ERIK MARTIN WILLÈN: November 2026

Monday, November 2, 2026

November’s Night Sky Notes: Light-Day Away

NASA's Voyager mission took advantage of a once-every-175-year alignment of the outer planets for a grand tour of the solar system. The twin spacecraft revealed details about Jupiter, Saturn, Uranus and Neptune – using each planet's gravity to send them on to the next destination. Voyager set the stage for such ambitious orbiter missions as Galileo to Jupiter and Cassini to Saturn. Today both Voyager spacecraft continue to return valuable science from the far reaches of our solar system.

NASA/JPL-Caltech

Twin Travelers

In 1977, NASA launched twin spacecraft Voyager 1 and 2, taking advantage of a once-every-175-year planetary alignment of the four largest planets in our solar system: Jupiter, Saturn, Uranus, and Neptune. Using six gravity assists between them, this Grand Tour gave us up-close views of the gas and ice giants, including several moons. By the 1980s, the two probes went their separate ways at Saturn. As Voyager 2 continued toward Uranus and Neptune, Voyager 1 grabbed one more portrait of the solar system (excluding Mercury and Mars), including a final image of the pale blue dot we call home.

The Golden Record Cover

NASA/JPL-Caltech

Playlist

“Hello from the children of planet Earth.”

Every good road trip needs some music to match. In this case, each craft carries the Golden Record, a 12-inch phonograph record with spoken greetings in 55 languages, 27 musical tracks, 116 images, and other sounds from Earth. Each record is protected by an outer cover featuring etchings showing our Sun's location relative to 14 pulsars, along with instructions on how to play it. The design used various metals to protect the information encoded from space radiation: the record used copper and gold plating, and the cover used aluminum. The cover was electroplated with an ultra-pure sample of the isotope uranium-238. Uranium-238 has a half-life of 4.468 billion years.

Are We There Yet?

Did you know that a light-minute is a measure of distance, not time? In August 2012 and November 2018, Voyager 1 and 2 crossed the heliopause, the boundary where the Sun’s solar wind meets the interstellar medium. Using NASA’s Deep Space Network, Earth communicates with both spacecraft and tracks each on its journey. At the time of this article, the Canberra antenna tracked Voyager 1 at 25.80 billion km, or just over 16 billion miles.

This graphic shows the position of NASA's Voyager 1 and Voyager 2 probes, outside of the heliosphere, a protective bubble created by the Sun that extends well past the orbit of Pluto.

NASA/JPL-Caltech

On November 18, 2026, 49 years after its launch, Voyager 1 will cross the one-light-day mark, 16.1 billion miles from the Sun. You may have heard the term light-year in your favorite sci-fi movie or show, or when stargazing and referring to an object outside of our solar system. This video best demonstrates the different distances between the inner solar system, outer solar system, and beyond, using light measurements. Additionally, track each Voyager spacecraft here.

You can get a real understanding of what a gravity assist might be like with our Gravity Assist activity and learn what it’s like to measure a “light minute” with our Measuring a Kid Minute activity guide!

Kat Troche

Source: November’s Night Sky Notes: Light-Day Away - NASA Science

Aspirin and Dementia: A Genetic Clue, and a Catch

Low-dose aspirin is one of the cheapest and most widely used drugs in the world, so any hint that it could help protect the aging brain gets attention. The catch is that the big trials so far have been disappointing: when older adults are studied as one group, aspirin does not prevent dementia. A new analysis from Monash University suggests that this overall result may hide something. In one genetically defined slice of the participants, aspirin looked very different – and so did its risks.

Looking inside a trial that found nothing

The data come from ASPREE (Aspirin in Reducing Events in the Elderly), a large randomized, placebo-controlled trial of low-dose aspirin in older adults. The researchers used genetic data from 13,541 participants and asked a simple question: could differences in people’s DNA explain why aspirin might help some and not others?

To find out, they screened 5,182 polygenic scores from a public catalog. A polygenic score adds up the small effects of many genetic variants into a single number that estimates a person’s inherited tendency toward a trait. For each score, the team checked whether it changed how aspirin affected dementia and major bleeding compared with placebo.

The platelet signal

The strongest result came from scores built to predict platelet count. Platelets are the small blood cell fragments that help form clots. Participants were ranked by their score, and the top 20 percent were compared with everyone else.

In that top group, 1 percent of people taking aspirin developed dementia, against 3.3 percent of those on placebo. That works out to roughly a 70 percent lower relative risk; in the paper’s terms, a hazard ratio of 0.28. Outside that top group, dementia rates were similar with aspirin and placebo, which fits with the trial’s original null result.

The authors point out that the signal did not involve the well-known genetic risk factors for Alzheimer’s disease. Instead it points toward platelet biology, an area where researchers have already linked platelet activation and clumping to dementia, while the role of platelet count itself has been much less clear.

The catch

In the same genetic group, major bleeding occurred in 4.4 percent of people taking aspirin and 2.1 percent of those on placebo. Put the two sets of numbers side by side and the absolute differences are strikingly close: about 2.3 percentage points fewer people with dementia, and about 2.3 percentage points more with major bleeding. That is simple arithmetic on the reported figures, not a conclusion from the study, and the two outcomes are not equal in severity or in how patients weigh them. But it shows why a headline of “70 percent lower risk” tells only half of the story.

Why caution is warranted

· It is a secondary look at an existing trial. ASPREE was not designed to test aspirin in people grouped by platelet-count genetics. This is a post hoc analysis.

· Many scores were tested. When thousands of scores are screened, some will look significant by chance, which is why corrections for multiple testing matter. The authors themselves describe the results as hypothesis-generating and in need of validation.

· The scores are a proxy. They estimate genetic tendency toward a higher platelet count; they are not direct measurements of platelet activity in the individual.

· Replication comes first. The lead author says the finding must be confirmed in other studies and then tested in a trial built specifically for people with this genetic profile.

What it could mean

If the result holds up, it would be a textbook case of personalized prevention: a cheap, familiar drug that is useless on average but useful for a genetically identifiable group, whose bleeding risk could be weighed against the benefit before anyone takes it. If it does not hold up, it will be a useful reminder of how easy it is to find patterns in large genetic datasets.

For now, the researchers are clear that nobody should start taking aspirin to prevent dementia on the basis of this study, and that anyone considering it should talk to their doctor first, especially given the bleeding risk.

Sources

· Original press release: Monash University, Genetic analysis reveals potential benefit of aspirin for reducing dementia risk (29 September 2026)

· Original journal paper: Fransquet PD, Yu C, Tran C, et al. Platelet count polygenic scores may modify the effect of aspirin in primary prevention of dementia. Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, 2026. DOI: 10.1002/alz.71817

This post is for general information and is not medical advice. Talk to a doctor before starting or stopping any medication.

Source: Aspirin and Dementia: A Genetic Clue, and a Catch