Racial Disparities Found in Alzheimer Disease Biomarkers


Investigators decipher the differences along racial lines for cerebrospinal fluid amyloid, tau biomarkers and associated cutoffs for patients with mild cognitive impairment.

Stephanie Garrett, MD

Stephanie Garrett, MD

Race may play a key role when interpreting cerebrospinal fluid (CSF) biomarkers, while the ratio of phosphorylated tau 181 to β-amyloid 1-42 may have less racial differences than other biomarkers.

A team, led by Stephanie L. Garrett, MD, Division of General Medicine and Geriatrics, Department of Medicine, Wesley Woods Health Center, Emory University School of Medicine, compared cerebrospinal fluid biomarkers in African American and white patients with normal cognition and mild cognitive impairment (MCI) to estimate race-based cutoffs that maximize diagnostic discrimination between normal cognition and MCI.

“This study found that African American individuals had lower levels of tau-based biomarkers that were not likely explained by the degree of disease stage or neurodegeneration reflected by hippocampal volumes,” the authors wrote. “This study suggests that race is an important factor when interpreting CSF biomarkers, especially in the clinical diagnosis of prodromal [Alzheimer disease] AD.”

The investigators believe that using the pTau181 to Aβ1-42 ratio may ameliorate these differences.

In the case-control study involving 362 patients at least 50 years old, the investigators studied the link between demographic characteristics, cognitive performance, and common vascular risk factors. The study included patients who participated in the Brain Stress Hypertension and Aging Research Program cohort undergoing baseline assessment.

The investigators found that African American patients with mild cognitive impairment had lower biomarker levels than the white participants with mild cognitive impairment, after they adjusted for demographic characteristics.

After the investigators adjusted for demographic characteristics and cognitive performance, lower mean levels were found in African American vs white individuals with MCI for tau (52.40 [5.90] vs 78.98 [5.02] pg/mL; P = .001) and pTau181 (15.42 [2.06] vs 25.24 [1.75] pg/mL; P = .001).

They also found a lower pTau181 to Aβ1-42 ratio (0.07 [0.02] vs 0.14 [0.01]; P = .003).

“There were no racial differences in the normal cognition group or in hippocampal volumes in the MCI group,” the authors wrote.

African Americans also had higher levels of β-amyloid 1-42, which were not significant after adjusting for demographic characteristics and cognitive performance. Diagnostic discrimination cutoffs were higher for β-amyloid 1-42 and lower for tau biomarkers in African American participants, except for the ratio of phosphorylated tau 181 to β-amyloid 1-42.

Cutoffs for cerebrospinal fluid biomarkers were higher for Aβ1-42 in African American compared to white individuals (208 [95% CI, 126-321] vs 197 [95% CI, 183-245] pg/mL) and lower for tau (51 [95% CI, 31-59] vs 59 [95% CI, 56-92] pg/mL) and pTau181 (12 [95% CI, 12-19] vs 20 [95% CI, 12-27] pg/mL) levels.

Overall, African Americans have an increased risk of developing Alzheimer disease compared to white patients. Previous evidence shows that racial differences exist in tau biomarkers in mild cognitive impairment and Alzheimer disease.

The study, “Racial Disparity in Cerebrospinal Fluid Amyloid and Tau Biomarkers and Associated Cutoffs for Mild Cognitive Impairment,” was published online in JAMA Network Open.

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