Epidemiology has played a crucial role over the decades in understanding Alzheimer’s Disease and other common causes of dementia, like vascular disease and Lewy body disease. Yet, there are still more questions than answers about the causes, appropriate treatment, and preventive measures for dementia-related diseases.
The World Health Organization estimates 50 million people are affected by dementia worldwide, and nearly 10 million new cases are diagnosed each year. Progress in the field of dementia epidemiology is critical.
According to a group of international researchers led by Dr. Mary Ganguli from the University of Pittsburgh, an interdisciplinary population-focused approach to this public health issue is needed to push scientific discovery forward.
In a special submission piece published in the January issue of the Alzheimer’s Disease and Associated Disorders, the researchers propose reframing the current study of dementia epidemiology toward a more inclusive and perhaps more commonly understandable term: “population neuroscience.” This broader term would better reflect the multidisciplinary collaboration needed to effectively address these diseases and would also serve as a segue toward precision medicine and population health.
The paper outlines how population neuroscience would put epidemiological population studies at the heart of neuroscience in order to study the “full range of brain disease, risk factors, genomics and underlying biological pathways as they present in the population at large.”
As some breakthroughs continue to challenge our knowledge of dementia and related illnesses, researchers have also discovered some setbacks. For example, AD is likely begin in the brain 10 to 25 years prior to any dementia symptoms, thus the data collected in clinical settings on persons who already have dementia symptoms can oftentimes lead to comparisons with persons who harbor disease but have not yet developed symptoms. This could cause researchers to miss important risk factors. Further, limiting studies to clinic settings or solicited volunteers may fail to reflect how these diseases commonly co-occur in the population, as well as how they may act synergistically, antagonistically or independently to cause dementia in the population as a whole.
“We’ve come to a point where we really have to turn our eyes out toward the general population, so we can figure out how to address this issue and know we aren’t just dealing with very odd cases in clinical settings,” said co-author Walter Kukull, a professor of epidemiology at the University of Washington’s School of Public Health.
Population neuroscience describes a multidisciplinary collaborative effort to study the causes of dementia through multiple approaches, some harnessing recent advances in technology. For example, establishing large longitudinal population-based cohort studies beginning with unaffected persons could potentially take advantage of new technologies to identify disease processes well before any cognitive symptoms appear, and increase our understanding of how the underlying diseases may be able to be treated, ultimately preventing dementia symptoms. Data mined from Electronic Health Records could help build a database, similar to the National Program of Cancer Registries, to facilitate future research studies. Expansion of bioinformatics and other “-omics” to the population level would also help identify potential risk factors and undetected early stages in the disease.
Other approaches in population neuroscience include exploring the links between disease patterns and the environment, looking at specific generational risk factors (such as sleep disturbances, work stress, etc.), and observing the effectiveness of interventions among different races and ethnicities.
Each approach would help paint a fuller picture of dementia while taking into account the disease biology, personal and environmental factors, and social determinants of health at the community level.
“Alzheimer’s disease occurs together with a background of other brain diseases that cause dementia, and we don’t always realize it’s happening at the same time,” said Kukull. “This is one reason why we need to move to a population-based setting to better understand how the etiologic causes of dementia might interact.”
Authors to this article include: Drs. Mary Ganguli (University of Pittsburgh), Emiliano Albanese (University of Geneva, Switzerland), Sudha Seshadri (Boston University), David A. Bennett (Rush University Medical Center), Constantine Lyketsos (Johns Hopkins University), Walter Kukull (University of Washington), Ingmar Skoog (Gothenburg University, Sweden), and Hugh Hendrie (Indiana University Center for Aging Research).
This paper was supported in part by grants from the National Institute of Aging of the National Institutes of Health (K07AG044395; U01AG016976; P30AG10133; R01AG045350; P50AG005146; R01AG054076; P30AG10161, and R01AG17917), and from Vetenskapsrådet, Sweden (2015-02830).