Old galaxies in a young universe?
Analysis of 31 high-redshift galaxies observed with JWST indicates average stellar ages of about 600 million years, close to the universe's age at that epoch (~700 Myr), with some cases, such as JADES-1050323, appearing older than the universe at their redshift. These findings challenge the standard Lambda-CDM model and suggest a need for further investigation.

The standard cosmological model (present-day version of "Big Bang," called Lambda-CDM) gives an age of the universe close to 13.8 billion years and much younger when we explore the universe at high-redshift. The redshift of galaxies is produced by the expansion of the universe, which causes emitted wavelengths to lengthen and move toward the red end of the electromagnetic spectrum.

The further away a galaxy is, the more rapidly it is moving with respect to us, and so the greater is its redshift; and, given that the speed of light is finite, the more we travel to the past. Hence, measuring the age of very high redshift galaxies would be a way to test the cosmological model. Galaxies cannot be older than the age of the universe in which they are; it would be absurd, like a son older than his mother.\

In work carried out  by researchers at the Canary Islands Astrophysics Institute (IAC; Spain), we analyzed 31 galaxies with average redshift 7.3 (when the universe was 700 Myr old, according to the standard model) observed with the most powerful available telescope available: the James Webb Space Telescope (JWST).

The findings are published in the journal Monthly Notices of the Royal Astronomical Society.

As a result, they found that they are on average ~600 Myr old, according to the comparison with theoretical models based on previous knowledge of nearby galaxies. Our models include all of the known possibilities: old and young stellar populations, thermally-pulsating AGB stars, emission lines associated with HII regions, black holes in active galactic nuclei (AGN), interstellar dust extinction, and intergalactic extinction from neutral hydrogen.

There were other independent works that also pointed out  strong anomalies with JWST galaxies, including the existence of old galaxies (e.g., Steinhardt et al. 2024, ApJ, 967, 172; Wang et al. 2024, ApJL, 969, L13; Martínez-García 2025, MNRAS, 541, 1988). If this result is correct, we would have to think about how it is possible that these massive and luminous galaxies were formed and started to produce stars in a short time. It is a challenge.

The fact that some of these galaxies might be older than the universe within some significant confidence level is even more challenging.

M López-Corredoira et al, Improved measurements of the age of JWST galaxies at z = 6 − 10, Monthly Notices of the Royal Astronomical Society (2026). DOI: 10.1093/mnras/stag089

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Boxfish

Fever chills explained: How brain signals push warmth-seeking to fight infection

When running a fever during infection, we often feel chills, which prompt us to take action to warm ourselves, such as turning on a heater or adding layers of clothing. Increased body temperature helps inhibit pathogen growth and boosts immune cell activity.

A recent rat study by researchers identified the neural mechanism underlying chills, a cold sensation that supports the body's response to infection. The findings were published in The Journal of Physiology.

When mammals are infected, their immune system produces a pyrogenic mediator, prostaglandin E₂ (PGE₂), in the brain's vascular cells. PGE₂ acts on the preoptic area, the brain's thermoregulatory center, and triggers autonomic fever responses, such as shivering, increased heat production in brown adipose tissue, and constriction of skin blood vessels.

PGE₂ is known to trigger not only autonomic fever responses but also behavioral fever responses including warming behaviors with chills.

The team hypothesized that PGE₂ acts on the lateral parabrachial nucleus (LPB) in the brain, which relays sensory signals, to trigger chills and warmth-seeking behaviors during infection. This was based on their 2023 study showing that LPB neurons transmit skin-temperature sensations to the forebrain and influence body temperature regulation. To test this hypothesis, the team conducted experiments on rats.

The researchers found that the rats' axons primarily target the central nucleus of the amygdala, which regulates emotions such as discomfort and fear, with minimal projections to the preoptic area.

The team also found that the pathway from EP3-expressing neurons to the amygdala is activated in cold environments and transmits cold sensations.

These findings suggest that during infection, PGE₂ boosts cold signals from the LPB to the central nucleus of the amygdala via EP3 receptors, triggering chills and promoting warmth-seeking behaviour.

This study demonstrates that PGE₂ increases body temperature by acting on two brain regions: the preoptic area, which drives autonomous thermogenic responses, and the lateral parabrachial nucleus (LPB), which mediates behavioural responses.

The pyrogenic mediator prostaglandin E2 elicits warmth seeking via EP3 receptor-expressing parabrachial neurons: a potential mechanism of chills, The Journal of Physiology (2026). DOI: 10.1113/JP289466