Protein from the liver may cause Alzheimer’s disease in the brain
The liver's amyloid protein can promote brain dementia, reports PLOS Biology. The data show that the liver may play a significant role in the initiation or progression of Alzheimer's disease.
Deposits of amyloid-beta (A-beta) in the brain are one of the pathological hallmarks of Alzheimer's disease (AD) and are implicated in neurodegeneration in both human patients and animal models of the disease. But A-beta is also present in peripheral organs, and blood levels of A-beta correlate with cerebral amyloid burden and cognitive decline, raising the possibility that peripherally produced a-beta may contribute to the disease. The scientists discovered that mice exhibited neurodegeneration and brain atrophy, as well as neurovascular inflammation and capillary malfunction, both hallmarks of Alzheimer's disease.
This study's findings show that A-beta produced in the liver may contribute to human disease. They may have huge consequences for understanding Alzheimer's if that contribution is large. Most disease models to far have focused on A-beta overproduction in the brain, which resembles rare genetic Alzheimer's cases. The vast majority of AD cases, however, do not appear to be caused by A-beta overproduction in the brain. A high-fat diet, for example, may increase A-beta liver production.
Its effects on brain capillaries could be crucial in the illness process. This discovery demonstrates that a person's diet and some medications that target lipoprotein amyloid could potentially reduce their risk or halt the progression of Alzheimer's disease.