Could Your Liver be a Factor in the Development of Alzheimer’s Disease?
Written by Susan Parker | Updated on June 22, 2025
Reviewed by Susan Parker
11 sources cited
Overview
A recent study conducted by researchers from Australia has uncovered a potential mechanism behind Alzheimer's disease. They have identified a harmful protein produced in the liver that can travel through the bloodstream to the brain, causing cell damage, inflammation, and memory loss. This discovery opens up new possibilities for the development of preventive and therapeutic approaches for Alzheimer's disease.
Accumulation of the toxic protein beta amyloid is a critical characteristic of Alzheimer's disease. Recent research indicates that levels of amyloid in the blood of cognitively healthy individuals can accurately reflect the amount of amyloid present in the brain. Moreover, blood tests have shown high accuracy in predicting individuals at risk of developing Alzheimer's in the future. These findings suggest that amyloid-related damage may originate from sources other than the brain and reach the brain via the bloodstream.
Role of Blood in Transporting Brain-Damaging Material
Prior groundbreaking research carried out by scientists from Curtin University revealed that beta amyloid, a key factor in Alzheimer's disease, is not only generated in the brain but is also transported by molecules produced in the liver called triglyceride-rich lipoproteins (TRL). These TRLs can breach the blood-brain barrier and contribute to the onset of Alzheimer's disease. Through genetic manipulation of mice to produce human beta amyloid exclusively in the liver, researchers observed the protein's transfer through the bloodstream by lipoproteins, leading to its entry into the brain. This process resulted in neurodegeneration, brain shrinkage, inflammation, and cognitive decline in the mice.
According to the researchers, their findings support the hypothesis put forth by another research team that the liver, rather than the brain, may act as the primary source of toxic beta amyloid deposits that harm the brain. This may explain why not all individuals with beta amyloid deposits in the brain develop Alzheimer's disease, as the protein's origin could be a crucial factor.
Impact of Diet and Exercise
Scientists believe that issues related to TRL-amyloid metabolism could contribute to the development of Alzheimer's disease. They stress that addressing this metabolic pathway could create new avenues for prevention through dietary and lifestyle changes. While specific strategies were not outlined, it is recommended to follow a diet rich in healthy fats, avoid processed and trans fats, and engage in regular physical activity to regulate blood fats. Additionally, targeting lipid metabolism issues with medications like cholesterol-lowering drugs could be beneficial.
Senior research scientist John Mamo emphasized the importance of managing lipoprotein-amyloid levels in the blood to prevent their seepage into the brain. This approach could potentially lead to novel Alzheimer's disease treatments and help mitigate memory loss.
