According to a recent research published in the open-access journal PLOS Biology by John Mamo of Curtin University in Bentley, Australia, and colleagues, liver-produced amyloid protein may induce neurodegeneration in the brain. These findings indicate that the liver may be involved in the start or progression of Alzheimer’s disease (AD) since the protein is a known risk factor for the illness. Amyloid-beta (A-beta) deposits in the brain are one of the illness’s pathological hallmarks and have been linked to neurodegeneration in both human patients and animal models of the disease. However, A-beta is also found in peripheral organs, and blood levels of A-beta are linked to cerebral amyloid load and cognitive loss, suggesting the idea that peripherally generated a-beta may be a factor in the illness. A-beta is produced in the brain as well, and it’s difficult to tell one source of protein from the other.
A new mouse model was created by the authors of the present research to overcome this problem. This animal generates human a-beta only in liver cells. They discovered that the protein was transported to the brain from the periphery via triglyceride-rich lipoproteins, exactly as it is in humans. Neurodegeneration and brain shrinkage were detected in mice, along with neurovascular inflammation and malfunction of cerebral capillaries, all of which are often reported in Alzheimer’s disease patients. Those mice failed miserably in a learning test that gauges how well the hippocampus, a brain region critical to the development of new memories, functions. According to the results of this research, peripherally generated A-beta has the potential to induce neurodegeneration, and A-beta produced in the liver may also be a factor in human disease development. If that’s the case, the results may have a substantial impact on our knowledge of Alzheimer’s disease. A-beta brain overproduction in most illness models is based on rare hereditary instances of Alzheimer’s disease in humans. Overproduction of A-beta in the brain isn’t believed to be the cause of Alzheimer’s disease in the overwhelming majority of people. A high-fat diet, for example, may speed up the liver’s synthesis of A-beta, making lifestyle variables more relevant. Mamo adds that the effects of peripheral A-beta on brain capillaries may be crucial throughout the illness process. As a result of this study’s findings, further research is required to determine if a person’s diet and some medicines that target lipoprotein amyloid may reduce or delay the development of Alzheimer’s disease. Further research is needed.