Laurens Zwanenburg: “Ik heb in het verleden een brede medische achtergrond kunnen opbouwen. Ik ben werkzaam geweest binnen de radiologie, neurologie en als arts-instructeur bij Defensie. Thans heb ik meer dan tien jaar werkervaring in het verrichten van verzekeringsgeneeskundige diensten in de private sector.”

Wij zijn verheugd dat Laurens Zwanenburg zijn kennis en ervaring inzet voor EC VerzuimDiagnostiek. We kijken uit naar een prettige samenwerking!

Bekijk het cv van verzekeringsarts Laurens Zwanenburg

The brain has two important “changes of gear” in adult life: one when it reaches maturity at about 24 and another when the biological effects of ageing become much more apparent at about 60, a study suggests.

The findings are part of PsychAD, an ambitious project dedicated to producing a uniquely detailed map of the prefrontal cortex, the region of the brain responsible for higher-level thinking, personality and complex behaviour, and tracking how it changes over time.
The results showed that during childhood and adolescence the proportions of different types of brain cells changed rapidly as the brain developed and its connections were reorganised.

The rate of change dropped sharply at about 24. From then until late middle age, the make-up of the brain cells was comparatively stable.
At about 60 the pattern changed again. Cells that maintain and protect the brain became much more active in dealing with inflammation and abnormal or faulty proteins.

The brain’s internal clock also appeared to change. In younger adults nerve cells involved in planning, decision-making and memory followed a clear 24-hour timetable and different biological processes became more active at predictable times of day and night. After 60, that orderly pattern started to break down.
Obituaries

Instead, some of the brain’s immune cells and the cells that insulate nerve fibres developed a new daily routine. They appeared to become more active in dealing with damaged proteins, which can contribute to disease, towards the end of the day.

The project, which was led by researchers at the Icahn School of Medicine at Mount Sinai, in New York, studied thousands of genes inside different types of brain cells.

Genes contain the instructions a cell uses to carry out its work. By analysing the RNA, a type of genetic material that is produced when different genes are active, the scientists could compare what different cells were up to in brains of different ages. The technique opened a window on how different tasks and processes became more or less important as people aged.

Across the project scientists analysed more than 6.3 million cells from nearly 1,500 donated brains. Nine studies have been published this week that draw on the data, in Nature and other journals.

One study may help to explain one of the puzzles of Alzheimer’s: why some people retain their mental abilities despite having advanced signs of the disease in their brains.

The researchers compared people who had dementia with others whose thinking remained relatively sharp, despite them having similar levels in the brain of a toxic protein known as tau, which is seen as a hallmark of the disease. Differences could be seen both in nerve cells and in astrocytes, cells that help keep nerve cells functioning and can mount protective responses when the brain is under stress.

Some forms of these astrocytes showed signs of helping nerve cells to survive damage, potentially offering clues to why certain brains are more resilient to Alzheimer’s than others.

Bron: The times.com / 23 september 2026

The tiny plastic particles, smaller than 5 mm, are found throughout the environment and can be inhaled or ingested into the body, but previous evidence on their health risks remained inconclusive. A new study, published in the European Heart Journal, included 61 adults, 19 of whom experienced STEMI, who were treated at hospitals in Italy. Researchers collected separate blood samples from vessels supplying the heart and limbs, and they estimated air pollution exposure via home addresses.

Microplastics and nanoplastics were detected in 84% of patients with STEMI, who also showed a broader array of plastic types compared with 40% of patients with chronic coronary syndromes and 32% of those with healthy coronary arteries. Samples with more microplastics also had elevated tumor necrosis factor α (TNF-α) and interleukin-6, suggesting an inflammatory response, according to researchers.

People who smoked were more likely to have microplastics in their blood than those who did not. Researchers also detected microplastics in all people with higher pollution exposure who smoked, in contrast with 12.5% of people who didn’t smoke with lower exposure. Researchers noted these findings demonstrate a link among environmental exposures, bloodstream microplastics, and heart disease, but they “do not prove that microplastics cause heart attacks,” the lead author concluded in a news release.

Bron: Jama /  September 11, 2026

Een medewerker met te veel werk klaagt hierover, bij een collega, in een functioneringsgesprek, soms zelfs bij de bedrijfsarts. Maar wie te weinig te doen heeft, houdt dat meestal voor zich. Niemand zegt hardop: ik verveel me.

Toch is onderbelasting volgens Madelon van Hooff, hoogleraar Gezondheid, welzijn en motivatie op het werk aan de Open Universiteit, net zo’n serieus arbeidsrisico als overbelasting. Ze onderzoekt al sinds 2014 wat er gebeurt als mensen zich structureel vervelen in hun werk. Vorig jaar schreef ze er het boek Meer dan nietsdoen over, verschenen bij Boom uitgevers.

Haar boodschap is niet dat verveling een nieuw probleem is. Het bestond al. Wat ontbreekt, is een gewoonte om erover te praten.

Onderbelasting is geen onschuldig ongemak. Verveling op het werk hangt samen met dezelfde problemen waar HR al langer op let bij overbelasting: verminderde motivatie, meer burn-outklachten, minder werktevredenheid. Alleen krijgt het niet de aandacht die overbelasting wel krijgt.

Zelfs een simpele vraag als hoeveel mensen hiermee te maken hebben, levert geen eenduidig antwoord op. “Dat weten we dus niet,” zegt Van Hooff. “Over burn-outs wordt veel onderzoek gedaan, maar verveling is nog een onderwerp in de marge. Onderzoeken die er wel zijn laten zien dat 15 tot 86 procent van de mensen op werk ermee te maken heeft. Dat is natuurlijk een te grote marge om met zekerheid te kunnen zeggen om hoeveel mensen het gaat.”

Dat wil niet zeggen dat het onderwerp er niet toe doet. In breed onderzoek naar verveling, niet beperkt tot de werkvloer, staat werk op de derde plek van situaties waarin mensen zich vervelen, vertelt Van Hooff. Verveling op het werk is dus geen zeldzaamheid.

Het is eerder iets waar HR-afdelingen nog geen taal voor hebben ontwikkeld, terwijl overbelasting inmiddels dus een vaste plek heeft op de agenda: verzuimcijfers, werkdrukmetingen, protocollen voor burn-outpreventie.

Dat verschil in aandacht zegt weinig over hoe vaak beide problemen voorkomen, en meer over wat organisaties gewend zijn te meten. Overbelasting laat zich aflezen aan verzuim, verloop en klachten. Voor onderbelasting zijn er nog geen duidelijk meetbare data. Wie zich verveelt, blijft doorgaans gewoon op zijn plek zitten, en levert zijn werk vaak uiteindelijk wel af.

Erover praten voelt als een bekentenis

Wie te weinig te doen heeft, zegt dat zelden hardop. “Ik denk dat het een vrij onderbelicht begrip is in organisaties,” stelt Van Hooff. “Voor veel mensen zit er toch een beetje een soort van schaamte of aarzeling in om het ter sprake te brengen, omdat het natuurlijk niet goed overkomt.” Om te zeggen: ‘Ik heb te weinig te doen’ klinkt voor veel mensen als een bekentenis, niet als een signaal dat iemand serieus mag nemen.

Dat gebrek aan openheid heeft een merkwaardig gevolg. Uit onderzoek blijkt dat mensen die zich vervelen actief gedrag gaan vertonen om dat te verbergen. “Mensen die zich vervelen,” legt Van Hooff uit, “gaan juist soms doen alsof ze druk hebben om die verveling te maskeren.”

Zo ‘maskeren’ ze hun eigen verveling. Dat kost energie, meer dan gewoon eerlijk zijn zou kosten, maar wordt toch verkozen boven het risico dat iemand ziet hoe weinig er eigenlijk te doen is.

Verveling is niet hetzelfde als een zinloze baan

Daar komt bij dat onderbelasting eenvoudig te verwarren is met een heel ander probleem: zinloos werk. Want verveling en betekenisloosheid zijn niet hetzelfde, legt Van Hooff uit. Ze illustreert dat met een voorbeeld.

“Niet alle mensen in bullshit jobs vervelen zich,” zegt ze, “omdat bijvoorbeeld een hedgefondsmanager alsnog voor zichzelf wel veel betekenis uit dat werk kan halen, omdat hij lol heeft in die competitie en in het geld verdienen. Dat verschilt per individu.”

Andersom kan iemand met ogenschijnlijk zinvol werk zich alsnog dood vervelen als de taken te makkelijk of te eenzijdig zijn. Wie dat verschil niet maakt, mist het eigenlijke probleem.

En dan is er nog de manier waarop werk zelf is ingericht. Bijvoorbeeld in grote distributiecentra, waar technologie steeds meer taken overneemt, wordt het overgebleven werk vaak juist eenzijdiger.

“Dan heb je een technologische ontwikkeling,” aldus Van Hooff, “die het werk zo verandert dat het minder interessant wordt.” Dat is geen kwestie van individuele werknemers die zich makkelijk vervelen. Het zit in hoe het werk is vormgegeven.

Twee bronnen van verveling

Dat voorbeeld sluit aan bij het dieper begrijpen van verveling. Verveling heeft namelijk niet één oorzaak. Van Hooff onderscheidt een deel dat in de persoon zit en een deel dat in het werk zit. Sommige mensen hebben simpelweg meer behoefte aan afwisseling en nieuwe prikkels dan anderen.

“Sommige mensen hebben nou eenmaal van nature meer behoefte aan afwisseling,” zegt Van Hooff. “Wij noemen dat boredom proneness, ofwel ‘vervelingsgeneigdheid’.”

Als je je verveelt en op je smartphone gaat zitten, voel je je daar alleen maar verveelder door.

Het andere deel zit in het werk zelf, en dat is waar HR wél iets aan kan doen. Allereerst de kwantiteit: simpelweg te weinig te doen hebben. Daarnaast de kwaliteit, en dat is genuanceerder dan het klinkt.

“Je moet denken aan te makkelijk, maar ook veel te moeilijk werk,” legt Van Hooff uit. “Dat wordt nog weleens vergeten, maar als taken veel te moeilijk zijn, denk maar aan de wiskunde op school, dan gaan mensen zich ook vervelen.” Te weinig afwisseling en te weinig autonomie vergroten dat risico verder.

Dat overbelasting en onderbelasting twee kanten van dezelfde medaille zijn, is geen toevallige waarneming. Het is precies waarom Van Hooff dit onderzoeksterrein instapte. Tijdens haar studie leerde ze de Yerkes-Dodsonwet: een omgekeerde U die de relatie tussen activatie en prestatie weergeeft.

Te veel stress laat de prestatie dalen, maar te weinig activatie doet dat net zo goed. “Het verbaasde mij,” vertelt Van Hooff, “dat die andere kant, dus die onderbelasting, dat daar eigenlijk zo weinig over bekend was.”

Wat er misgaat als je verveling negeert

Een veelgehoorde aanname is dat verveling wel iets oplevert: rustige momenten die ruimte geven voor creativiteit. Uit onderzoek blijkt daar weinig van. “In organisaties,” zegt Van Hooff, “laten de weinige studies die er zijn dat helemaal niet zien. We zien vooral negatieve gevolgen van verveling.”

Deze negatieve gevolgen zijn bijvoorbeeld: te laat komen, langzamer werken, langere pauzes of jezelf sneller ziek melden terwijl je niet ziek bent. “Dat noemen wij contraproductief werkgedrag,” aldus Van Hooff.

Ook het zoeken van afleiding op de smartphone hoort daarbij, en dat werkt averechts: “Als je je verveelt en op je smartphone gaat zitten, voel je je daar alleen maar verveelder door,” legt ze uit.

Ook op het gebied van welzijn blijft het niet zonder gevolgen. Verveling is geassocieerd met burn-outklachten, met stress en met depressieve gevoelens, niet alleen met verminderde werktevredenheid.

Recent onderzoek van Van Hooff laat zien dat een toename van verveling binnen een periode van zes weken samengaat met een toename van diezelfde depressieve gevoelens en van contraproductief gedrag.

Wat HR kan doen tegen verveling op het werk

De meest concrete stap is de eenvoudigste: het onderwerp een plek geven naast werkdruk, in plaats van er alleen naar te vragen als er al iets misgaat.

“Praat met je medewerker,” herhaalt Van Hooff. “Niet alleen over de werkdruk van je werknemer: heeft hij te veel te doen, loopt hij risico op overbelasting, maar ook: loopt hij risico op onderbelasting.” Dat vraagt om een klimaat waarin een eerlijk antwoord ook veilig voelt, anders krijgt een leidinggevende alleen het antwoord dat sociaal gewenst is.

Bron: hrmorgen.nl / 15 september

Lees het volledige artikel via medisch contact

“What can I do to prevent dementia?” patients implore.

Image description not available.(opens in new tab)
It’s no wonder they’re concerned. There is no cure, and the 2 so-called disease-modifying therapies available for Alzheimer disease, the most common cause of dementia, are expensive and only modestly effective at best.

Meanwhile, the numbers of people with dementia are climbing as populations around the world age. According to a 2025 US estimate, the lifetime risk of dementia after age 55 years is 42%, with higher rates among women, Black adults, and carriers of the apolipoprotein ε4 (APOE ε4) allele, the primary genetic risk factor for sporadic Alzheimer disease. The authors projected that the number of people in the US who develop dementia each year will rise from the 514 000 seen in 2020 to approximately 1 million in 2060.

More than 7 million people in the US are living with Alzheimer disease, and the cost of caring for them and others with dementia is projected to reach $409 billion this year, according to the Alzheimer’s Association. Worldwide, the number of people with Alzheimer disease is expected to reach 78 million in 2030 and nearly double that in 2050, according to estimates from Alzheimer’s Disease International, a global federation of Alzheimer and dementia organizations.

Those projected case numbers aren’t a forgone conclusion, though. As many as 45% of dementia cases might be preventable if people eliminated risk factors ranging from hearing loss to high levels of low-density lipoprotein cholesterol to social isolation, the Lancet Commission on dementia estimated in its 2024 report.

“It’s so much more efficient to prevent the disease from happening in the first place,” noted Gold, an advanced heart disease fellow at Cedars-Sinai Medical Center in Los Angeles.

For now, there are no proven treatments to reduce the risk of mild cognitive impairment or dementia in people with normal cognition, although a clinical trial of lecanemab (Leqembi), currently approved only for people with Alzheimer-related mild cognitive impairment or early-stage dementia, is under way in individuals described as presymptomatic.

Lecanemab is a monoclonal antibody that clears amyloid plaque deposits in the brain, a hallmark of Alzheimer disease. Presymptomatic people enrolled in the trial were cognitively intact at baseline but had an above-average risk of Alzheimer disease because they carried at least one copy of APOE ε4 or had elevated brain amyloid levels.

Even if lecanemab is found to prevent or delay the onset of cognitive impairment, the treatment is expensive and cumbersome, requiring infusions or injections. Plus, at least in people who already have Alzheimer-related cognitive impairment or dementia, lecanemab and donanemab (Kisunla)—the other antiamyloid monoclonal antibody on the market—carry the risk of an adverse event called amyloid-related imaging abnormalities (ARIA). ARIA, characterized by brain swelling or microbleeds, is often asymptomatic, but in about 5% of cases, it can result in hospitalization, permanent disability, or death.

For lack of a silver bullet to prevent cognitive decline, scientists increasingly have been investigating the brain health effects of modifiable risk factors such as hypertension, diabetes, and poor sleep, whose role in the development of cardiovascular disease is well-documented. Adhering to the American Heart Association’s Life’s Essential 8, 4 health behaviors and 4 health factors for improving and maintaining cardiovascular health, may also promote optimal brain and cognitive health, Gold and his coauthors concluded in a narrative review published in July in the Journal of the American Heart Association.

Much of the evidence about these risk factors comes from observational studies, which is unsurprising, given the challenges of conducting a clinical trial powered to detect dementia in people who were asymptomatic at baseline. But observational studies can show only correlation, not causation, and the findings of clinical trials have been mixed.

Still, “I think there’s very good evidence for a lot of these risk factors” related to brain health, said Kristine Yaffe, MD, a cognitive aging and dementia researcher, although some have more evidence than others.

She and other experts in the field point out that tackling modifiable risk factors—especially in midlife—can’t hurt, for the most part, and likely will help improve overall health as well as brain health and quality of life.

Quantifying the Risks
A study published last month suggested that tackling major cardiovascular risk factors in middle age can benefit the brain years later.

Researchers calculated the associated risk of midlife hypertension, diabetes, and current smoking with dementia risk using an easy-to-understand metric: dementia-free survival years, which integrates incident dementia and death before dementia.

“We wanted 3 big risk factors that were easy to classify as yes or no,” explained coauthor Josef Coresh, MD, PhD, a professor of population health and the founding director of the Optimal Aging Institute at the NYU Grossman School of Medicine. Type 2 diabetes alone may double the risk of dementia, noted Mark Espeland, PhD, a professor of internal medicine and public health sciences at Wake Forest University School of Medicine who was not involved in the study.

Coresh’s observational study included about 12 000 US adults with an average age of 56 years who did not have dementia at baseline. Participants were followed up over a median of 26 years. Having none of the vascular risk factors was associated with nearly twice as many dementia-free survival years (30 years) as having all 3 of them (17.5 years), the researchers found.

As for hypertension, at least 2 randomized trials have found that aggressive treatment can reduce not only the risk of heart attack and stroke but also of cognitive impairment, Coresh said.

One trial, the China Rural Hypertension Control Project Phase-3 (CRHCP-3) study, enrolled nearly 34 000 people aged 40 years or older with uncontrolled hypertension. Participants were randomly assigned to the intervention group, which set a goal of lowering systolic blood pressure to less than 130 mm Hg and diastolic blood pressure to less than 80 mm Hg, or usual care. After 48 months, those in the intervention group had a significantly lower risk of all-cause dementia, investigators reported in 2025. New long-term data demonstrate sustained benefits. Over 7 years, the intensive blood pressure intervention resulted in a significant 15% reduction in dementia risk compared with usual care, the researchers reported late last month at the European Society of Cardiology meeting.

The other trial, the Systolic Blood Pressure Intervention Trial Memory and Cognition in Decreased Hypertension (SPRINT MIND) study, first published in JAMA in 2019, randomly assigned people with hypertension to intensive treatment targeting a systolic blood pressure of less than 120 mm Hg or to usual treatment targeting less than 140 mm Hg.

SPRINT MIND found that after a median follow-up of 5 years, intensive blood pressure control had significantly reduced the risk of developing mild cognitive impairment, an intermediate stage between normal aging and dementia. However, the study did not find a statistically significant reduction in the risk of dementia. The authors speculated that was due to fewer-than-expected dementia cases or the decision to halt SPRINT early after a median intervention period of a little over 3 years because of its success in reducing cardiovascular disease.

Citing both CRHCP-3 and SPRINT MIND, the American Heart Association and the American College of Cardiology now recommend that adults with hypertension reduce their systolic blood pressure to less than 130 mm Hg to prevent mild cognitive impairment and dementia.

Pointing Fingers at Multidomain Interventions
In recent years, evidence about modifiable dementia risk factors from randomized trials testing multidomain interventions has been growing.

The first randomized clinical study to demonstrate that lifestyle factors can help prevent cognitive decline was published in 2015. The Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) enrolled approximately 1300 individuals, aged 60 through 77 years, who had an increased risk of dementia. Over 2 years, the intervention group received about 360 hours of lifestyle-based strategies targeting diet, exercise, cognitive training, and vascular risk monitoring, while the control group received general health advice.

Cognitive performance improved among both groups, but the average total improvement was 25% higher in the intervention group than in the control group. (A recent JAMA Neurology editorial noted that even the control groups of FINGER and other multidomain intervention trials may appear to improve due to the practice effect of repeatedly taking a cognitive test or because they modify their behavior as a result of being observed.)

FINGER has given rise to multiple randomized trials in more than 70 countries to assess the effects of multidomain lifestyle interventions on brain health.

One of them, the US Study to Protect Brain Health Through Lifestyle Intervention to Reduce Risk (US POINTER) trial, published in JAMA in 2025, enrolled about 2100 people aged 60 to 79 years who had an elevated risk of cognitive decline. After 2 years, the trial’s structured, higher-intensity intervention had a greater benefit on global cognition than a self-guided intervention. This July, researchers reported similar findings from a trial in 11 Latin American countries called the Latin American-FINGERS trial, which used a culturally adapted multidomain lifestyle intervention.

Whether the “fairly modest” benefit will prove to be clinically important and translate into a reduced risk of dementia remains to be seen, said Espeland, one of the leaders of the US POINTER trial.

Espeland is also an investigator on a trial examining the effect on cognition of a 10-year multidomain weight-loss intervention in people with diabetes.

The Action for Health in Diabetes (Look AHEAD) trial randomly assigned nearly 3700 adults either to the intensive lifestyle intervention, which included caloric restriction and increased physical activity, or to a control group that received diabetes support and education.

The researchers published their results in July. As in the US POINTER trial, “the differences in cognitive function were also pretty small” in Look AHEAD, Espeland said.

After the trial concluded, the researchers continued to follow up participants for 12 to 14 years. They found that the intensive lifestyle intervention’s impact on the incidence of mild cognitive impairment or dementia depended on baseline body mass index (BMI).

Among those who were overweight at baseline, incident cognitive impairment was reduced. But among those who were obese at baseline, it was neither reduced nor increased, and among those with the greatest obesity, the intensive lifestyle intervention actually increased the incidence of cognitive impairment. These head-scratching findings appeared to be unrelated to the amount or trajectory of weight loss.

Observational studies in people with prediabetes or type 2 diabetes and the general population have suggested that higher adiposity is linked with slower cognitive decline, the authors noted. One possible explanation for why adiposity appears to protect the brain later in life is that unintended weight loss could be a precursor to dementia, due to such factors as a poorer sense of taste and smell and apathy about eating, Espeland noted.

The study’s findings shouldn’t stop people from deliberately losing weight if they are overweight or obese, he cautioned. “Losing weight is great for preventing diabetes and for the heart,” he said. “Following the goals of the POINTER trial is probably great for the brain.”

Refining the Trials
Scientists are hopeful that the advent of blood biomarker tests will enable clinical trials to offer insights at a faster pace.

Typically, researchers must follow up participants for many years to see whether modifying factors such as diabetes or hypertension reduces dementia risk.

Except perhaps after having a stroke, “you don’t wake up and have dementia,” emphasized Yaffe, director of the Center for Population Brain Health at the University of California San Francisco. “It’s a progressive thing.”

Dementia, and cognitive decline in general, can happen 20 years or more after underlying biological processes begin to develop, noted Sokratis Charisis, MD, a fellow in neurology at Massachusetts General Hospital. “It’s hard for studies to sustain these long periods of follow-up.” And, he pointed out, some study participants will die before their incipient cognitive decline is detected.

But the recently available plasma tests for Alzheimer disease biomarkers hold promise for monitoring the biological effects of interventions such as a healthier diet for which clinical trials are lacking, said Charisis, who coauthored a recent commentary in JAMA Network Open that touched on the tests’ use in research. Although their applications in caring for asymptomatic individuals are limited for now, he said, “we’re hoping these new biomarkers will help us refine clinical trial designs.”

Yaffe was the senior author of a preprint study posted in April that investigated midlife cardiovascular health and Alzheimer disease biomarkers.

The study, which has not been peer-reviewed, found that poorer cardiovascular health in early midlife, as defined by Life’s Essential 8, was linked to less-favorable early Alzheimer disease biomarker profiles in late midlife, particularly reflecting greater amyloid burden and structural brain changes.

Yaffe said clinical trials of lifestyle interventions for dementia are starting to incorporate biomarker tests. “If you’re doing a FINGER trial, I’d like to see how the biomarkers move,” she said. “I think that’s an exciting area now.”

In the meantime, Espeland noted, for both brain and cardiovascular health, “adopting a healthy lifestyle should be good for you.”

Bron: JAMA / September 4, 2026.

The findings suggest that chronic fatigue syndrome (also known as ME), long COVID, post-traumatic stress disorder (PTSD), rheumatoid arthritis and multiple sclerosis (MS) may be driven by common underlying mechanisms.

This is despite the conditions being triggered by different events—from viral infections to psychological trauma or autoimmune responses.

Lead researcher Professor Dmitry Pshezhetskiy, from UEA’s Norwich Medical School, said, “Until now, illnesses including long COVID, PTSD, ME/CFS, multiple sclerosis and rheumatoid arthritis were viewed as seemingly unrelated and triggered by completely different events.

“ME/CFS often follows viral infection. Long COVID develops after SARS-CoV-2 infection. PTSD emerges after traumatic experiences. Rheumatoid arthritis is an autoimmune disease attacking the joints, while multiple sclerosis attacks the nervous system.

“But one thing that links them all is that patients frequently report remarkably similar symptoms—overwhelming fatigue, brain fog, poor concentration, disturbed sleep, autonomic dysfunction and a dramatic reduction in everyday functioning.

“We wanted to find out why this is.

“What we discovered is something approaching a biological unifying theory of fatigue.”

How the research happened
Rather than conventionally analyzing DNA sequences, researchers from UEA used Oxford BioDynamics’ innovative EpiSwitch Orion platform, which examines the three-dimensional architecture of the genome, essentially studying how DNA folds and interacts inside living cells.

The analysis was computational. Published genomic data for long COVID, PTSD, rheumatoid arthritis and multiple sclerosis, drawn from existing genome-wide association studies, were combined with 3D genomic data from an earlier ME/CFS patient study, without needing to collect new patient samples.

“DNA is folded in our cells, so regions far apart in the linear sequence can touch, and those contact points are where genes get controlled. Orion predicts where these contact points are likely to be,” said Dr. Ewan Hunter, chief data officer at Oxford BioDynamics.

Applied to the five conditions, Orion found that genetic changes that appeared to have little in common connected into the same regulatory circuitry.

Pshezhetskiy said, “We expected to find at least some overlap in genes across the conditions. But we actually found the opposite.

“At an individual gene level, there was surprisingly little direct overlap between long COVID, ME/CFS, PTSD, multiple sclerosis and rheumatoid arthritis.

“But when we analyzed how those genes interact in complex biological networks, a completely different picture emerged. Suddenly, the diseases appeared deeply connected.

“This is not something you can see by reading the genetic sequence alone, which is why these conditions may have looked unrelated for so long.

“Although these conditions are triggered by completely different events, they may ultimately disrupt the same fundamental biological systems and produce the similarly devastating exhaustion experienced by millions worldwide.”

The study found that genes linked to each illness fed into the same major biological systems—including immune and inflammatory signaling, mitochondrial energy production, metabolic regulation, stress-response mechanisms and neuroendocrine signaling.

Why trauma and viruses can produce the same symptoms
The team said the study could help explain why people who have experienced a viral infection or psychological trauma can go on to develop similar symptoms.

“We now think the answer may lie in shared regulatory networks embedded within the body’s immune and metabolic systems,” Pshezhetskiy said.

“A COVID infection may trigger prolonged immune activation. Traumatic stress may disrupt stress-hormone pathways and inflammatory responses.

“But both disturbances appear capable of converging on common biological circuits controlling energy production, immune regulation and cellular resilience.

“When those systems become persistently dysregulated, the result may be the profound and disabling fatigue seen across multiple disorders.”

A new role for the immune system
The study also highlighted several “hub genes” that sit at the busiest points within these shared networks.

Among them were genes involved in immune regulation, inflammatory signaling and mitochondrial energy production. The authors stress that these are candidates identified by the analysis, and more work is needed to confirm their role.

One part of the analysis, looking specifically at ME/CFS, flagged LAG3 as a gene to investigate. This is a molecule associated with ‘T-cell exhaustion,’ a state in which immune cells become worn out after prolonged activation.

The team said that if this can be confirmed in further studies, it could help explain why many patients appear to be stuck in a state of chronic illness long after the original trigger has disappeared.

“This work adds to a growing body of evidence suggesting that persistent immune dysfunction may play a far larger role in chronic fatigue-related illnesses than previously recognized,” Pshezhetskiy said.

Paving the way for blood tests and treatments
“Perhaps the most significant implication is what this could mean for diagnosis.

“ME/CFS and long COVID are currently diagnosed largely through symptoms, with no universally accepted laboratory test available.

“That has left many patients facing years of uncertainty.”

Separate earlier work using the EpiSwitch platform had already produced a blood-based ME/CFS test that showed promise for high levels of diagnostic accuracy and was ready for further validation needed for clinical use.

The new findings raise the prospect of signatures shared across several conditions, beyond ME/CFS alone.

“We hope our work could pave the way for objective blood tests capable of identifying underlying biological signatures rather than relying solely on patient-reported symptoms,” Pshezhetskiy said.

Now, the team hopes the newly identified shared biological pathways could eventually lead to broader diagnostic tools and even treatments that work across several chronic conditions.

“Rather than viewing long COVID, ME/CFS, PTSD, rheumatoid arthritis and multiple sclerosis as entirely separate disorders, we now think they may be different manifestations of disturbed biological networks operating throughout the body.

“In that scenario, chronic exhaustion is not simply a symptom. It is the visible consequence of a deeper system failure affecting immune function, metabolism and stress-response pathways.

“This study offers a framework for understanding how different triggers can converge to cause the same profound clinical exhaustion.”

This research was led by the University of East Anglia in collaboration with Oxford BioDynamics, the London School of Hygiene and Tropical Medicine, and Cornwall Partnership NHS Foundation Trust.

Bron: medical express – 2 September 2026

De verwachtingen zijn hoog: AI moet bijdragen aan lagere administratieve lasten, efficiëntere zorgprocessen en meer tijd voor de patiënt. Tegelijkertijd laten twee recente onderzoeken zien dat juist de volgende stap – het structureel opschalen van succesvolle toepassingen – veel lastiger is dan het ontwikkelen van nieuwe pilots.

Die conclusie komt naar voren uit zowel de AI Monitor Ziekenhuizen 2026 van M&I/Partners uit maart van dit jaar als de recente whitepaper De weg naar volwassen AI in de zorg van IG&H (de links naar de onderzoeken staan onderaan het artikel). Hoewel beide onderzoeken een andere invalshoek kiezen, schetsen ze een vergelijkbaar beeld. Nederlandse ziekenhuizen investeren steeds meer in AI en boeken aantoonbare vooruitgang, maar het realiseren van blijvende organisatiebrede impact is vooralsnog weerbarstig.

Vaste voet aan de grond

Dat ziekenhuizen AI steeds serieuzer nemen, blijkt uit verschillende ontwikkelingen. Volgens de AI Monitor beschikt inmiddels bijna de helft van de ziekenhuizen over een uitgewerkte AI-visie en -strategie, terwijl driekwart AI-beleid heeft vastgesteld. Ook hebben veel organisaties AI-boards of regiegroepen ingericht die zich bezighouden met governance, prioritering en naleving van wet- en regelgeving.

De aard van de toepassingen verandert eveneens. Diagnostiek was jarenlang het meest zichtbare domein voor AI, maar inmiddels verschuift de aandacht naar toepassingen die de dagelijkse werkzaamheden van zorgprofessionals ondersteunen. Zo wordt AI steeds vaker ingezet voor administratieve processen, verslaglegging, communicatie en logistiek. Vrijwel alle ziekenhuizen experimenteren daarnaast met generatieve AI, zoals veilige interne varianten van tools zoals ChatGPT en Copilot, spraakgestuurde verslaglegging en AI-ondersteuning bij correspondentie.

Tegelijk blijkt uit de AI Monitor dat de meeste ziekenhuizen weliswaar veel AI-initiatieven hebben, maar dat slechts een klein deel daarvan daadwerkelijk wordt opgeschaald. Ook toepassingen als ambient listening bevinden zich in veel organisaties nog vooral in de pilotfase. Daarmee blijft de gerealiseerde impact vooralsnog achter bij de hoge verwachtingen die ziekenhuizen van AI hebben.

Organisatie bepaalt succes

Volgens IG&H ligt de verklaring daarvoor niet in de technologie zelf. De onderzoekers wijzen juist op organisatorische factoren die succesvolle opschaling in de weg staan. Datakwaliteit blijft een belangrijk aandachtspunt, mede doordat gegevens historisch zijn ingericht om bestaande zorgprocessen te ondersteunen en niet om AI-toepassingen organisatiebreed te voeden.

Ook eigenaarschap blijkt lang niet altijd duidelijk belegd. Wanneer onduidelijk is wie verantwoordelijk is voor beheer, doorontwikkeling en besluitvorming, blijft een succesvolle pilot vaak hangen binnen één afdeling of een kleine groep enthousiaste gebruikers.

Losse toepassingen

Een ander probleem is het opstarten van nieuwe AI-pilots zonder eerst bestaande pilots goed te integreren in processen. “Veel ziekenhuizen starten nieuwe AI-projecten terwijl eerdere initiatieven nog niet structureel zijn verankerd”, stelt Femke Keijzer, Managing Director Healthcare bij IG&H. “Zonder aandacht voor de basis ontstaat stapeling van technologie, terwijl gebruik en opbrengst nauwelijks toenemen.” AI wordt dan toegevoegd aan bestaande werkwijzen, in plaats van dat processen worden heringericht rond de mogelijkheden die de technologie biedt.

Volgens IG&H zijn organisaties die eerst investeren in hun zwakste schakels uiteindelijk beter in staat AI succesvol op te schalen. Dat kan betekenen dat eerst wordt gewerkt aan datakwaliteit, governance, AI-geletterdheid of de betrokkenheid van eindgebruikers, voordat nieuwe toepassingen worden toegevoegd. Ook bestuurlijke betrokkenheid speelt daarbij een belangrijke rol. Organisaties waarin AI expliciet onderdeel is van de bestuursagenda blijken vaker samenhang aan te brengen tussen strategie, uitvoering en investeringen.

Van technologie naar organisatie

Waar M&I laat zien dat ziekenhuizen de afgelopen jaren veel hebben geïnvesteerd in AI-strategieën, AI-beleid en organisatorische randvoorwaarden, probeert IG&H te verklaren waarom verdere groei op veel plaatsen toch stokt. Samen schetsen de studies een sector die de experimentele fase grotendeels achter zich heeft gelaten, maar nog volop zoekt naar manieren om AI duurzaam onderdeel te maken van de dagelijkse zorgpraktijk.

Dat betekent ook dat de discussie verandert. Enkele jaren geleden draaide AI vooral om technologische mogelijkheden en nieuwe toepassingen. Inmiddels verschuift de aandacht naar vragen als: hoe organiseer je eigenaarschap, hoe borg je datakwaliteit, hoe neem je medewerkers mee in veranderingen en hoe bepaal je welke toepassingen daadwerkelijk waarde toevoegen?

De volgende ontwikkelfase draait dan ook minder om het ontwikkelen van nóg meer AI-toepassingen en steeds meer om het creëren van de organisatorische voorwaarden. Zo kunnen succesvolle pilots uitgroeien tot een vast onderdeel van de zorgverlening.

Beide onderzoeken laten dan ook zien dat AI geleidelijk verandert van een technologische innovatie in een bestuurlijk en organisatorisch vraagstuk. Uiteindelijk zal niet de techniek bepalen hoeveel waarde AI toevoegt aan de zorg, maar de manier waarop ziekenhuizen hun organisatie daarop weten in te richten.

Vijf lessen uit twee AI-onderzoeken

AI is definitief doorgebroken in ziekenhuizen. Vrijwel alle ziekenhuizen werken inmiddels met AI-toepassingen of ontwikkelen daarvoor beleid en strategie.

De aandacht verschuift van diagnostiek naar ondersteuning van zorgprofessionals. Vooral toepassingen voor verslaglegging, administratie, communicatie en logistiek groeien snel.

Opschalen blijft de grootste uitdaging. Veel AI-toepassingen leveren lokaal resultaat op, maar groeien niet uit tot organisatiebrede voorzieningen.

Succes hangt minder af van technologie dan van organisatie. Datakwaliteit, governance, eigenaarschap, AI-geletterdheid en adoptie bepalen steeds vaker of AI daadwerkelijk waarde oplevert.

De volgende fase vraagt om bestuurlijke keuzes. AI ontwikkelt zich van een innovatieproject naar een vast onderdeel van de strategie en bedrijfsvoering van ziekenhuizen.

In ICT&health 4, die 21 augustus verschijnt, staat een achtergrondartikel over de conclusies uit beide onderzoeken.

Bron: ICT & Health / 3 juli 2026

Long COVID is estimated to affect 5% of the world’s population and is characterized by a wide range of persistent and sometimes debilitating symptoms, including brain-related ones such as fatigue, brain fog, memory problems or low mood, that continue for at least three months following the initial COVID-19 infection.

Despite its prevalence, no evidence-based treatments currently exist, largely due to limited understanding of the underlying brain pathology.

Brain scans point to dopamine loss

In the new study, researchers used positron emission tomography (PET) brain imaging to measure a well-established marker of dopamine neuron integrity in people with long COVID and healthy individuals.

The team found significantly lower levels of the imaging marker—indicating reduced dopamine nerve terminal density—across all major regions of the striatum, the brain structure that plays a central role in motivation, movement and thinking, in people with long COVID compared with healthy individuals. Specifically, lower markers in the ventral striatum were associated with greater loss of motivation, marker reductions in the dorsal putamen were associated with slowed movement speed, and marker loss in the caudate putamen was linked to memory difficulties.

“Our findings provide compelling evidence that long COVID involves the loss of dopamine-releasing neurons,” says Dr. Jeffrey Meyer, senior scientist at the Brain Health Imaging Center, Canada Research Chair, and senior author of the study.

“This kind of injury is well known to produce symptoms like lack of motivation and motor slowing, and may contribute to memory difficulties in other neurological conditions. Our results suggest a similar process is occurring in long COVID.”

Building on earlier evidence

The findings build on the team’s earlier work showing that people with long COVID have elevated levels of inflammation in the brain, especially in regions that are rich in dopamine-releasing neurons.

“We know that inflammation can injure dopamine neurons. While our earlier research showed high levels of inflammation in those regions, this study provides direct evidence that the dopamine neuron marker is reduced in the same regions—and that this loss correlates with patients’ symptoms,” explains Meyer.

The study represents a notable shift in how long COVID may be understood and treated. Previous studies predominantly focused on brain inflammation and immune changes that occur during long COVID, with almost no clinical trials targeting the dopamine-releasing neurons.

“These results indicate that long COVID is, at least in part, a disorder of the brain’s dopamine system,” adds Meyer. “This suggests that repurposing medications that augment the function of dopamine-releasing neurons, including dopamine precursors and inhibitors of dopamine metabolism, could be a promising approach.”

Hope and a trial ahead

For individuals affected by long COVID, the new findings offer hope.

“For five years I have been seeking answers about what happened to me after I contracted COVID in 2021,” says Susan Deuville, lived experience research adviser to Meyer. “It was a crushing loss of the life I had and the person I was before. Meyer’s research brings hope. It also validates what long COVID sufferers have always known—long COVID is real and the effects are devastating.”

Based on the new findings, the team plans to launch a clinical trial targeting dopamine function to help with memory, motivation and fatigue in people with long COVID in the next couple of months, in collaboration with University Health Network (UHN), as part of the hospitals’ partnership to help bridge the gap between mental and physical health care.

Bron: Medical express / 10 juli 2026

Nearly half of dementia cases may be connected to risk factors that people can potentially change, including smoking and high blood pressure. New research from Lund University has identified how specific risk factors are associated with Alzheimer’s disease and vascular dementia, the two most common causes of dementia.

A person’s dementia risk is shaped partly by factors that cannot be altered, including age, gender and genetics. Other influences may be modifiable, such as smoking, cardiovascular disease, high blood lipids, physical activity, alcohol consumption, hearing loss and high blood pressure.

Dementia is not a single disease. It is a collection of symptoms that can result from several different disorders, which means the risks may vary depending on the underlying cause. Researchers at Lund University examined how individual risk factors are connected to brain changes associated with Alzheimer’s disease and vascular dementia.

“Much of the research available on the risk factors that we ourselves can influence does not take into account the different causes of dementia. This means that we have had limited knowledge of how individual risk factors affect the underlying disease mechanisms in the brain,” explains Sebastian Palmqvist, senior lecturer in neurology at Lund University and senior physician at the Memory Clinic at Skåne University Hospital.

Researchers Tracked Brain Changes for Four Years

The study involved almost 500 participants who had an average age of 65 and showed no signs of cognitive impairment. Researchers followed them for four years, measuring changes in the brain’s white matter, the nerve fibers that are often damaged in vascular dementia.

The team also monitored levels of amyloid β and tau, two proteins associated with Alzheimer’s disease. Their goal was to determine how both modifiable and nonmodifiable risk factors were related to changes in the brain over time.

Vascular Risks Were Linked to White Matter Damage

Most of the modifiable factors examined, including smoking, cardiovascular disease, high blood lipids and high blood pressure, were associated with damage to blood vessels in the brain. They were also linked to a more rapid buildup of changes in white matter.

“We saw that most modifiable risk factors — smoking, cardiovascular disease, high blood lipids and high blood pressure, among others — were linked to damage to the brain’s blood vessels and a faster accumulation of so-called white matter changes. This damage impairs the function of the blood vessels and leads to vascular brain damage – and can ultimately lead to vascular dementia,” says Isabelle Glans, doctoral student at Lund University and resident in neurology at Skåne University Hospital.

The researchers also identified possible connections between certain risk factors and the proteins involved in Alzheimer’s disease.

“Diabetes was associated with increased accumulation of amyloid β, while people with lower BMI had faster accumulation of tau. However, these findings need to be investigated further and validated in future studies,” continues Isabelle Glans.

Healthy Habits May Reduce Multiple Forms of Damage

Adopting healthier habits and addressing modifiable risks may help delay the appearance of Alzheimer’s symptoms. This may be especially important because many people with dementia have more than one type of disease process occurring in the brain, including both vascular damage and Alzheimer’s related changes.

Palmqvist said that improving vascular and metabolic health may therefore remain valuable even for people at risk of Alzheimer’s disease.

“Focusing on vascular and metabolic risk factors can still help reduce the combined effects of several brain changes that occur simultaneously,” he concludes.

Bron: Lund University / August 6, 2026