A new study says CTE should be recognised as a cause of dementia, with those in the most advanced stages facing a 4.5-fold higher lifetime risk.

Chronic traumatic encephalopathy (CTE) is a degenerative brain condition seen in some athletes.

Linked to repeated head impacts, it can cause memory loss, mood changes, poor coordination and suicidal thoughts. Diagnosis is only possible after death.

People with the most advanced CTE were 4.5 times more likely to develop dementia during life than people without CTE, researchers found.

Many former NHL and NFL players have been posthumously diagnosed with CTE, including Junior Seau, Frank Gifford and Ken Stabler.

The study from researchers at the Boston University CTE Center provides what the centre describes as the clearest evidence yet linking CTE to dementia risk.

The centre says these findings indicate CTE should be known as a cause of dementia.

“This study provides evidence of a robust association between CTE and dementia as well as cognitive symptoms, supporting our suspicions of CTE being a possible cause of dementia,” said Dr Michael Alosco, an associate professor of neurology and co-director of clinical research at the BU CTE Center.

“Establishing that cognitive symptoms and dementia are outcomes of CTE moves us closer to being able to accurately detect and diagnose CTE during life, which is urgently needed.”

Researchers studied brain tissue from more than 600 donors, the majority men.

The donors, primarily contact sport athletes, had known exposure to repetitive head impacts, but none had Alzheimer’s disease, Lewy body disease or frontotemporal lobar degeneration.

They found that 366 male donors had CTE. After examining the donor brains, they calculated the odds of developing dementia across CTE stages I to IV.

Donors with stages III and IV had the worst cognitive and functional symptoms, regardless of age or history of substance use treatment.

Lower stages were not associated with dementia, cognitive impairment or functional decline.

The team also found no link between less severe CTE and changes in mood or thinking, suggesting observed changes may stem from other effects of repetitive head impacts or unrelated medical or environmental factors.

“Understanding which brain changes drive cognitive decline is essential,” said Dr Richard Hodes, director of the National Institute of Health’s National Institute on Aging.

“This study shows that only severe CTE has a clear link to dementia, which provides an important distinction for researchers, healthcare providers and families.”

The study also found that dementia due to CTE is often misdiagnosed as Alzheimer’s disease.

Both conditions are marked by abnormal tau proteins that build up in brain cells and affect blood vessels, although the tau differs in each disease.

Of donors with CTE who had received a dementia diagnosis during life, 40 per cent were told they had Alzheimer’s disease but showed no evidence of it at autopsy.

A further 38 per cent of families were told the cause of dementia was unknown or could not be specified.

A UK university will become one of the first in the country to make improving the health and well-being of the elderly one of its six ‘mission-led’ research priorities.

Bournemouth University’s choice to focus on pensioners is partly the result of the Labour Government’s wish for universities to specialise, whilst also reflecting the area’s demographics – the south-coast city has one of the one of the oldest populations in the world.

“Our demographics are much older than other places – about 10 years older on average compared to the rest of the UK,” explained Tom Wainwright, professor of orthopaedics at Bournemouth.

Vary your exercise

The university’s Orthopaedic Research Institute is already heavily involved in work with the surrounding area and its recently published study, in The Lancet, showed that over-65s with osteoarthritis who undertook group-based cycle classes enjoyed much better outcomes than those receiving one-to-one physiotherapy.

Research published in leading British doctors’ publication the BMJ Journal, which tracked 100,000 people over the last 30 years, has shown that mixed exercise routines can have a significant impact on overall health and longevity.

The study tracked the cohorts exercise habits over three decades and found that participants who engaged in the highest variety of exercises had a 19% lower risk of death, compared to those who engaged in the lowest variety.

Benefits were even bigger when looking at specific causes like heart disease, cancer, and respiratory illness, with risk reductions ranging from 13 to 41 percent.

“People naturally choose different activities over time based on their preferences and health conditions,” says Yang Hu, corresponding author and research scientist in the Harvard TH Chan Department of Nutrition.

“When deciding how to exercise, keep in mind that there may be extra health benefits to engaging in multiple types of physical activity, rather than relying on a single type alone.”

US researchers have identified over five dozen new potential blood-based metabolites which could predict a Type 2 diabetes risk, years in advance.

Key Alzheimer trigger identified

Scientists at Mass General Brigham and Albert Einstein College of Medicine, followed 23,634 participants for up to 26 years and over that time analysed 469 metabolites in blood samples, alongside additional genetic, diet and lifestyle data.

In doing so they identified 235 metabolites associated with higher or lower diabetes risk, including 67 new molecules previously unreported.

The researchers say their work supports a shift toward precision prevention strategies which are more reliable than current indicators such as BMI or family history.

Further research into the Alzheimer’s predicting APOE (apolipoprotein E) gene has left UK researchers with renewed conviction of their ability to develop preventive measures, earlier in life.

Researchers at University College London analysed nearly 470,000 people across four major studies, focusing on participants aged 60 and older with confirmed Alzheimer’s diagnoses and genetic data.

Whilst previous studies had identified the ε4 allele of APOE as the one most predictive of Alzheimer’s development the UCL researchers also highlighted how allele ε3 may also carry a significant risk

Dr Dylan Williams, the study’s lead author, explained that the APOE gene’s contribution to the prevalence of Alzheimer’s has been significantly underestimated for a long time, and that the ε3 allele has historically been misunderstood as having a neutral effect on risk.

He said: “Intervening on the APOE gene, or the molecular pathway between the gene and Alzheimer’s, could have huge potential for preventing or treating a large majority of cases.”

Fibre first

Researchers say that fibre – found in beans, lentils, chia seeds, oats, bran, and certain fruits – is emerging as the ‘new hero’ of nutrition science.

Longevity expert Dr Vassily Eliopoulos, MD, who trained at Cornell, highlights how protein has ruled diet trends for years, but says fibre is now stepping into the spotlight.

“Everyone’s chasing protein, but the next big longevity macro is fibre. And fibre might be the most under-appreciated longevity nutrient that you’re missing daily.”

Explaining why fibre plays such a crucial role, he highlights the connection between gut health and overall well-being.

“Here’s the secret, your gut microbes eat what you don’t digest. These microbes convert fibre into powerful compounds that protect the body. They turn fibre into short-chain fatty acids, which act as your body’s natural anti-inflammatory molecules,”

Dr Eliopoulos highlights how chronic inflammation is closely linked to ageing and disease and he recommends aiming for 30 to 40 grams of fibre a day.

New research links gut inflammation to Alzheimer’s, with higher levels associated with more amyloid plaque in the brain.

Animal studies have shown Alzheimer’s can be passed to young mice through gut microbe transfer, strengthening the link between the gut and the brain.

A 2023 study adds support to inflammation as a possible mechanism.

Barbara Bendlin, psychologist at the University of Wisconsin, said: “We showed people with Alzheimer’s disease have more gut inflammation, and among people with Alzheimer’s, when we looked at brain imaging, those with higher gut inflammation had higher levels of amyloid plaque accumulation in their brains.”

Margo Heston, pathologist at the University of Wisconsin, and an international team tested faecal calprotectin, a marker of gut inflammation, in stool samples from 125 individuals in two Alzheimer’s prevention cohorts.

Participants completed cognitive tests at enrolment, family history interviews and testing for a high-risk Alzheimer’s gene. Amyloid plaques are abnormal protein clumps in the brain that signal disease processes.

A subset of participants took clinical tests for signs of amyloid protein clumps.

Whilst calprotectin levels were generally higher in older participants, they were even more pronounced in those with Alzheimer’s-characteristic amyloid plaques.

Levels of other Alzheimer’s biomarkers also rose with inflammation, and memory scores fell as calprotectin increased. Even participants without an Alzheimer’s diagnosis recorded poorer memory with higher calprotectin.

Heston said: “We can’t infer causality from this study; for that, we need to do animal studies.”

Laboratory analyses have shown gut-bacteria chemicals can stimulate inflammatory signals in the brain. Other studies have reported increased gut inflammation in patients with Alzheimer’s compared with controls.

The researchers suspect microbiome shifts trigger gut changes that lead to mild but chronic, system-wide inflammation, gradually weakening the body’s protective barriers.

Federico Rey, bacteriologist at the University of Wisconsin, said: “Increased gut permeability could result in higher blood levels of inflammatory molecules and toxins derived from gut lumen, leading to systemic inflammation, which in turn may impair the blood-brain barrier and may promote neuroinflammation, and potentially neural injury and neurodegeneration.”

The team is now testing whether diet-induced inflammation in mice can trigger the rodent version of Alzheimer’s.