  Oxidative stress is a pathological hallmark of neurodegenerative tauopathic
disorders such as Alzheimer's disease and Parkinson's disease-related dementia,
which are characterized by altered forms of the microtubule-associated protein
(MAP) tau. MAP tau is a key protein in stabilizing the microtubule architecture
that regulates neuron morphology and synaptic strength. The precise role of
reactive oxygen species (ROS) in the tauopathic disease process, however, is
poorly understood. It is known that the production of ROS by mitochondria can
result in ultraweak photon emission (UPE) within cells. One likely absorber of
these photons is the microtubule cytoskeleton, as it forms a vast network
spanning neurons, is highly co-localized with mitochondria, and shows a high
density of aromatic amino acids. Functional microtubule networks may traffic
this ROS-generated endogenous photon energy for cellular signaling, or they may
serve as dissipaters/conduits of such energy. Experimentally, after in vitro
exposure to exogenous photons, microtubules have been shown to reorient and
reorganize in a dose-dependent manner with the greatest effect being observed
around 280 nm, in the tryptophan and tyrosine absorption range. In this paper,
recent modeling efforts based on ambient temperature experiment are presented,
showing that tubulin polymers can feasibly absorb and channel these
photoexcitations via resonance energy transfer, on the order of dendritic
length scales. Since microtubule networks are compromised in tauopathic
diseases, patients with these illnesses would be unable to support effective
channeling of these photons for signaling or dissipation. Consequent emission
surplus due to increased UPE production or decreased ability to absorb and
transfer may lead to increased cellular oxidative damage, thus hastening the
neurodegenerative process.
