain vasculature. We generated and compared 3D reconstructions of GFP-labelled blood vessels of the zebrafish forebrain from heterozygous psen1 mutant zebrafish and their wild type siblings. We observed no statistically significant differences in vessel density, surface area, overall mean diameter, overall straightness, or total vessel length normalised to the volume of the telencephalon. Our findings do not support that changes in vascular morphology are responsible for the increased basal expression of hypoxia responsive genes in psen1 heterozygous mutant brains.
Keyphrases
- wild type
- early onset
- genome wide
- genome wide identification
- endothelial cells
- poor prognosis
- white matter
- cognitive decline
- copy number
- resting state
- cancer therapy
- dna methylation
- transcription factor
- intellectual disability
- multiple sclerosis
- binding protein
- gene expression
- functional connectivity
- autism spectrum disorder
- young adults
- high resolution
- bioinformatics analysis
- cerebral ischemia
- blood brain barrier
- mass spectrometry
- mild cognitive impairment
- pluripotent stem cells
- childhood cancer
- optical coherence tomography