According to Creationists, everything about biology and human anatomy and physiology especially, is definitely not the result of natural, evolutionary forces and the operation of random chance. Instead, it is all designed by their reputedly omnipotent, omniscient god who knew exactly what it was designing and designed if for the particular purpose which it serves - which means it is responsible for both the good and the bad in its 'designs', of course.
So, playing at Intelligent [sic] Design advocates for a moment, we have in this scientific paper an example of the sheer mendacious nastiness of Creationism's divine malevolence. It shows how, just to make sure it's victims get Alzheimer's disease in later life, it has designed a mechanism in the liver that manufactures one of the proteins which has been implicated in the progress of this ghastly disease which robs the sufferer of their dignity, their memory, their personality and eventually their life.
The study, published open access in PLOS Biology, was carried out by John Mamo of Curtin University in Bentley, Australia, and colleagues.
According to the press release from PLOS:
Deposits of amyloid-beta (A-beta) in the brain are one of the pathological hallmarks of AD and are implicated in neurodegeneration in both human patients and animal models of the disease. But A-beta is also present in periphereral 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. Testing that hypothesis has been difficult, since the brain also produces A-beta, and distinguishing protein from the two sources is challenging.
In the current study, the authors surmounted that challenge by developing a mouse that produces human a-beta only in liver cells. They showed that the protein was carried in the blood by triglyceride-rich lipoproteins, just as it is in humans, and passed from the periphery into the brain. They found that mice developed neurodegeneration and brain atrophy, which was accompanied by neurovascular inflammation and dysfunction of cerebral capillaries, both commonly observed with Alzheimer's disease. Affected mice performed poorly on a learning test that depends on function of the hippocampus, the brain structure that is essential for the formation of new memories.
The findings from this study indicate that peripherally derived A-beta has the ability to cause neurodegeneration and suggest that A-beta made in the liver is a potential contributor to human disease. If that contribution is significant, the findings may have major implications for understanding Alzheimer's disease. To date, most models of the disease have focused on brain overproduction of A-beta, which mimics the rare genetic cases of human Alzheimer's. But for the vast majority of AD cases, overproduction of A-beta in the brain is not thought to be central to the disease etiology. Instead, lifestyle factors may play a more important role, including a high-fat diet, which might accelerate liver production of A-beta.