Tiny vesicles from damaged mitochondria spread Alzheimer’s in mice
Alzheimer’s disease spreads through the brain. But how exactly? New research points to an unexpected driver: tiny vesicles shed by damaged mitochondria that accelerate the disease in mice.
Mitochondria are the power plants of cells. When they are damaged, they can release tiny packets called mitovesicles. Until now, the role of these packets in Alzheimer's disease had barely been studied. The researchers, publishing in Nature Aging, found that brain cells from Alzheimer's patients and from a mouse version of the disease released substantially more of these packets than healthy brain cells.
Injecting vesicles triggers disease in healthy mice
That was not all. When the researchers injected vesicles derived from Alzheimer’s mouse brains directly into the brains of healthy mice, those animals developed Alzheimer’s-like changes: memory impairment, activation and inflammation of glial cells, and abnormalities in the synaptic connections between neurons. The same vesicles also accelerated disease progression when injected into mice already in an early stage of Alzheimer’s.
The protein that causes the damage
Through protein analysis, the researchers identified a specific protein that was highly concentrated in the harmful packets: Ggt1. This enzyme breaks down glutathione, a molecule that protects cells against damage caused by harmful chemical reactions. When Ggt1 was blocked or inhibited, Alzheimer's-like features in the mice decreased and packet-induced disease progression slowed. The researchers regard both the mitovesicles and Ggt1 as potential treatment targets.
This is research in mice and brain tissue from patients. Whether the same mechanisms play the same role in living humans has not yet been established.
Search terms to explore further: mitovesicles brain cell death | extracellular vesicles Alzheimer's pathology | glutathione cell damage brain