Alzheimer’s disease is a form of dementia that progressively hinders memory and thinking skills among older people. This irreversible brain disorder cannot be cured as of now, but current studies are progressing towards developing treatments and preventative measures.
A process of removing a protein linked to higher risk of Alzheimer’s from the brains of mice without obstructing learning and memory has been found, according to a study from the Peter O’Donnell Jr. Brain Institute (1).
The protein focused on was a specific form of apolipoprotein E (ApoE), which is known to cause toxic plaque build-up in the brains of Alzheimer’s patients (1). Its direct effects, however, are on the cardiovascular system. Although minimizing the effect of ApoE can potentially treat Alzheimer’s disease, researchers are still unsure of whether or not the protein is needed for normal brain function.
The research team at the Peter O’Donnell Jr. Brain Institute tested the absence of ApoE in the brains of mice (2). Their experimental design consisted of developing a novel mouse model that expressed normal levels of ApoE in peripheral tissues but significantly reduced ApoE levels in the brain. This allowed the team to evaluate the loss of ApoE compared to a normal plasma lipid profile (2). They found that, if ApoE was still present in the liver to filter cholesterol after its removal from the brain, the mice could keep their memory and learning abilities (1).
If not properly filtered, ApoE can transport cholesterol and similar molecules like b-amyloid throughout the body, creating plaques in the brains of Alzheimer’s patients (1). The ApoE gene produces different types of ApoE, which each have varying capabilities in removing the amyloid (1). ApoE2, ApoE3, and ApoE4 all lead to potential amyloid plaque buildup, with ApoE2 being the least hazardous and ApoE4 being the most so (1). Alzheimer’s is therefore associated with genes producing ApoE4 (1).
Although additional findings are required to determine why cardiovascular problems affect the brain, this study supports the claim that reducing ApoE can become an effective treatment for Alzheimer’s. Research facilities, such as UT Southwestern, look to further study the effects of ApoE4 removal on brain function. Dr. Herz, holder of the Thomas O. and Cinda Hicks Family Distinguished Chair in Alzheimer’s Disease Research and Director of the Center for Translational Neurodegeneration Research, supports this area of research, claiming, “This approach still holds potential (1).”
- UT Southwestern Medical Center. (2016). Protein linked to high risk of Alzheimer’s can be removed from brain without hindering learning, memory. ScienceDaily. Retrieved from www.sciencedaily.com/releases/2016/10/161004130341.htm
- C. Lane-Donovan, W. M. Wong, M. S. Durakoglugil, C. R. Wasser, S. Jiang, X. Xian, J. Herz (2016). Genetic Restoration of Plasma ApoE Improves Cognition and Partially Restores Synaptic Defects in ApoE-Deficient Mice. Journal of Neuroscience, 2016; 36 (39): 10141 DOI:10.1523/JNEUROSCI.1054-16.2016