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Listening to happy tunes helped study participants with motion sickness get over their predisposition and recover better, according to new research.

Motion sickness is a common condition that happens when you’re moving while sitting still, such as riding in a car. It occurs when our eyes, inner ear and body send conflicting messages to the brain, resulting in nausea, headaches, or breaking out in a cold sweat.

Now, Chinese scientists studying ways for improving the condition have published a study in the journal Frontiers in Human Neuroscience showing that playing different types of music may help people recover more effectively.

Using a specially calibrated driving simulator, they induced car sickness in participants and then played different types of music while they tried to recover. Soft and joyful music produced the best recovery effects, while sad tunes were even less effective than doing nothing at all.

“Motion sickness significantly impairs the travel experience for many individuals, and existing pharmacological interventions often carry side-effects such as drowsiness,” said study author Dr. Qizong Yue of Southwest University in China.

“Music represents a non-invasive, low-cost, and personalized intervention strategy.”

The researchers explained that feeling tense in anticipation of possible car sickness can trigger a physical reaction, bringing sickness on more quickly. Because music can be used to alleviate tension, Dr Yue and his team wondered if it could help people who get carsick.

The team began by developing a model to induce motion sickness. They recruited 40 participants to screen routes on a driving simulator and chose the most effective route for making people feel carsick.

30 people who reported moderate levels of previous carsickness then wore electroencephalogram (EEG) caps, to try to identify quantifiable signals of carsickness in the brain’s activity.

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They were divided into six groups – four that received a music intervention, one that received no music, and one whose simulators were stopped when they started to report that they might feel slightly carsick.

The last group acted as a comparative sample for the EEG data. They had received the same stimuli as the other 25 participants, but weren’t allowed to become nauseous, so the difference between their brain activity and the other participants’ would help identify signals characteristic of carsickness.

To begin with, the participants sat still in the simulator for a few minutes to capture EEG signals from their brains. Then they performed a driving task and reported their level of carsickness to the research team. Once they stopped driving, the participants in the music groups were played tunes for 60 seconds, and then asked to report how sick they felt.

Joyful music alleviated carsickness by 57%

The scientists found that joyful music alleviated carsickness the most, reducing it by 57.3%—followed very closely by soft music, at 56.7%.

Passionate music reduced motion sickness by 48.3%, while playing sad music turned out to be slightly worse than doing nothing.

The control group reported a reduction of carsickness symptoms by 43.3% after their rest, while those who listened to sad music reported a reduction of just 40%.

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The EEG data showed that participants’ brain activity in the occipital lobe changed when they reported carsickness, measureing less complex activity in this brain region when participants said they felt quite sick.

The better the said they felt as they recovered, the more the activity measured by the EEG returned to normal levels.

Joyful or soft music?

The researchers believe it’s possible that soft music relaxes people, relieving the tension that exacerbates carsickness, while joyful music might distract people by activating brain reward systems.

But sad music could have the opposite effect, by amplifying negative emotions and increasing overall discomfort.

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The researchers say further work with a larger sample size is needed to confirm the results. They plan to follow up the experiments with investigations of different forms of travel-sickness and the role played by personal musical taste.

“Based on our conclusions, individuals experiencing motion sickness symptoms during travel can listen to cheerful or gentle music to achieve relief,” said Dr. Yue, who believes the findings of this study would “likely extend to motion sickness experienced during air or sea travel,” as well.

SHARE THIS GOOD NEWS TIP With Families Who Have Carsick Kids…

Microscopic pores in brain cells may hold vital clues to Parkinson’s disease. Scientists have tracked these disruptions in real time, revealing how toxic protein clusters interact with membranes.

The findings point toward a new explanation for how Parkinson’s symptoms develop, beginning at the molecular level of cell membranes.

The quiet onset of Parkinson’s

Parkinson’s often begins quietly. A tremor in the hand, a stiffness in movement, or slowed responses mark the earliest signs.

Beneath these symptoms lies a gradual loss of brain cells. For decades, the trigger behind this degeneration remained unclear. Now, the focus has shifted to α-synuclein, a protein abundant in nerve cells.

In its healthy state, α-synuclein supports communication between neurons. In Parkinson’s, it misfolds and forms clumps.

Earlier studies focused on fibrils, the large clumps seen in brain tissue. The new research highlights oligomers, smaller assemblies that prove more toxic because of their ability to pierce cell membranes.

Proteins create shifting pores

“We are the first to directly observe how these oligomers form pores – and how the pores behave,” said Mette Galsgaard Malle, postdoctoral researcher at both Aarhus University and Harvard University.

Oligomers do not create static damage. Instead, they attach to curved membrane regions, insert partly, and then complete pores that open and close like revolving doors.

“This dynamic behavior may help explain why the cells don’t die immediately,” said Bo Volf Brøchner, PhD student and first author of the study.

“If the pores remained open, the cells would likely collapse very quickly. But because they open and close, the cell’s own pumps might be able to temporarily compensate.”

Watching molecules move

To capture this activity, the researchers used a single-vesicle analysis platform. These vesicles, artificial bubbles resembling cell membranes, allowed scientists to record oligomer activity in real time.

The team even watched fluorescent dyes move through pores, confirming that molecules can cross once pores form.

“It’s like watching a molecular movie in slow motion,” explained Galsgaard Malle. “Not only can we see what happens – we can also test how different molecules affect the process. That makes the platform a valuable tool for drug screening.”

Distinct steps of Parkinson’s

The team proposes a three-stage model: initial recruitment to membranes, partial insertion, and full pore formation.

Interestingly, recruitment occurs more often on curved membranes, while full pore creation favors flatter ones. This means the first and final steps are distinct processes shaped by membrane geometry and charge.

Negatively charged lipids, abundant in mitochondria and synaptic vesicles, seem particularly vulnerable. This supports the idea that energy-producing cell regions may be among the first harmed in Parkinson’s.

Pore formation and cell risk

The studies also show that neutral membranes can recruit oligomers, but only negative charges activate pores. Recruitment is enhanced by curvature, likely because tightly bent membranes expose more defects that oligomers can latch onto.

Yet, pore formation itself works best on flat, low-curvature membranes, which offer more stability for the pore to open fully.

This separation between binding and pore creation clarifies earlier contradictions in research. It suggests that cells might not be equally at risk, depending on membrane composition and shape.

Nanobodies and detection

The researchers also tested nanobodies, tiny antibody fragments that bind specifically to oligomers. These nanobodies did not block pore formation, but they helped reveal how pores change dynamics.

One nanobody increased pore turnover, making oligomers more flexible and interactive, while another reduced activity.

“The nanobodies did not block the pore formation,” said Volf Brøchner. “But they may still help detect oligomers at very early stages of the disease. That’s crucial, since Parkinson’s is typically diagnosed only after significant neuronal damage has occurred.”

Implications beyond Parkinson’s

These findings may apply beyond Parkinson’s. The same methods could explore other protein aggregates, such as tau in Alzheimer’s disease, which may also damage membranes in subtle but progressive ways.

The single-vesicle platform offers a high-resolution way to track protein-membrane interactions across different neurodegenerative conditions.

For now, these experiments remain in artificial models. Real brain cells are far more complex, with diverse lipids and interacting proteins. The next challenge is to confirm whether pores form in living tissue and how they contribute to cell death.

“We created a clean experimental setup where we can measure one thing at a time. That’s the strength of this platform,” said Galsgaard Malle. “But now we need to take the next step and investigate what happens in more complex biological systems.”

The study is published in the journal ACS Nano.

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