A growing body of research on Alzheimer’s disease suggests an infectious trigger for the development of the disease. According to Brian Balin, PhD, professor of pathology and chair of bio-medical sciences at Philadelphia College of Osteopathic Medicine, this could be the key to stopping the destructive process of Alzheimer’s before it even starts.
For the past several decades, Balin—who recently co-authored an editorial in the Journal of Alzheimer’s Disease which called for more focus and funding on this area of research—and his colleagues have operated under the hypothesis that infection is the root cause of Alzheimer’s disease—the first link in a chain of events that causes cells in the brain to malfunction and produce too much waste, which then causes the brain to defend itself by creating the tau and amyloid buildup that is synonymous with the disease.
“The ‘waste’ blocks the ability of the cell to create chemical messengers within the cells as well as the ability to communicate with other cells,” said Balin. “Once the cells begin to misbehave, they continue until they die. As these cells die, the ones they communicate with die. This process then continues along typical cognitive pathways leading to further functional and cognitive deficits.”
Existing research has shown that a change in the sense of smell is one of the earliest symptoms of Alzheimer’s, along with early learning and memory deficits. Balin explains that the path from the nose to the brain—the olfactory pathway—is highly and directly connected to the brain’s learning and memory centers. To that end, he and his team hypothesize that breathing in harmful pathogens could trigger the malfunctioning of cells in the brain.
Balin and his team have studied the brain tissues of those who died of Alzheimer’s, and were able to identify the bacteria Chlamydia pneumoniae in the cells of 85-90 percent of those brains. That bacteria (different from the sexually transmitted form), can enter through the nose via that olfactory pathway, and could trigger the process of cell damage.
“It is possible to catch an infection that would require the use of valuable brain energy to defend. When the brain defends against an infection, you get inflammation in the brain,” said Balin. “The inflammatory response, once triggered, can hang out, damaging the cells. So, if the infection was a gun, the inflammatory response would be the bullet. With repeated firing, your brain cells begin to malfunction and die.”
Balin likens this process to those who are predisposed toward depression. “One person could go through life without developing the disease, while another person could experience it. For the latter individual, they may have experienced an environmental episode, like losing a mother, which would trigger a biological response. So, the gun (that biological predisposition) wouldn’t be a problem until there was a bullet (the mother’s death). Then, that person would experience depression.”
Now that Balin and other researchers are honing in on infection as a suspected trigger to Alzheimer’s, he says the next step is to focus on avoiding and combatting infection, which could ultimately prevent the disease. “This prevention is just as important, if not more, as the majority of research currently focuses on slowing down the progression of cell damage after disease diagnosis,” said Balin. “The latter is just a Band-Aid approach. But the former could stop the process before it starts.”
Source: Philadelphia College of Osteopathic Medicine