Alzheimer's-linked tau disrupts mitochondria, reversing electron flow in nerve cells
A protein named tau, which has been strongly implicated in the world's No. 1 cause of dementia—Alzheimer's disease—and several other neurodegenerative disorders, may spur these diseases in a way that differs greatly from the pathological pathway usually ascribed to it.
Alzheimer's-linked tau disrupts mitochondria, reversing electron flow in nerve cells, according to a recent study published in Neuron. Tau, a protein associated with Alzheimer's disease and several other neurodegenerative disorders, seems to play a significant role in these conditions in a manner distinct from previously believed pathways.
The research conducted by Stanford Medicine scientists reveals that tau molecules, once they detach from microtubules – structures crucial for the proper functioning of nerve cells – become prone to modifications by enzymes. These modifications, particularly the addition of phosphate groups, make tau prone to aggregation and the formation of neurofibrillary tangles, a hallmark of tauopathies.
A key finding of the study is that hyperphosphorylated tau can interact with mitochondria, the cell's powerhouses responsible for converting nutrients into energy. This interaction leads to a phenomenon known as reverse electron transport, where the flow of electrons is reversed, causing the production of harmful molecules, inflammation, and damage to proteins.
This reverse electron transport has been observed in various tauopathies, including Alzheimer's disease, Parkinson's disease, and Huntington's disease, as well as other rare conditions.
Previously, scientists were unsure about the mechanism by which tau contributed to these disorders. However, this new study provides a clear pathway showing how tau disruptions in mitochondria can lead to pathological events within these powerhouses and the nerve cells they support. The discovery opens up new possibilities for therapeutic interventions targeting tau's effects on mitochondria, potentially offering new treatments for these debilitating diseases.
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