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.”

A recent international study that pooled brain scans and memory tests from thousands of adults has shed new light on how structural brain changes are tied to memory decline as people age.

The findings show that the connection between shrinking brain tissue and declining memory is nonlinear, stronger in older adults, and not solely driven by known Alzheimer’s-associated genes like APOE ε4.

This suggests that brain ageing is more complex than previously thought, and that memory vulnerability reflects broad structural changes across multiple regions, not just isolated pathology.

Alvaro Pascual-Leone, MD, PhD is senior scientist at the Hinda and Arthur Marcus Institute for Aging Research and medical director at the Deanna and Sidney Wolk Center for Memory Health.

The researcher said: “By integrating data across dozens of research cohorts, we now have the most detailed picture yet of how structural changes in the brain unfold with age and how they relate to memory.”

The study found that structural brain change associated with memory decline is widespread, rather than confined to a single region.

While the hippocampus showed the strongest association between volume loss and declining memory performance, many other cortical and subcortical regions also demonstrated significant relationships.

This suggests that cognitive decline in ageing reflects a distributed macrostructural brain vulnerability, rather than deterioration in a few specific brain regions.

The pattern across regions formed a gradient, with the hippocampus at the high end and progressively smaller but still meaningful effects across large portions of the brain.

Importantly, the relationship between regional brain atrophy and memory decline was not only variable across individuals but also highly nonlinear.

Individuals with above-average rates of structural loss experienced disproportionately greater declines in memory, suggesting that once brain shrinkage reaches higher levels, cognitive consequences accelerate rather than progress evenly.

This nonlinear pattern was consistent across multiple brain regions, reinforcing the conclusion that memory decline in cognitively healthy ageing is linked to global and network-level structural changes, with the hippocampus playing a particularly sensitive role but not acting alone.

Pascual-Leone said: “Cognitive decline and memory loss are not simply the consequence of ageing, but manifestations of individual predispositions and age-related processes enabling neurodegenerative processes and diseases.

“These results suggest that memory decline in ageing is not just about one region or one gene — it reflects a broad biological vulnerability in brain structure that accumulates over decades.

“Understanding this can help researchers identify individuals at risk early, and develop more precise and personalized interventions that support cognitive health across the lifespan and prevent cognitive disability.”

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.