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Dementia resistance may be hereditary, linked to protein
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Relatives of those who were free of dementia and had high levels of C-reactive protein were relatively likely to remain free of dementia themselves, according to study results published in Neurology.
C-reactive protein (CRP) is a biomarker for cardiovascular risk factors and systemic inflammation and has been associated with worse cognition in the earlier stages of old age.
“Thus, for very old people who remain cognitively healthy, those with a high protein level may be more resistant to dementia,” study researcher Jeremy M. Silverman, PhD, of the Mount Sinai School of Medicine in New York, said in a press release. “Our study shows that this protection may be passed on to immediate relatives.”
Silverman and colleagues identified 277 cognitively healthy male veterans aged at least 75 years who provided blood samples to measure CRP levels.
The researchers interviewed the veterans about 1,329 parents and siblings to determine whether the veterans’ relatives had dementia, which was identified in 40 relatives from 37 families. A second group of 51 community-dwelling men and women aged 85 years or older with no dementia symptoms were interviewed about 202 of their relatives, nine of whom were identified with dementia.
Silverman and colleagues found that higher levels of CRP were strongly associated with lower risk for dementia in relatives (HR=0.55; 95% CI, 0.41-0.74). The second sample exhibited a similar association, but even stronger in magnitude (HR=0.15; 95% CI, 0.06-0.37).
“Relatives of successful cognitive aging individuals with high levels of CRP are relatively likely to remain free of dementia,” the researchers wrote. “High CRP in successful cognitive aging individuals may constitute a phenotype for familial — and thus possibly genetic — successful cognitive aging.”
Disclosure: The researchers report no relevant financial disclosures.
Perspective
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Robert Zimmerman, MD, FACR
In this paper, the authors identified a relationship between high levels of C-reactive protein (an inflammatory and cardiovascular risk factor marker) and high levels of cognitive function in individuals aged older than 75 years. As more and more genomic and/or proteomic markers for degenerative disease are discovered, the relationship between these markers and imaging studies of dementia represents a fertile area for interdisciplinary translational research. Routine structural imaging in demented or mildly impaired elderly patients typically yields non-specific results that provide little if any prognostic information. Sophisticated MRI techniques such as morphometry, spectroscopy, diffusion tensor imaging, functional MRI and perfusion imaging have revealed findings that allow more precise identification of abnormalities in patients with a variety of neurodegenerative conditions, including Alzheimer’s disease. However, variations exist between individual patients that make broad application of advanced imaging findings to specific patients problematic. By combining imaging with genomic/proteomic information, it should be possible to more accurately characterize differences between groups of patients and eventually to provide information about treatment and prognosis in individual patients.
My father suffered from Alzheimer’s disease. He had a slow but inexorable decline that lasted more than 15 years. Watching him change (it seemed like in slow motion) was one of the most painful experiences of my life. He had several imaging studies early in the course of his disease that were completely non-specific. I have always asked myself why his disease took the course that it did. Within the disease designation of Alzheimer’s disease, are there different subtypes that might explain differences in clinical manifestations and disease course? Could knowledge of these different disease types (assuming they exist) allow better prognostic information and at some point targeted therapies? Developing a profile of biologic and imaging markers could aid enormously in this endeavor.
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