- Previously, experts viewed modest reductions in clinical cognitive test scores as predictors of future risk of progression to Alzheimer’s disease.
- Lower education, lower income and social isolation contribute to lower performance of cognitive tests, called “cognitive frailty”.
- In a new study, despite lower test scores, cognitively frail participants performed complex mental tasks at a similar level to healthy controls.
- Researchers at the University of Cambridge concluded that clinical cognitive testing alone was not accurate in predicting an individual’s likelihood of progressing to mild cognitive impairment (MCI) or Alzheimer’s disease.
Currently, more than 6 million people in the United States are living with Alzheimer’s disease. This number is estimated to rise to over 13 million by 2050.
Although deaths from heart disease decreased by 7.3%, those from Alzheimer’s disease increased by 145.2%. Additionally, projected public health costs related to Alzheimer’s could increase from current estimates of $ 355 billion annually to $ 1.1 trillion by 2050.
Regarding all causes of dementia, an item suggests that a serious underestimation of the risk of dementia is at stake. The authors predict that 152 million or more people worldwide will be living with dementia by 2050.
Researchers looked for meaningful treatments or a cure. However, only five drugs in the United States and four in the European Union have received approval for the treatment of Alzheimer’s disease since 1994.
These drugs are not curative, but they intervene in the disease process by reducing symptoms or decreasing inflammation of the brain cells. These drugs represent the paucity of options for people living with the condition.
The lack of attempts is not to blame for this lack of treatment options. Clinical scientists and researchers have attacked Alzheimer’s on multiple fronts.
Most of the research in recent decades has been based on the “amyloid cascade hypothesis,” which refers to the significant presence of a protein called amyloid that first instigates inflammation, disrupts neuronal function, and ultimately contributes to the breakdown of messages. in the brain.
For Medical news today, Dr. Scott Kaiser, director of geriatric cognitive health for the Pacific Neuroscience Institute at Providence Saint John’s Health Center in Santa Monica, California, elaborated:
“I suspect they are multifactorial processes. Instead of saying that the amyloid hypothesis is or isn’t correct, let’s start looking [it] as part of a larger and more complex equation. [T]here are more factors […]. The amyloid load is only one of the factors. There are some questions as to how much amyloid accumulation is causal rather than just a by-product, a marker. I think these are areas of exploration. ”
– Dr. Scott Kaiser
Dr. Kaiser added: “I predict that the definitions of dementia and various types of dementia and various clinical syndromes surrounding dementia will change. […] in the next future. They will continue to evolve ”.
This basic scientific research has led to the most recent breakthrough in the treatment of Alzheimer’s disease: the development of anti-amyloid monoclonal antibodies to remove amyloid plaques known to disrupt brain communication.
The Food and Drug Administration (FDA) recently approved aducanumab (Aduhelm), the first drug in its class, for limited use, and related drug studies are ongoing. Although research has shown the reduction of brain amyloid deposits using this drug, its clinical benefit is still being studied.
More and more doctors and scientists are taking a combined therapeutic approach to treat Alzheimer’s disease, using symptomatic and disease-modifying therapies.
In addition to drug therapies, researchers are also looking at Alzheimer’s through a lifelong lens of individual and public health. Why do some people develop the condition and others don’t? And, as treatment options improve, how do we identify people at risk and those in the early stages of the disease for intervention?
Prof. James Rowe, a Cambridge University researcher and senior author of the paper, and his collaborators sought to answer these questions and investigate the underlying causes in their new study.
The results appear in the Journal of Neuroscience.
Clinical researchers are increasingly focused on accurately identifying those people who may be at risk of developing Alzheimer’s disease. One such group of individuals are those that the medical community classifies as cognitively frail: people who do not perform well on the cognitive tests they undergo as part of a comprehensive health assessment.
On Monday, scientists from the Cambridge Center for Frontotemporal Dementia and Related Disorders revealed the results of their study comparing cognitively frail people with those living with healthy cognition, MCI and Alzheimer’s disease.
The first author, Dr Ece Kocagoncu, noted that the team’s work is unique in that it is “[t]was the first to take a multimodal and in-depth approach and to test the cognitive impairments using electroencephalogram (EEG), magnetoencephalogram (MEG) and magnetic resonance imaging (MRI). “
With Prof. Rowe and other colleagues from the University of Cambridge, Dr. Kocagoncu first recruited participants using a large-scale cross-sectional population from the Cambridge Center for Aging and Neuroscience study (Cam-CAN Frail project).
From this intensive home community-based study, the researchers identified people to undergo extensive cognitive testing and assigned them to categories.
By definition, cognitively frail people are those who find cognitive testing difficult but show none of the clinically observed memory or learning deficits in MCI or late Alzheimer’s disease.
For MNT, Dr. Kocagoncu drew up the study design:
“To measure their neural activity,” he continued, “we used a special activity we designed, called whimsical crossmodal activity, in the scanner. This task was specially designed to separate healthy individuals from Alzheimer’s disease patients.”
“It measures the ability to make connections between information (associative processing) and to recognize new information (novelty processing), which are functions known to be impaired in Alzheimer’s.”
The results were not predictable.
On the EEG and MEG (neurophysiological tests), cognitively frail individuals behaved robustly, that is, just like those without cognitive impairment. And, structurally, the brains of cognitively frail people were similar to that of cognitively healthy individuals.
The brains of cognitively frail individuals were clearly different from that of people with MCI or Alzheimer’s disease. What does this mean? Dr. Kocagoncu explained:
“Our results have been amazing and very encouraging! We found that when we look closely at the brain structure and neural function of the cognitively frail, they are just like healthy older adults. They show no volume loss in brain areas associated with Alzheimer’s disease and show no functional alterations in associative and novelty processing. “
In this way, Dr Kocagoncu and her colleagues from Cambridge showed that cognitive frailty was not a quick and accurate predictor of future MCI or Alzheimer’s disease.
So, what does this mean for screening individuals in the community who may be scoring in the cognitive frailty bracket?
Scientists conclude that cognitive frailty may be on the spectrum of normal aging rather than a precursor to Alzheimer’s disease.
Dr Kocagoncu reflected: “First, the tests that are often used in the clinic to help diagnose dementia – such as the Mini-Mental Status Examination (MMSE) – are unlikely to provide an accurate picture of our cognitive health when used. alone”.
“Cognitive test results should be interpreted with caution and we should consider other factors that could contribute to suboptimal performance.”
“Second, cognitive underperformance could instead be the result of an accumulation of psychosocial, lifestyle and medical risk factors.”
“Factors such as malnutrition, social isolation, stress, depression, sedentary lifestyle, hearing / vision problems, cardiovascular disease, chronic inflammation and lower education levels are known to contribute to the worsening of cognitive function.”
– Dr. Kocagoncu
Prof. Rowe, Dr. Kocagoncu and their colleagues postulate that their research opens the door to further study. They note that the use of increasingly available biomarkers – blood measurements of Alzheimer’s disease-specific proteins – can further help identify people at risk or in the early stages of Alzheimer’s disease.
Their lab plans to take a closer look at the risk factors associated with cognitive frailty, as well as the protective factors associated with healthy cognitive aging.
Dr. Scott Kaiser concluded:
“We know that there are modifiable risk factors. By addressing these risk factors, you can reduce your risk of dementia. [S]something on the order of a third of dementia cases could be prevented entirely by addressing a profile of risk factors. Some of them are individual, such as diet, exercise and sleep. Others are more related to public health, such as air pollution and even noise pollution. “
“[W]These factors must be addressed throughout the life span […] – early diagnosis is essential. [W]and the need to detect problems early so that we can be more aggressive to promptly address the factors that could fuel the disease, even if they are cardiovascular risk factors, [i.e.,] be more aggressive in treating high blood pressure, hyperglycemia and high cholesterol. ”
“[T]The fact is that we have an aging population and, consequently, a growing burden of people who are significantly cognitively impaired […]. We need to start thinking about modifiable risk factors, from prenatal to end of life, [in order] prioritize brain health, regardless of particular pathophysiology.
For MNT, Keiland Cooper, Ph.D. (c), a neuroscientist in the Department of Neurobiology and Behavior at the University of California, Irvine, summarized the study:
“This paper fits into an ongoing discussion and evolving framework in the field of how to classify patients, perhaps galvanized by the recent prevalence and use of biomarkers. I find the paper’s perspective in this regard interesting and am excited to see further use of biomarker-based studies to distinguish or potentially find similarities between groups, especially on longitudinal time paths.