In a new study, researchers at the ASU-Banner Neurodegenerative Disease Research Center examine the effects of Alzheimer’s 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.

The research findings appear in “Oligomeric Amyloid Beta Preferentially Targets Neuronal and Not Glial Mitochondrial Encoded mRNAs,” made available online by Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association as an article in press corrected proof.

Two pathological hallmarks are observed in AD brains at autopsy: intracellular neurofibrillary tangles and extracellular senile plaques, which tend to occur in the neocortex, hippocampus, and other subcortical regions crucial for cognitive function. These observations have led to a dominant theory of Alzheimer’s causality, known as the amyloid hypothesis.

The theory points to accumulations of the sticky protein substance amyloid beta as the critical factor initiating the chain of events leading to development of Alzheimer’s disease. While the amyloid hypothesis continues to exert a considerable hold on the field, an increasing consensus among researchers is moving away from the idea of amyloid beta accumulation as the primary event that sets the disease in motion. The new study focuses on mitochondria, which are currently under intense investigation for their early role in AD pathology.

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