Are you looking to explore Cerebral Amyloid Angiopathy (CAA) as an independent risk factor for cognitive dysfunction or Alzheimer’s disease? QPS Austria, one of the top preclinical and clinical CROs in Europe, is ready to partner with you to provide visualization and quantification of CAA in murine tissues.
In the last five years, there has been a significant increase in publications and research relating to CAA, including the development of new biomarkers. Research has suggested that CAA is associated with cognitive impairment, and QPS recently took part in a study whose results indicated that CAA is a risk factor for cognitive dysfunction and Alzheimer’s.
In this study, we evaluated CAA in APPSL and 5xFAD transgenic animals by measuring the overlap of 6E10 and collagen IV in the isocortex and hippocampus. We identified the strongest progressive increase of the CAA signal in APPSL mice from 6 to 12 months old. In 5xFAD mice, the total CAA signal was already high at 6 months of age, resulting in a weaker signal increase in later age groups.
This data suggests that both mouse models display a progressive and robust vascular CAA pathology, an independent risk factor for cognitive dysfunction and Alzheimer’s disease.
In the figures above, you can see representative images of amyloid by 6E10 labeling (marked in green) on collagen IV (marked in red) positive vessels (submeningeal arteries) in APPSL mice over age compared to a non-transgenic (ntg) littermate. The nuclei are labeled with DAPI (in blue).
Since 1995, QPS has provided discovery, preclinical, and clinical drug development services. An award-winning leader focused on bioanalytics and clinical trials, QPS is known for proven quality standards, technical expertise, a flexible approach to research, client satisfaction, and turnkey laboratories and facilities. For more information, please email [email protected] or visit www.qpsneuro.com. You can also learn more about QPS Austria’s CAA research in our June 2019 newsletter, which you can find at https://qpsneuro.com/newsletter.