It is known that A-beta is also present in other peripheral organs, and these increased levels of the protein in the blood raise the possibility of AD. But it has been difficult to trace out this hypothesis as the protein is also produced by the brain and distinguishing this protein from the two sources is challenging.
The present study thereby investigated the role of these proteins in the mouse model that produces human a-beta only in liver cells.
Liver Protein and Alzheimer’s Disease
It was found that these mice had developed neurodegeneration and brain atrophy, accompanied by neurovascular inflammation and dysfunction of cerebral capillaries, as observed in AD.
Moreover, these mice also performed poorly on a learning test that was conclusive of hippocampus function – the brain structure essential for the formation of new memories.
The study thereby portrays that peripherally derived A-beta can cause neurodegeneration, especially those in the liver that serves as a potential contributor to human disease.
“While further studies are now needed, this finding shows the abundance of these toxic protein deposits in the blood could potentially be addressed through a person’s diet and some drugs that could specifically target lipoprotein amyloid, therefore reducing their risk or slowing the progression of Alzheimer’s disease,” says John Mamo, who led the study at the Curtin University in Bentley, Australia.
Source: Medindia
