Dr. Brian Balin is an experimental neuropathologist who studies the link between infection and inflammation in the body and neurological disorders. He is an internationally recognized expert in the field of Alzheimer’s disease research. Among his research interests are: Infection with Chlamydia pneumoniae as a trigger in the neuroinflammation and neurodegeneration in Alzheimer’s disease, effects of infection and inflammation on the blood brain barrier in cerebrovascular disease, and pathogenesis of chronic disease associated with the aging process. He received his PhD from the University of Maryland School of Medicine at Baltimore and a bachelor’s degree in Microbiology from the University of Maryland.
Late-onset Alzheimer’s disease, occurring after age 65, accounts for the majority of all cases.
Prevailing theories suggest age as the number one risk factor, followed by variations of a gene that helps carry cholesterol in the blood.
But what if that’s not the whole story?
For 20 years, we have been studying links between infection and late-onset Alzheimer’s. We found that a respiratory organism, Chlamydia pneumoniae, infected a large percentage of brain tissues of those who died from Alzheimer’s. It’s a bacterium that acts similar to a virus as it enters into our bodies’ cells, and our evidence shows that it can infect nasal cells responsible for detecting smell.
The organism travels from the nose to the olfactory regions of the brain where early symptoms of Alzheimer’s may first occur, including changes in sense of smell and short-term memory problems. This suggests that this area of the brain can be vulnerable, and that infection here may cause the damage leading to those changes. Mice infected intranasally with this organism develop some of the same pathological deposits seen in Alzheimer’s, suggesting that infection entering the brain in this way could trigger damage and neurodegeneration.
Other experiments have shown that this organism can lead to long-term infections in the brain; that inflammation occurs following the infection; and that it can accumulate in brains of those with genetic risk factors. These findings could link infection and certain genetic profiles seen in Alzheimer’s.
More research is needed to clarify how infection triggers neurodegeneration in this disease.
Biomarkers of infection and inflammation may hold the key to eventual diagnosis and provide clues as to who may be at greatest risk for late-onset Alzheimer’s. This knowledge could lead to the development of anti-infective and anti-inflammatory therapies that not only treat the disease, but prevent it entirely.