Contrary to popular “scientific” belief, we aren’t really that sure what causes the neurodegeneration of brain tissue in Alzheimer’s Disease (AD) patients. Thus, amyloid beta (AB) plaques are not nearly as deserving a scapegoat as is often thought.
If we investigate the chemical properties of AB depositions, we find that AB doesn’t exhibit the ability to make reactive oxygen species; rather AB exhibits anti-oxidant properties, implying that AB should be neuroprotective.
If AB is neurotoxic, we might expect to observe deleterious affects whenever AB production is increased, however AB increases are observed after instances of neuronal stress, as in cases of hypoglycemia and brain trauma. This result gives merit to the hypothesis: AB increases serve as a neuroprotective pathway due to physical stresses. So what is the role of AB plaques in the brain?
An alternative hypothesis to the origin of AB is that neuronal energy shortages coupled with Ca2+ overloads promote a fundamental switch in the metabolism route of Amyloid-Beta Precursor Protein (ABPP) from a non-amyloidogenic to an amyloidogenic pathway, i.e. it switches from the body making no AB plaques to the body making AB plaques. Since AB plaques show up after neuronal stress, induced by decreased energy production and higher Ca2+ concentrations (key symptoms exhibited by concussion patients), it appears that AB plaques play a protective role in the brain, and that ABPP is the necessary built-in protective system that is always on standby ready to create protective plaques.
So, even though AB plaques are always observed in AD patients, the presence of AB plaques is not unique to AD patients and thus is likely a bystander of the damaging effects of AD. Considering this information and that of the AD article we read, there are obviously mixed opinions regarding the role AB plays in AD. The article focused on in our neurochemistry course suggests that AB plaques are toxic, while other literature sources claim that AB is either a benign byproduct of AD or that it plays an active role in protecting the brain from the neurodegenerative nature of AD. Only future research will illuminate the true role AB plays in AD.
Amyloid Beta Plaques: Destructive or Protective?
