Return to search

Analyzing perivascular collagen IV density and cognitive decline in hypertensive rhesus macaques

Cognitive decline is one of the most common symptoms from neuropathology as well as a part of natural aging. While there may be a number of factors that contribute to age-related cognitive decline, previous research has shed a light on the role of chronic hypertension. The effect of hypertension on cognitive decline through small vessel disease is referred to as Vascular Cognitive Impairment and Dementia (VCID). However, the exact molecular pathology behind VCID is not very well understood. Using a non-human primate model of hypertensive aging with the Macaca mulatta, (more commonly known as the Rhesus Macaque) this project builds on previous research implicating collagen IV as part of the cascade of molecular changes that occur in VCID.
This project evaluated collagen IV thickness around blood vessels in the corpus callosum and cingulum bundle of normotensive and hypertensive monkeys. as well as determined vessel properties such as total vessel area and perimeter length to evaluate the relationship to scores from the subjects cognitive testing batteries. The results from this project will allow for an examination of the effects on hypertension on vascular properties and possible mechanisms for the development of cognitive impairments.
Data collected from this research shows significant differences of collagen IV thickness in the Corpus Callosum between hypertensive and normotensive groups. Similarly, in the cingulum bundle we see that the difference between these groups in collagen IV thickness is trending towards significance. The relationship between average collagen IV densities, blood pressure at perfusion, and cognitive testing scores also showed trending relationships in both the cingulum bundle and the corpus callosum. These results demonstrate how prolonged hypertension can negatively influence cognitive abilities and implicates increases in collagen IV around small vessels in white matter as a significant factor in the molecular cascade which results in cognitive impairment.

Identiferoai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/38677
Date10 October 2019
CreatorsLobo, Alexander
ContributorsRosene, Doug L., Moore, Tara L.
Source SetsBoston University
Languageen_US
Detected LanguageEnglish
TypeThesis/Dissertation

Page generated in 0.0026 seconds