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Midlife pollution exposure linked to brain decline
Exposure to air pollution in midlife may slow thinking and cause brain changes in later life, potentially affecting cognitive health as people age.
A 26-year study tracked 1,761 people aged 45 and over, assessing their exposure to air pollutants and testing their cognitive function at four points between ages 43 and 69.
Researchers from King’s College London’s Institute of Psychiatry, Psychology & Neuroscience (IoPPN), in collaboration with University College London, the University of Leicester and Alzheimer’s Research UK, found that those exposed to higher pollution levels from age 45 scored lower on cognitive screening tests at age 69.
The Addenbrooke’s Cognitive Examination, which assesses attention, memory, language, perception and verbal fluency, showed poorer results among those with greater exposure to air pollution. Participants exposed to high levels of nitrogen dioxide (NO₂) and particulate matter (PM₁₀) also demonstrated slower processing speeds between ages 43 and 69.
Brain scans from a subgroup of participants aged 69 to 71 revealed physical differences linked to pollution exposure. High exposure to nitrogen oxides (NOₓ) was associated with a smaller hippocampus – a brain region involved in memory. Greater exposure to NO₂ and PM₁₀ was linked to larger ventricular volume, which tends to increase when brain tissue reduces.
Both outcomes are associated with cognitive decline and dementia. These associations remained even after adjusting for childhood cognitive scores and pollution exposure before age 45. However, no clear link was found between air pollution and verbal memory alone.
“153 million people are predicted to be living with dementia by 2050. Our study represents one of the longest follow ups that seeks to understand the impact of air pollution on a broad range of cognitive outcomes and on brain health as we age. Most of the world’s population is breathing toxic air above World Health Organization recommended limits, which could partly explain the increased dementia risk as people age,” said Professor Ioannis Bakolis, deputy director at the Centre for Mental Health Policy and Evaluation at King’s IoPPN and the study’s principal investigator.
Thomas Canning, one of the study’s first authors from King’s IoPPN, added: “For some time, researchers have been seeking to highlight the long term and potentially permanent effects of air pollution on the brain. Our study highlights that reducing people’s exposure has the potential to help conserve cognition and brain structure as they age, even if this happens once they reach mid-life.”
The findings suggest that even small reductions in air pollution exposure during midlife could help preserve cognitive function and brain structure in later years. With most of the global population breathing air above World Health Organization limits, the results add to evidence linking air quality with long-term health outcomes.
The study was part-funded by the National Institute for Health and Care Research Maudsley Biomedical Research Centre, with further support from the Medical Research Council, Alzheimer’s Research UK, Alzheimer’s Association, MRC Dementias Platform UK, Wolfson Foundation and Brain Research UK.
An Alzheimer’s mutation may delay disease onset by about 20 years in people otherwise expected to develop memory loss in their mid-40s.
The mutation affects a protein called reelin, which directs brain cells to break down amyloid plaques and tau tangles, harmful protein build-ups linked to Alzheimer’s.
New research suggests the mutation makes reelin work much more efficiently.
The discovery follows decades of work in the valleys near Medellin, Colombia, where thousands of people carry a rare inherited form of Alzheimer’s caused by a mutation in the presenilin 1, or PSEN1, gene.
Anyone carrying even one copy of the altered gene would be expected to lose their memory in their mid-40s.
The late neurologist Francisco Lopera, who grew up in the region, spent years mapping the affected population.
A year before his death in 2024, he co-authored a paper on a patient who carried the PSEN1 mutation but lived well into his 60s before developing Alzheimer’s.
Lopera found that the man’s brain was protected by another mutation, dubbed COLBOS after the research centres in Colombia and Boston that characterised it.
Research published in December 2025 by molecular biologist Chunyu Wang and colleagues at Rensselaer Polytechnic Institute in New York has now shown how COLBOS works.
The mutation alters how reelin binds to a sugar molecule called heparan sulfate on the surface of brain cells, strengthening that bond and helping reelin build up where its protective signalling is most effective.
There, reelin can help slow key disease processes, including phosphorylation of tau, a chemical change that destabilises the protein and causes toxic tangles to build up in neurons, the brain’s nerve cells.
Joachim Herz, a neuroscientist at the University of Texas Southwestern Medical Center who was not involved in the research, said: “I would never have expected that it would be so protective that it actually negates the effect of a dominant early onset Alzheimer’s disease mutation.
“That I would never have in my wildest dreams predicted.”
Herz, who mapped much of the reelin pathway 20 years ago in mice, believes the COLBOS mutation may make the process of feeding harmful proteins into cell structures that break them down more effective.
However, as the brain ages, defects in those structures may become harder to overcome despite reelin’s effects, meaning the mutation may delay Alzheimer’s rather than prevent it.
The findings could still have implications for future therapies for the far larger number of patients who do not carry high-risk PSEN1 mutations.
Wang pointed to recent research showing that reelin-producing neurons are among the first to die in Alzheimer’s, and suggested that making reelin work more efficiently at brain cell surfaces, even when less of it is present, could protect people from further symptoms.
He is now discussing the development of a gene therapy to enhance reelin signalling based on the findings.
Wang said that even delaying Alzheimer’s by a fraction of the two decades linked to the COLBOS mutation would be a major advance.
Current drugs on the market may extend independent living by two to three years at most, he said, so “20 years is amazing.”
Super-ageing key, Seaweed’s special, hair-raising breakthrough and more
The secret of how ‘super-agers’ have the mental agility of people decades younger is centred around brain health, say US researchers.
Some elderly people are able to regenerate brain cells twice as quickly as other, healthy adults, of the same age.
While it has recently been established that we continue creating brain cells throughout our lives, the new research suggests that some people age without any signs of cognitive decline because their bodies are much better at renewing brain cells.
This is known as neurogenesis and happens in the hippocampus – which is crucial for memory.
“Super agers had twice the neurogenesis of the other healthy older adults,” said Professor Orly Lazarov, of the University of Illinois at Chicago.
“Something in their brains enables them to maintain a superior memory. I believe hippocampal neurogenesis is the secret ingredient, and the data support that.
Amino acid alert
“This is a big step forward in understanding how the human brain processes cognition, forms memories and ages.”
A super-ager is someone aged 80 or older who exhibits cognitive function that is comparable to an average person who is middle-aged.
A study of more than 270,000 participants from the UK Biobank has uncovered a link between a common amino acid and how long men live.
Researchers found that higher levels of tyrosine – an amino acid found in protein-rich foods and often marketed as a focus-boosting supplement – were associated with shorter life expectancy in men.
The study published in Aging-US, from the University of Hong Kong and the University of Georgia, examined the role of phenylalanine and tyrosine in longevity.
Their findings suggest that higher tyrosine levels are associated with shorter life expectancy in men, raising the possibility that longevity strategies may need to differ by sex.
‘Seaing’ into the future
Researchers are using a unique Australian seaweed that mimics the biological functions of human skin to develop sustainable, regenerative wound-healing, anti-ageing solutions for complex skin injuries and burns.
The healing power of seaweed is not a new discovery.
There is evidence that it was chewed medicinally in what is now Chile more than 14,000 years ago, and that seaweed has been a versatile resource for Indigenous Australians for millennia.
It is now believed there are some 12,000 species of seaweed around the world, and that current scientific understanding of the possible benefits of those species is just scratching the surface.
Over the last decade, University of Wollongong researchers at the Intelligent Polymer Research Institute (IPRI) have been investigating a unique Australian green seaweed with antibacterial, anti-inflammatory and regenerative properties.
The team believes this discovery could revolutionise complex wound healing and boost longevity.
Link between obesity and muscle loss
Researchers at the UK’s University of Birmingham have identified a new mechanism by which obesity may contribute to muscle loss in older adults.
The study, published in the Journal of Cachexia, Sarcopenia and Muscle and delivered through the National Institute for Health and Care Research (NIHR) Birmingham Biomedical Research Centre (BRC) shows for the first time that extracellular vesicles – tiny particles released by fat tissue – can directly trigger muscle atrophy in human cells.
Sarcopenic obesity, where excess body fat coexists with reduced muscle mass and strength, is an increasingly common condition in ageing populations and is associated with frailty, reduced mobility, and poorer overall health outcomes.
It is estimated to affect around 11 per cent of the population.
In the study, researchers found that extracellular vesicles released from obese adipose tissue caused significant thinning of muscle fibres derived from older adults, whilst researchers found
that muscle cells derived from younger adults were resilient to these effects.
Lead researcher Dr Joshua Price, first author and Postdoctoral Researcher, said: “It isn’t just having more fat tissue that matters.
“Obesity changes how fat tissue behaves and how it communicates with muscle.
“Ageing muscle is far more vulnerable to these altered signals, which helps explain why muscle loss accelerates with obesity later in life.”
Hair-raising breakthrough
Japanese regenerative health firm OrganTech has pinpointed the trio of cells required to prevent hair loss.
The Tokyo-based biotech said its researchers have defined a three-cell configuration capable of reconstructing hair follicle organ germs to sustain a hair growth cycle.
The work, published in Biochemical and Biophysical Research Communications, provides a potential blueprint for regeneration of hair follicles; which are complex, mini-organs that repeatedly manifest through growth, regression, rest and shedding cycles.
Previous regenerative approaches have combined epithelial stem cells and dermal papilla cells to form early follicular structures.
But, working with researchers at the RIKEN Center for Biosystems Dynamics Research, OrganTech identified a third, previously uncharacterised, cell type that appears to be essential for complete regeneration.
This mesenchymal cell was shown to play a critical role in triggering the transition from the resting to the growth phase of the hair cycle and in driving the follicle’s downward extension into surrounding tissue.
OrganTech CEO Yoshio Shimo, said: “This work defines a foundational cellular configuration for functional hair follicle regeneration.
“Beyond hair biology, it reinforces our broader strategy of organ-level regenerative medicine, where precisely orchestrated epithelial and mesenchymal interactions enable stable and functional tissue reconstruction.”
Low-dose lithium may slow verbal memory decline linked to Alzheimer’s disease in older adults, according to a pilot clinical trial.
The two-year trial enrolled adults aged 60 and older with mild cognitive impairment, a condition where people develop noticeable memory or thinking problems beyond what is typical for their age.
Participants were randomly assigned to receive either a low dose of lithium, a drug long used to treat bipolar disorder, or a placebo.
Over the study period, those receiving lithium showed a slower decline on a sensitive test of verbal memory, the ability to remember and recall words and sentences, which often worsens early in Alzheimer’s disease.
The research was led by Dr Ariel Gildengers, professor of psychiatry at the University of Pittsburgh and a geriatric psychiatrist whose previous work has suggested long-term lithium use in older adults with bipolar disorder is linked with better brain integrity.
“In a prior study, we observed that older adults with bipolar disorder who take lithium long-term tend to show markers of better brain integrity,” Gildengers said.
“The new question was whether those apparent neuroprotective effects might extend beyond mood disorders, and whether we could test that rigorously in a prospective clinical trial.”
Brain imaging showed that the hippocampus, a region of the brain important for memory, shrank over time in both groups.
Although the overall difference between groups did not reach statistical significance, further analysis suggested stronger protective effects among participants who tested positive for amyloid beta, a protein widely considered one of the key biological indicators of Alzheimer’s disease.
The study also found that low-dose lithium was safe and well tolerated in older adults when carefully monitored.
“The key point is that lithium doesn’t restore lost memory,” Gildengers said.
“What it appears to do, if the signal holds up, is slow deterioration. That distinction matters enormously when you’re designing trials and interpreting results.”
However, the trial had limitations. When it began nearly a decade ago, blood-based tests for Alzheimer’s disease were not yet available, meaning participants were enrolled based on clinical symptoms alone.
Only a subset were later found to have amyloid, which may have reduced the study’s ability to detect stronger effects.
“If we were designing this study today, we would enrol participants based on amyloid status from the start,” Gildengers said.
“That’s exactly what we’re planning for next.”
The research team is now seeking support for a larger trial that would use blood-based biomarkers, measurable biological indicators in the blood, to identify individuals most likely to benefit.
“This study tells us that the approach is feasible, safe and worth pursuing,” Gildengers said.
“But it also reminds us why careful, adequately powered trials are essential, especially when the stakes are this high.”
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