Shielding from Earth's Magnetic Field Extended Lifespan by 20% in Flies with a Parkinson's Gene, While Healthy Flies Gained Mobility Instead

Shielding from Earth's Magnetic Field Extended Lifespan by 20% in Flies with a Parkinson's Gene, While Healthy Flies Gained Mobility Instead

Scientists at the University of Nottingham nearly completely shielded Drosophila from Earth's magnetic field and compared healthy flies with flies carrying a PINK1 gene mutation that models early-onset Parkinson's disease. In the mutant flies, the absence of the field extended lifespan by roughly 20% but impaired mobility; in healthy flies, the effect ran in the opposite direction. The causes were traced to a specific node of the mitochondrial respiratory chain and to free radical levels.

The paper was published on September 23 in the journal Aging. The team placed flies for 10 or 20 days inside a container made of mu-metal, an alloy that shields magnetic fields, reducing the ambient field from the usual 25 to 60 microtesla down to 0.006 microtesla. Some flies were healthy; others carried a mutation in the PINK1 gene, which in humans is responsible for early hereditary Parkinson's disease. In flies the gene sits on the X chromosome, so only males were used to keep the gene effect separate from sex. The PINK1 protein normally tags damaged mitochondria, the cell's power plants, for disposal; without it, defective mitochondria accumulate and the cell is poisoned by its own malfunctioning machinery.

Twenty days without the field cut the mortality risk of mutant flies roughly in half relative to controls, corresponding to a lifespan increase of approximately 20%; ten days produced almost no change. The same mutant flies showed impaired climbing ability on the wall of a vial, the standard motor assay for Drosophila. In healthy flies, climbing improved, while lifespan dipped only slightly, a shift that was statistically less robust than the effect seen in mutants.

The source of the paradox was sought in the mitochondria. Respiration was measured with a high-resolution respirometer, and free radicals, the harmful byproducts of respiration, were detected with quantum sensors based on defects in diamond crystals. Without the field, the contribution of one link in the respiratory chain, Complex II, increased. Earlier data had shown that Complex I is selectively damaged in PINK1-mutant flies. The authors propose that the boosted Complex II compensates for the missing Complex I function in diseased flies, which explains the survival gain, while in healthy flies it amounts to an unnecessary burden on an already intact system. In roundworms, a comparable dissection of the respiratory chain showed the same pattern: when Complex I is broken, electrons enter through Complex II, whereas Complex IV has no such backup route. The idea that a magnetic field can influence cellular chemistry was proposed earlier by physicists in the "radical pair" hypothesis, which also explains compass navigation in migratory birds: a weak field shifts the outcome of reactions involving magnetically sensitive electrons. The authors do not identify which molecular node senses the change in field strength inside the fly cell.

On the neighboring question of whether flies sense the magnetic field as a compass, the largest direct study to date (nearly 109,000 individuals, Nature, 2023) found no behavioral magnetosensitivity, although that finding was later reanalyzed and challenged by another paper in the same journal. The fact that healthy and diseased flies responded in opposite directions points to a direct biochemical action on mitochondria, independent of the fly's sensory organs.

Earth's magnetic field, the background in which all life evolved, thus becomes a variable in the biology of aging: it can be switched on and off externally, and its effects differ depending on mitochondrial health.

The lead researcher, Professor Lisa Chakrabarti, explains:

"Understanding how cells sense and respond to magnetic fields could ultimately open new ways of managing mitochondrial function in aging and disease."