Medical hypothesis: Neurodegenerative diseases arise from oxidative damage to electron tunneling proteins in mitochondria.

Mitochondria likely arose from serial endosymbiosis by early eukaryotic cells and control electron flow to molecular oxygen to facilitate energy transformation. Mitochondria translate between the quantum and macroscopic worlds and utilize quantum tunneling of electrons to reduce activation energy barriers to electron flow. Electron tunneling has been extensively characterized in Complex I of the electron transport chain. Age-related increases in oxidative damage to these electron tunneling systems may account for decreased energy storage found in aged and neurodegenerative disease tissues, such as those from sufferers of amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD) and Parkinson's disease (PD). This hypothesis is testable. If correct, this hypothesis supports pre-symptomatic, mitochondrially-directed oxygen free radical scavenging therapies.