ApoA-I Deficiency Increases Cortical Amyloid Deposition, Cerebral Amyloid Angiopathy, Cortical and Hippocampal Astrogliosis, and Amyloid-Associated Astrocyte Reactivity in APP/PS1 Mice
This week we profile a recent publication in Alzheimer’s Research & Therapy from Emily Button (pictured, 4th from left) in the laboratory of Dr. Cheryl Wellington (3rd from left) at the Djavad Mowafaghian Centre for Brain Health.
Can you provide a brief overview of your lab’s current research focus?
Our lab is interested in both Alzheimer’s disease and traumatic brain injury and especially on the role of vascular health within the brain during these diseases. This particular study is part of our focus on how components in the blood, such as high-density lipoproteins (HDL), can affect brain health by promoting health of cerebral vessels.
What is the significance of the findings in this publication?
This publication shows that mice with low levels of HDL (commonly known as the “good cholesterol”) in the blood have worsened brain vascular inflammation in a model of Alzheimer’s disease. Others have previously suggested that high blood levels of HDL reduces Alzheimer’s disease risk however it was not completely understood how this protective effect works. The findings in this publication, together with our previous publication using an in vitro 3-dimensional bioengineered artery model (Robert et al (2017) Molecular Neurodegeneration. 12(1):60) suggest that one way that HDL protects against Alzheimer’s disease is by reducing vascular inflammation in the brain. These findings further support the idea that a healthy diet and physical activity, two factors that can improve HDL levels, are good for brain health.
What are the next steps for this research?
We next plan to bring our research on HDL and the brain vascular system back to humans. We know from the work of others that HDL can lose its protective functions in disease, therefore we are very interested to learn if this protective HDL function on brain vessel inflammation is altered in people with Alzheimer’s disease or other diseases that are risk factors for Alzheimer’s, such as Type 2 Diabetes.
This work was funded by:
This work was supported by operating grants from the Canadian Institutes of Health Research (CIHR), the Canadian Consortium on Neurodegeneration and Aging (CCNA), a Djavad Mowafaghian Centre for Brain Health Catalyst grant, philanthropic funding from the Jack Brown and Family Alzheimer’s Research Foundation, and the Y.P. Heung Foundation. Investigators were also supported by funding from CIHR, UBC, BrightFocus and MSFHR/CCNA doctoral and post-doctoral fellowships.
For more information about her research, check out this Brain Bytes video!