Repetitive Negative Thinking Linked To Higher Alzheimer’s Risk

Repetitive negative thinking, including constant worry and rumination, has been linked to Alzheimer’s-related brain changes. Here’s what researchers found and whether a 90-minute nature walk helps.

If you are someone who constantly replays the bad days in their mind, or are worrying about what would happen next or dwelling on everything that can go wrong, it's time that you start relooking your thought process. That's because this pattern of overthinking over the negatives of life could be doing more harm to you than simply affecting your mood. Research has found that their is a link between this pattern of negative thinking and other biological changes that are associated with Alzheimer’s disease, although scientists also stress that it does not clearly prove that overthinking causes Alzheimer’s.

The research that was published in Alzheimer’s & Dementia in 2020, looked at 292 older adults, including participants who underwent brain scans to measure amyloid and tau. These are two proteins that are strongly associated with Alzheimer’s pathology. Researchers assessed what they called repetitive negative thinking (RNT), which includes two familiar behaviours: worrying about the future and ruminating over negative experiences from the past.

Does Rumination Cause Alzheimer’s?

The researchers found that people with higher levels of repetitive negative thinking showed greater decline in global cognition as well as immediate and delayed memory. Higher RNT was also associated with greater amyloid deposition and entorhinal tau deposition. These associations remained even after researchers adjusted for potential confounding factors, including depression and anxiety.

This is where the findings of the research become all the more interesting. The researchers have proposed the concept of 'Cognitive Debt,' a hypothesis which suggests that repetitive negative thinking could potentially be one pathway through which psychological stress factors are associated with the risk of Alzheimer’s disease. However, this remains a hypothesis for now. The study was also observational, which means that it could identify an association but could not establish that negative thinking or rumination caused the protein build-up or cognitive decline. The researchers specifically called for intervention studies to determine whether reducing RNT could actually alter Alzheimer’s risk.

So, Can A 90-minute Walk Help?

This is where another study has entered the conversation online. A separate 2015 Stanford-led study, published in PNAS, looked at whether spending time in nature could reduce rumination. Researchers randomly assigned 38 healthy adults to either a 90-minute walk through a natural setting or a 90-minute walk in an urban environment. Those who walked in nature reported reduced rumination and also showed reduced activity in the subgenual prefrontal cortex, a brain region associated with rumination.

However, there is an important distinction: the 90-minute nature-walk study did not study Alzheimer’s disease, amyloid or tau. It cannot therefore be used to claim that walking in nature prevents Alzheimer’s or clears Alzheimer’s proteins from the brain.

What the evidence does suggest is that repetitive negative thinking is worth paying attention to as a potentially modifiable behaviour, while activities such as spending time in nature may help reduce rumination in the short term. Whether changing these thought patterns can actually reduce future Alzheimer’s risk is a question researchers are still investigating.

So, the takeaway isn't that every anxious thought is damaging your brain. Rather, persistent patterns of worry and rumination may deserve attention, and finding healthy ways to interrupt that cycle could benefit mental and potentially long-term cognitive health.

 

 

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UK Drug Opening a New Chapter in the Fight Against Alzheimer's

In the ongoing battle against Alzheimer's disease, a new development presents a beacon of hope. A drug known as Donanemab is earning accolades in the scientific and medical communities due to its effectiveness in slowing cognitive decline, as demonstrated in a recent global trial. This drug, which operates as an antibody medication, shows promise in the early stages of Alzheimer's by effectively reducing the buildup of a protein that tends to accumulate in the brains of individuals afflicted with this type of dementia.

While Donanemab doesn't represent a cure, its significance can't be overstated, as charities and medical organizations hail its efficacy as a milestone in Alzheimer's treatment. This is particularly heartening, considering the vast scope of the disease's impact on patients, their families, and health systems across the globe. The drug, having passed the rigorous phase of clinical trials, is now under the evaluation process for potential use within the National Health Service in the United Kingdom.

Donanemab is primarily effective against Alzheimer's, and not other types of dementia, such as vascular dementia. Its mode of operation involves the deceleration of the disease's progression, helping affected individuals retain more of their daily routines, such as preparing meals and engaging in recreational activities. During the trials, donanemab slowed the disease's pace by approximately a third, which is a notable achievement in Alzheimer's research.

The development of donanemab is attributed to Eli Lilly, a prominent player in the pharmaceutical industry. Donanemab functions similarly to another drug, lecanemab, which is a joint creation by Eisai and Biogen. Lecanemab made headlines for its proven ability to slow down Alzheimer's, a feat also achieved by donanemab. However, it's important to note that while these drugs bring hope, they're not without their risks. 

 

One of the common side effects experienced in the donanemab trials was brain swelling, impacting up to a third of the participants. Although the majority of these cases resolved without producing symptoms, there were unfortunate incidents where a few volunteers suffered dangerous levels of brain swelling, leading to fatal outcomes.

During the donanemab trial, the research team conducted an in-depth examination of 1,736 individuals, aged 60 to 85, all of whom were in the early stages of Alzheimer's disease. The group was split in half, with one part receiving a monthly infusion of donanemab treatment, while the other half was administered a placebo over a period of 18 months. 

 

The results of this comprehensive trial have yielded several critical observations. For starters, donanemab seems to offer a tangible benefit for some patients, with those in the earlier stages of the disease and lesser brain amyloid at baseline deriving more significant advantages. Those administered the drug were able to maintain more of their day-to-day lives, such as discussing current events, answering phone calls, or pursuing hobbies. The rate at which the disease progressed, as determined by what people could still do on a daily basis, was slowed by about 20-30% overall, and by 30-40% in a set of patients who were identified as more likely to respond. 

 

While the effects of the drug could be described as modest, they do confirm the notion that removing amyloid from the brain may alter the course of Alzheimer's. This could potentially benefit people affected by this devastating disease if they're given the treatment at the right time. However, as is the case with any new treatment, patients will need to be aware of the associated risks. 

 

The availability and potential cost of donanemab in the UK market remain uncertain, but Alzheimer's experts predict that the presence of two drugs could foster competition in terms of pricing. As for the UK's drug watchdog, NICE, they have already begun assessing donanemab's potential application in treating mild cognitive impairment or mild dementia resulting from Alzheimer's disease.

Despite this promising development, it's crucial to highlight that delivering such treatments on a large scale presents a formidable challenge. According to the Alzheimer's Society, the National Health Service is currently not equipped to provide these new, promising Alzheimer's treatments at the necessary scale. Timely, accurate diagnosis is key, and only a small percentage of individuals currently receive their diagnosis through the specialist investigations needed to be eligible for these treatments. Moreover, these drugs necessitate regular infusions and monitoring, which the NHS is not yet prepared to handle at a large scale. 

 

In conclusion, while donanemab isn't a magic bullet, its potential to slow down Alzheimer's progression marks a significant stride in dementia research. The momentum in Alzheimer's treatment research is gathering pace, and the medical community is optimistic about the potential of these new drugs. However, the road ahead also calls for preparedness and capacity building within health systems to make these treatments accessible to those in need.

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New studies support blood test for early detection of Alzheimer's disease

In three recent publications in Molecular Psychiatry, Brain and JAMA Neurology researchers from the University of Gothenburg provide convincing evidence that an in-house developed blood test for Alzheimer's disease can detect the disease early and track its course, which has major implications for a potential use in clinical practice and treatment trials.

"This is an extremely dynamic research field right now, thanks to the technological development and seminal scientific progress in the past years. The dream scenario is to have a blood test for the early detection and screening of Alzheimer's disease up and running. That would give significantly more people in the world access to testing and future treatments", says Michael Schöll, associate professor and one of the senior authors.

After decades of research, we now know that Alzheimer's disease-related memory problems are just the tip of the iceberg of underlying degenerative processes in the brain that have been silently developing over years or even decades.

These processes result from abnormal aggregation of amyloid and tau proteins in the brain, with these aggregates being the defining pathological features of Alzheimer's disease. Until recently, it was only possible to detect these protein aggregates in the brains of deceased patients at autopsy.

Recent research advances, however, have enabled the accurate detection of amyloid and tau pathology in the brain with imaging methods and in the cerebrospinal fluid of living individuals. These current so-called biomarker methods are either expensive, invasive, or only available at specialized centers; thus, only a fraction of patients suffering from the disease currently benefit from these advances.

An accessible, affordable, and minimally invasive biomarker for Alzheimer's disease would revolutionize care of patients worldwide, as well as boost the development of novel drugs for this presently still incurable disease.

In 2020, researchers at Sahlgrenska Academy, University of Gothenburg, have discovered such a biomarker: a cheap blood test capable to detect the presence of phosphorylated tau protein (p-tau181), a principal, defining hallmark of Alzheimer's disease. Three recent scientific articles from the same study group now focus on the diagnostic performance of this blood marker and how it changes over time during healthy aging and during disease.

The authors demonstrated great potential for the blood test to predict and monitor Alzheimer's disease progression in an unprecedently large study comprising more than 1100 subjects from the Alzheimer's Disease Neuroimage Initiative (ADNI), followed up over several years.

First authors are Thomas Karikari (the article in Molecular Psychiatry) and Alexis Moscoso (Brain and JAMA Neurology).

"The recent development of blood tests sensitive to Alzheimer's disease pathology is likely to provide a solution and has the potential to significantly change the way this disease can be managed in the near future", Moscoso says.

In the publication in Brain the researchers analyzed participants' blood samples acquired at different ages to construct the temporal trajectory of p-tau181 levels in blood across the long course of Alzheimer's disease.

Importantly, they found that the novel blood test could detect abnormalities in p-tau181 levels several years before the onset of memory loss, suggesting enormous potential for early disease detection.

This potential was further confirmed in another publication in Molecular Psychiatry, with first author Thomas Karikari, in which the investigators demonstrated the high clinical utility of p-tau181 in blood for predicting future Alzheimer's disease dementia, even among individuals who had not experienced any memory impairment in the moment of the blood test.

Finally, in the third and most recent publication in JAMA Neurology, the scientists demonstrated that annual increases of p-tau181 in blood were strongly coupled to the loss of nerve cells in Alzheimer's disease as well as to cognitive decline, suggesting not only potential for prediction but also for monitoring and identifying rapidly progressive forms of the disease in an affordable yet effective way. Professor Henrik Zetterberg:

"Our findings have clear and novel implications for the use of these tests, both as diagnostic tools, but also as outcome measures in clinical trials, as we showed that the levels of phosphorylated p-tau181 and Neurofilament light, NfL, in standard blood samples, are reliable biomarkers for Alzheimer's disease, specifically p-tau181, and for neurodegenerative diseases in general, NfL."

Together, these studies represent a crucial step towards the widespread use of biomarkers in clinical routine, making effective blood biomarker testing for Alzheimer's disease a reality for most clinical settings, including primary care. Professor Kaj Blennow:

"This is a major step forward showing that blood tests for tau pathology and neurodegeneration have clinical value to track disease progression in patients with Alzheimer's disease", he says.

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