MRI/PET scans reveal racial disparities in Alzheimer’s disease biomarkers

Racial differences in Alzheimer’s disease biomarkers may point to possible race-dependent biological mechanisms that contribute to how the disease is expressed, according to research published online Jan. 7 in JAMA Neurology.  

The findings suggest the evaluation of molecular biomarkers for Alzheimer’s disease should be adjusted for race, as African American patients were found to have lower levels of tau—a key biomarker used to identify the disease, according to John C. Morris, MD, of the Knight Alzheimer Disease Research Center (ADRC) at the Washington University School of Medicine in St. Louis, Missouri, and colleagues.  

A total of 1,255 participants (56 percent women, 14 percent African American, average age 71 years) were recruited and completed brain MRI or PET scans from January 1, 2004 through December 31, 2015.  

The scans were completed with Pittsburgh compound B (radioligand for aggregated amyloid-β) and/or CSF assays for the concentrations of amyloid-β42, total tau (t-tau) and phosphorylated tau (p-tau) 181, according to the researchers.    

From April 22, 2016 to August 27, 2018, independent cross-sectional analyses were blindly conducted for each biomarker modality and accompanied by an analysis of variance or covariance, including sex, educational level, race, apolipoprotein E (APOE) ε4 allele status and clinical status (normal cognition or dementia).  

Researchers found that for individuals with a reported family history of dementia, average total hippocampal volumes were lower for African American participants than their white counterparts. African American participants also had lower average CSF concentrations of t-tau and p-tau 181 than white participants, but there were non-racial differences in amyloid burden.  

Additionally, the lower levels of both t-tau and p-tau 181 among African American individuals were seen only in those with an APOE ε4 allele, the researchers noted.  

The lower CSF concentrations of t-tau and p-tau 181 in African American individuals suggest a different effect of Alzheimer’s risk variant as compared with white individuals.  

Furthermore, the researchers explained that normal and abnormal values of the biomarkers must be adjusted to factors in association with race—such as socioeconomic disparities, psychosocial factors and comorbid diseases like cardiovascular disease—when African Americans are considered for the framework's amyloid/tau/neurodegeneration (A/T/N) classification scheme for Alzheimer's disease.  

“Understanding how race may modify the risk and expression of Alzheimer’s disease may yield new insights into race-dependent biological mechanisms that in turn can inform future diagnostic and therapeutic advances,” the researchers concluded.  

In an accompanying editorial, Lisa L. Barnes, PhD, of the Rush Alzheimer’s Disease Center at Rush University Medical Center in Chicago, called the study and ensuring appropriate representation of minority populations in Alzheimer's research “a public health priority."

She also touched on the difficulty in recruiting African American participants for such invasive studies, but explained that not properly representing minority populations in Alzheimer's disease research will only impede any progress made in the field regarding new insight and treatment options.  

“Inclusion of African American individuals and other minority populations in biomarker studies is challenging, even for research centers that do this work well,” Barnes wrote. “But as the field moves toward a biological definition of Alzheimer’s disease, the under inclusion of minority populations in Alzheimer’s disease research will significantly hinder our progress as a field and the race to end Alzheimer’s disease will not be shared with our most vulnerable, at-risk populations.”