MRI Shows No Difference in Alzheimer’s Biomarkers in Patients Treated for Hypertension


Patients receiving standard therapy and intensive therapy for high blood pressure revealed no significant biomarker differences for Alzheimer’s disease on brain images.

There are no significant differences between the biomarkers for Alzheimer’s disease seen on the brain MRI scans of patients who are either on standard therapy or intensive blood pressure therapy, according to new study results.

In a study published March 8 in JAMA Neurology, a team of investigators from the University of Pennsylvania assessed brain MRI scans of these two groups of patients with hypertension. At comparison, they found nothing notable.

“There is no consistent or clinically meaningful difference in magnetic resonance imaging biomarkers of Alzheimer’s disease between intensive and standard blood pressure treatment,” wrote the team led by Ilya Nasrallah, M.D., Ph.D., assistant professor of radiology at the Hospital of the University of Pennsylvania.

Specifically, the team examined brain MRI scans from 454 patients with high blood pressure who were at least 50 years old. Participants underwent a baseline MRI with a follow-up scan in July 2016. Using the scans, the team compared changes in hippocampal volume, measures of Alzheimer’s disease regional atrophy, posterior cingulate cerebral blood flow, and mean fractional anisotropy in the cingulum bundle.

According to existing literature, treating high blood pressure can play a role in lowering the incidence of Alzheimer’s disease as vascular disease might be part of kick-starting two biomarkers for the condition – hippocampal atrophy or mild cognitive impairment. However, no clear mechanism has been identified to date.

At the outset of this study, Nasrallah’s team postulated the MRI scans would show less change in hippocampal volume and Alzheimer’s regional cortical thickness, signifying less atrophy. In addition, they said they anticipated an increase in posterior cingulate gyrus perfusion, as well as a decline in fractional anisotropy in the cingulum bundle.

For this study, investigators enrolled 454 participants who completed both MRI baseline scans that measured total brain volume, as well as follow-up studies. Average age at baseline was roughly 67 years, and approximately 40 percent of the group were women. Blood pressure was 138.1/77.9 mmHg, on average.

Based on their analysis, the team saw little difference between the treatment groups when it came to changes in hippocampal volume. The intensive treatment group experienced a decrease from 7.45 cm3 to 7.39 cm3 while the group receiving standard therapy saw a reduction from 7.48 cm3 to 7.46 cm3. They also saw no indications of differences for other neurodegeneration markers that are generally considered to be signs of Alzheimer’s advancement.

The team did note several limitations to their study in addition to the difficulty of even identifying early changes in Alzheimer’s disease. The four-year follow-up time frame may not have been long enough, they said, as Alzheimer’s is a particularly slow-developing disease.

But, changes are coming to, hopefully, facilitate research that can produce more disease-modifying treatments. This will be particularly important because recent clinical trial investigations for new drug therapies have come up relatively empty-handed, said Susan Landau, Ph.D., associate research scientist, and Theresa Harrison, Ph.D., post-doctoral fellow, both of the Helen Wills Neuroscience Institute at the University of California at Berkeley.

In an accompanying editorial, they outlined two new strategies that could potentially help investigators identify the underlying pathophysiology for Alzheimer’s. First, interventions are being launched earlier to pinpoint targets other than abnormal amyloid and tau proteins for individual who are at-risk but, yet, unaffected. Second, large, multi-site, longitudinal clinical trials will still be integral as their results could succeed where epidemiological data has not – they could unearth a causal link between high blood pressure and the brain, Landau and Harrison said.

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