- Previously, experts considered a modest reduction in the results of clinical cognitive testing to be a predictor of future risk of progression to Alzheimer’s disease.
- Lower education, lower income and social exclusion contribute to lower performance of cognitive testing – which is called “cognitive weakness”.
- In the new study, despite lower test scores, cognitively impaired participants performed complex mental tasks at a similar level as healthy controls.
- Researchers at the University of Cambridge have concluded that clinical cognitive testing alone is not accurate in predicting the likelihood of an individual progressing to mild cognitive impairment (MCI) or Alzheimer’s disease.
Currently, more than 6 million people in the United States live with Alzheimer’s disease. It is estimated that this number will increase to more than 13 million by 2050.
Although deaths from heart disease decreased by 7.3%, those resulting from Alzheimer’s disease increased by 145.2%. In addition, the expected cost of public health related to Alzheimer’s disease could rise from current estimates of $ 355 billion a year to $ 1.1 trillion by 2050.
As for all the causes of dementia, an
Beta-amyloid protein hypothesis – tested and true?
Researchers were looking for meaningful treatments or a cure. However, only five drugs in the United States and four in the European Union have been approved for the treatment of Alzheimer’s disease since 1994.
These drugs are not curative, but they intervene in the disease process by reducing the symptoms or inflammation of brain cells. These drugs represent a lack of opportunity for people living with this condition.
The lack of attempts is not to blame for this lack of treatment options. Scientists and clinicians-researchers have attacked Alzheimer’s disease on several fronts.
Most research in past decades has been based on the “amyloid cascade hypothesis,” which refers to the significant presence of a protein called amyloid that first stimulates inflammation, disrupts neuronal function and ultimately contributes to message breakdown in the brain.
For Micro B life, Dr. Scott Kaiser, director of geriatric cognitive health for the Pacific Neuroscience Institute at Providence Saint John’s Health Center in Santa Monica, CA, developed:
“I doubt that these are multifactorial processes. Instead of saying that the amyloid hypothesis is true or not true, let’s start looking [it] as part of a broader, complex equation. [T]there are several factors here […]. Amyloid load is only one factor. There are some questions about how much amyloid accumulation is the cause, not just a byproduct, a marker. I think those are areas of research. ”
– Dr. Scott Kaiser
Dr. Kaiser added: “I expect the definitions of dementia and the various types of dementia and the various clinical syndromes surrounding dementia to change […] in the near future. They will continue to evolve. ”
A moment of ‘eureka’?
This fundamental scientific research led to the latest discovery in the treatment of Alzheimer’s disease: the development of anti-amyloid monoclonal antibodies to remove amyloid plaques that are known to interfere with brain communication.
Clinicians and scientists are increasingly embracing the approach of combination therapy in the treatment of Alzheimer’s disease, using symptomatic therapies that modify the disease.
In addition to drug therapy, scientists are also observing Alzheimer’s disease through a lifelong lens of individual and public health. Why do some people develop this condition and others do not? And, how do therapeutic possibilities improve, how to identify those 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 explore the root causes in their new study.
Findings appear in Journal of Neuroscience.
Is it a normal part of aging or a disease?
Clinical researchers are increasingly focused on accurately identifying those people who could be at risk of developing Alzheimer’s disease. One such group of individuals is those classified by the medical community as cognitively impaired – people who do not perform well on the cognitive testing they undergo as part of a comprehensive health evaluation.
On Monday, researchers at the Cambridge Center for Frontotemporal Dementia and Related Disorders revealed the results of their study comparing cognitively impaired people with those living with healthy cognition, MCI and Alzheimer’s disease.
The first author, Dr. Ece Kocagoncu, pointed out that the work of the team is unique in that “[t]the first took a multimodal, in-depth approach and tested the cognitively impaired using electroencephalograms (EEG), magnetoencephalograms (MEG) and magnetic resonance imaging (MRI).
With prof. With Rowe and other colleagues at the University of Cambridge, Dr. Kocagoncu first recruited participants using a large cross-sectional population from a study by the Cambridge Center for Aging and Neuroscience (Cam-CAN Frail project).
From this intensive study in the home community, the researchers identified people who underwent extensive cognitive testing and assigned them to categories.
By definition, cognitively impaired people are those who find cognitive testing difficult, but do not show any memory or learning deficiency that is clinically observed in MCI or late Alzheimer’s disease.
For MBL, Dr. Kocagoncu elaborated on the design of the study:
“To measure their neural activity,” she continued, “we used a special task we devised – called a crossmodal oddball task – in the scanner. This task is specifically designed to separate healthy people from patients with Alzheimer’s disease. ”
“It measures the ability to make connections between pieces of information (associative processing) and recognize new information (novelty processing), functions that are known to be impaired in Alzheimer’s disease.”
‘Surprising and encouraging’ results
The results were not predictable.
On EEG and MEG (neurophysiological tests), cognitively impaired individuals performed robustly — that is, as well as those without cognitive impairment. And, structurally, the brains of cognitively weak people were similar to the brains of individuals who were cognitively healthy.
The brains of cognitively weak individuals were clearly different from the brains of people with MCI or Alzheimer’s disease. What does that mean? Dr. Kocagoncu explained:
“Our results were surprising and really encouraging! We found that when we look closely at the structure of the brain and the neural function of the cognitively weak, they are like healthy older adults. They do not show volume loss in areas of the brain associated with Alzheimer’s pathology and do not show functional impairment in associative and new processing. ”
Cognitive weakness may be part of normal aging
In this way, Dr. Kocagonac and her colleagues from Cambridge proved that cognitive weakness is not a solid and rapid predictor of future MCI or Alzheimer’s disease.
So what does it mean to screen individuals in the community who may be in the ranks of the cognitively weak?
Scientists conclude that cognitive weakness may be in the spectrum of normal aging, not a precursor to Alzheimer’s disease.
Dr. Kocagoncu thought, “First, tests that are often used in clinics to help diagnose dementia – such as the Mini-Mental Status Examination (MMSE) – are unlikely to give 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 impairment could be the result of an accumulation of psychosocial, life and medical risk factors.”
“Factors such as malnutrition, social isolation, stress, depression, sedentary lifestyle, hearing / vision impairment, cardiovascular disease, chronic inflammation and lower levels of education are known to contribute to impaired cognitive function.”
– Dr. Kocagoncu
What is the significance of the study?
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 measures of proteins specific for Alzheimer’s disease – can further help identify people at risk for Alzheimer’s disease or in the early stages of Alzheimer’s disease.
Their lab plans to take a closer look at risk factors associated with cognitive impairment as well as protective factors associated with healthy cognitive aging.
Dr. Scott Kaiser concluded:
“We know that there are variable risk factors. By eliminating these risk factors, you can reduce your risk of dementia. [S]some of one-third of dementia cases could be completely prevented by addressing the risk profile. Some of them are individual, such as diet, exercise and sleep. Others are more about public health, such as air pollution and even noise pollution. ”
“[W]These factors need to be addressed throughout life […] – Early detection is critical. [W]We need to detect problems early so that we can be more aggressive in dealing early with factors that can trigger 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 older population and, as a result, an increasing burden of people who are significantly cognitively impaired […]. We need to start thinking about changing risk factors, from prenatal to the end of life, [in order] give priority to brain health, regardless of the specific pathophysiology. ”
For MBL, Keiland Cooper, Ph.D., a neuroscientist in the Department of Neurobiology and Behavior at the University of California, Irvine, summarized the study:
“This paper fits into the ongoing discussion and development framework within the field of how to categorize patients, perhaps driven by the recent prevalence and use of biomarkers. I find the perspective of the work interesting in this regard and I am excited to see the continued use of biomarker-based studies to potentially differentiate or find similarities between groups, especially during longitudinal time courses. ”