Sharp rises in blood sugar after meals may raise Alzheimer’s risk, according to genetic analysis of more than 350,000 adults.

The findings point to after-meal glucose, rather than overall blood sugar, as a possible factor in long-term brain health.

Researchers examined genetic and health data from over 350,000 UK Biobank participants aged 40 to 69, focusing on fasting glucose, insulin, and blood sugar measured two hours after eating.

The team used Mendelian randomisation, a genetic method that helps test whether biological traits may play a direct role in disease risk.

People with higher after-meal glucose had a 69 per cent higher risk of Alzheimer’s disease.

This pattern, known as postprandial hyperglycaemia (elevated blood sugar after eating), stood out as a key factor.

The increased risk was not explained by overall brain shrinkage (atrophy) or white matter damage, suggesting after-meal glucose may affect the brain through other pathways not yet fully understood.

Dr Andrew Mason, lead author, said: “This finding could help shape future prevention strategies, highlighting the importance of managing blood sugar not just overall, but specifically after meals.”

Dr Vicky Garfield, senior author, added: “We first need to replicate these results in other populations and ancestries to confirm the link and better understand the underlying biology.

“If validated, the study could pave the way for new approaches to reduce dementia risk in people with diabetes.”

While a healthy lifestyle with regular exercise can improve longevity, the key to ageing well is determined by the brain, says a new paper.

Published earlier this month and entitled: ’The Brain Is the Rate-Limiting Organ of Longevity’ it contends that ‘Longevity is not limited by how long the body survives, but by how long the brain can sustain coherent function’.

It says the traditional emphasis on peripheral organ systems, metabolic optimisation, and molecular aging pathways are misplaced.

Authored by Shaheen Lakhan, MD, PhD, founding executive director, at the Miami-based Global Neuroscience Initiative Foundation, he says: “Peripheral organs may determine the final cause of death, but the brain determines the duration and quality of life that precedes it.

“Any longevity strategy that does not explicitly preserve and restore brain function will ultimately fail, regardless of how effectively it slows peripheral aging.

“Recognising the brain as the rate-limiting organ of longevity is therefore not a conceptual preference, but a biological imperative.”

The three ageing benchmarks

Exploring a similar theme, recent Chinese research has identified three ages where substantial brain changes occur.

The first significant change comes at 57, then 70, and then 78, with the researchers identifying biomarkers which indicate these cognitive slumps.

The first change at 57 is due to a reduction in brain volume brought about by a decline in ‘white matter’ – the network of nerve fibres which allows the different brain regions to communicate effectively, they say.

The research measured levels in the brain of 13 proteins that are associated with accelerated brain ageing and neurodegenerative diseases and went on to say that poor lifestyle choices are a key driver of premature decline.

It went to identify exercise as being neuro-protective, by increasing the size of the hippocampus and thereby improving memory.

Alzheimer’s enabler Identified

Researchers at the University of New Mexico have discovered that the enzyme Otulin, known for regulating the immune system, also drives the formation of tau – a protein linked to Alzheimer’s and other neurodegenerative diseases.

In their study, the team demonstrated that deactivating Otulin – either by administering a custom-designed small molecule or knocking out the gene responsible for it –  effectively halted tau production and removed the protein from neurons.

The experiments were conducted on two types of cells: one derived from a patient who had died from late-onset sporadic Alzheimer’s disease, and another from a human neuroblastoma cell line often used in neuroscience research.

“Pathological tau is the main player for both brain aging and neurodegenerative disease.

“If you stop tau synthesis by targeting Otulin in neurons, you can restore a healthy brain and prevent brain ageing,” said Dr Karthikeyan Tangavelou, a senior scientist in the department of molecular genetics & microbiology at the UNM School of Medicine.

US$44m for pan-Europe Alzheimer’s attack

A European initiative to accelerate the implementation of scientific innovations for Alzheimer’s disease (AD) management has been launched by the European Commission’s Innovative Health Initiative in Alzheimer’s disease (AD) management,

Over €38m has been secured by the ACCESS-AD consortium – co-led by King’s College London, Amsterdam UMC, Siemens Healthineers and Gates Ventures – for the five year project.

With AD expected to exceed 19 million people in Europe by 2050, ACCESS-AD aims to address the challenges this presents to healthcare systems by ‘accelerating innovation and strengthening equitable access to timely and effective care’.

“By combining technological innovation with economic, ethical, regulatory and patient perspectives, we aim to chart a sustainable, scalable and equitable pathway for the implementation of new AD diagnostics and therapies,” said Prof Dag Aarsland, head of the centre for healthy brain ageing at King’s college London and clinical co-lead of the project

A central focus of the project is the combination of advanced but accessible neuro-imaging with expanded use of fluid and digital biomarkers.

This will support early and accurate patient identification, enabling timely diagnosis and entry into personalised treatment pathways, targeted lifestyle interventions and nutritional strategies.

It’s never too late…

The benefits of regular exercise are highlighted in a 47 year Swedish study on a cohort first enrolled at the age of 16.

Published recently in the Journal of Cachexia, Sarcopenia and Muscle, the study was tasked with seeing how muscles and fitness changed over time in the 427 participants, now aged 63.

The authors found that our bodies start to age from 35, but that the rate of decline can be slowed down if we stay physically active.

The researchers examined the participants’ aerobic capacity, muscular endurance, muscle power and performance in strength training exercises, such as bench press and vertical jump.

The study’s main finding was that peak physical ability arrived before the age of 36, and that after 40, a decline begins, for both sexes.

The researchers found that adults who became physically active later in life improved their performance in the tests by 5 to 10%.

“It is never too late to start moving. Our study shows that physical activity can slow the decline in performance, even if it cannot completely stop it,” said the study’s lead Maria Westerståhl, of the Karolinska Institutet.

The longer someone has type 2 diabetes, the higher their cardiovascular disease risk, and changes in red blood cells may help explain it, new research suggests.

The study found red blood cells from patients with long-term diabetes harmed blood vessel function, while no such effect was seen in those newly diagnosed.

After seven years of follow-up, the blood cells of people initially diagnosed had developed the same harmful properties.

Zhichao Zhou, associate professor at Karolinska Institutet and lead author, said: “What really stands out in our study is that it is not only the presence of type 2 diabetes that matters, but how long you have had the disease.

“It is only after several years that red blood cells develop a harmful effect on blood vessels.”

Researchers at Karolinska Institutet in Sweden studied animals and patients with type 2 diabetes.

They identified microRNA-210, a small RNA that helps regulate gene activity, as a possible early biomarker of cardiovascular risk.

When its levels were restored in red blood cells, blood vessel function improved.

Eftychia Kontidou, doctoral student and first author, said: “If we can identify which patients are at greatest risk before vascular damage has already occurred, we can also become better at preventing complications.”

The researchers are now investigating whether the biomarker can be used in larger population studies.