Approximately 1 in 9 adults over the age of 65 have Alzheimer's disease, according to the CDC. The neurological disorder that causes our brains to shrink is the number one cause of dementia worldwide.
In a recent study published in the Proceedings of the National Academy of Sciences of the United States of America (PNAS), Hao Wang and his team found that cholesterol, specifically astrocyte-derived cholesterol, could be the key to understanding Alzheimer's disease.
Alzheimer’s is primarily caused by a protein called “tau”, which creates “tangles” in the brain neurons, and by a substance known as amyloid-beta (Aβ), which forms extracellular plaques.
In fact, several degenerative processes in our bodies can be traced back to plaque accumulation that disrupts the body’s natural function. There are several genetic amyloid diseases where amyloid particles amass in the kidneys or the heart and basically form a barrier of "gunk" that prevents the organs from functioning.
The most common type of plaque is created by LDL cholesterol, which can cause plaque in our blood vessels that harms healthy blood flow and leads to heart disease. But is cholesterol also the key to amyloid-beta accumulation in the brain that leads to Alzheimer’s?
In the PNAS study, the researchers found that astrocyte-derived cholesterol is crucial to balancing between APP, a protein that turns into Aβ, and a soluble called sAPPα, which is a protective product that prevents the amyloid clusters and protects our brain from degeneration. Their study found that the ratio of Aβ to sAPPα is regulated by astrocyte-derived cholesterol.
Astrocytes are types of cells in our brain that are the supporters, or the guards, of the central nervous system, protecting the neurons that oversee our thought and memory processes. The astrocytes are in charge of protecting the neurons from viruses and bacteria, maintaining specific electrolyte balances in the brain fluid and giving neurons the best surroundings in which to work.
The PNAS study found that astrocytes also control the cholesterol in the neurons and basically determine whether the brain will build up amyloid plaque or not. “The pathway establishes cholesterol as a critical lipid that controls the signaling state of a neuron,” claim the researchers. “The rise and fall of Aβ with cholesterol is striking.”
What does this mean? The study concludes that there is still a long way to go by means of researching how our cholesterol levels affect these mechanisms. Cutting back on cholesterol in our food is not likely to solve the problem by itself, but learning the ways in which astrocyte cells regulate cholesterol in the neuron may allow scientists to create ways to prevent Alzheimer’s medically, by inhibiting its pathways.
“This concept is likely important to other biological systems, given the profound effect of cholesterol on human health,” the researchers concluded.