Chronic Hepatitis and Enteritis May Signal Alzheimer's 20 Years Before Onset

An international team led by Stanford University published the results of a study in the New England Journal of Medicine. The findings indicate that a genetic analysis involving 500,000 people revealed that Alzheimer’s disease may not originate in the brain, but rather in other body tissues such as the intestines, liver, and adipose tissue, through chronic inflammatory responses that reach the brain via the bloodstream and the blood-brain barrier. The lead author, Dr. Tony Wyss-Coray, explained that they identified 17 genes associated with systemic inflammation that increase the risk of Alzheimer’s disease by 30 to 50 percent. These genes are strongly expressed in the intestines and liver, rather than in neuronal brain cells.

He added that the study opens the door to new preventive treatments focusing on reducing inflammation in peripheral organs rather than targeting the brain alone. The researchers noted that anti-inflammatory drugs such as canakinumab could delay the onset of Alzheimer’s disease if administered to at-risk patients.

• The team followed participants for up to 25 years and found that those with elevated levels of C-reactive protein (CRP) and interleukin-6 (IL-6) in midlife were 80 percent more likely to develop Alzheimer’s disease after age 60.

• Genetic analyses showed that 12 of the genes associated with Alzheimer’s disease regulate the innate immune response, rather than amyloid metabolism as previously believed.

The team plans to conduct a clinical trial using canakinumab (originally developed to treat heart disease) in individuals with chronic inflammation to determine whether it reduces the risk of Alzheimer’s disease. Researchers warned that current treatments targeting amyloid plaques in the brain may be “late-stage killers,” whereas the solution may lie in the intestines.