Mitochondria in Brain May Be Source of Alzheimer’s

05/02/2018

Alzheimer’s disease, a severely debilitating and ultimately fatal brain disorder, affects millions worldwide. To date, clinical efforts to find a cure or adequate treatment have met with dispiriting failure.

The disease is now on an ominous course of expansion, due in part to an aging population, and is poised to become a global health emergency. The enigmatic ailment–first described over 100 years ago–remains the only leading killer without effective treatment, prevention or cure.

In a new study, researchers at the ASU-Banner Neurodegenerative Disease Research Center examine the effects of the disease on the functioning of mitochondria–structures performing a variety of essential tasks, including supplying cells with energy.

The new research reveals that a highly toxic form of beta amyloid protein– known as oligomeric a-beta (OAβ)–disrupts the normal functioning of mitochondria. The result is a fateful cascade of events that appears early in the development of Alzheimer’s disease–decades before the onset of clinical symptoms.

The most promising finding in the new study is that human neuronal cells can be protected from OAβ-induced deterioration of their mitochondria when they are pre-treated with a custom-designed compound, suggesting an exciting avenue for future drug targeting.

“Mitochondria are the major source of energy in brain cells and deficiencies in energy metabolism have been shown to be one of the earliest events in Alzheimer’s disease pathobiology. This study reinforces the toxicity of oligomeric amyloid beta on neuronal mitochondria and stresses the importance for protective compounds to protect the mitochondria from oligomeric amyloid beta toxicity,” said Diego Mastroeni, a lead author of the new study.