Role of Beta-Amyloid (Aβ) Protein in Alzheimer’s Disease, and the Controversy Surrounding PIB-PET Imaging

Role of Beta-Amyloid (Aβ) Protein in Alzheimer’s Disease, and the Controversy Surrounding PIB-PET Imaging

Alvin Sherman Library 4009

Alzheimer’s disease (AD) is a highly complexed, enigmatic disease that affects nearly 4 million Americans. Surprisingly, over 99% of those affected have sporadic or late-onset AD (SAD), whose causes are unknown. Unfortunately, Alzheimer’s disease has no clear cause-and-effect relationship: like unsolved murders, an enormous body of evidence must be collected that can trace steps in order to form hypotheses or to form a consensus in the medical community.

This literature review project focuses on describing recent scientific research into beta- amyloid (Aβ) plaques as a potential cause of AD and methods of observing these plaques in the living human brain. Causes of Aβ plaque deposition relate to three factors which medical researchers aim to reverse: overproduction of Aβ protein, a decrease in catabolism of Aβ and/or a decrease in Aβ clearance out of the brain. Potential treatments include cleaving enzyme inhibitors, metal chelation therapy, and chaperone proteins.

Throughout history, scientists and physicians have been unable to view Aβ plaque deposition until after autopsy. Using specialized imaging such as PIB-PET, physicians are now able to observe Aβ plaques in the living human brain. However, PIB-PET imaging also brings about great social and legal consequences: defining who is eligible to receive the test, delineating an appropriate legal and medical plan of action once diagnosis is established, and clarifying who will have access to the results of these tests is only the beginning of the challenges that the health care system and legal system must strive to overcome.