One implication of the study results is that preventing formation of thrombogenic microvesicles may reduce the burden of WMH, which have been associated with memory loss and the risk of stroke.
The blood of healthy postmenopausal women may offer signs of increased risk of small areas of brain damage, dubbed white matter hyperintensities (WMH), which have been linked to memory loss, researchers reported.
In a prospective observational study, women who began with higher levels of thrombogenic microvesicles were more likely to have greater volumes of WMH 4 years later, according to Kejal Kantarci, MD, of the Mayo Clinic in Minneapolis, and colleagues.
One implication is that preventing formation of thrombogenic microvesicles may reduce the burden of WMH, which have been associated with memory loss and the risk of stroke, Kantarci and colleagues argued in the Feb. 13 issue of Neurology.
Thrombogenic microvesicles are shed by activated platelets, the researchers noted, and may affect the brain’s microstructure along with conventional risk factors such as hypertension, age, and smoking.
“This study suggests that these microvesicles in the blood may contribute to the development of white matter hyperintensities in women who have recently gone through menopause,” Kantarci said in a statement.
“Preventing the platelets from developing these microvesicles could be a way to stop the progression of white matter hyperintensities in the brain,” she added.
Because most studies examining the effects of WMH have been conducted in older and mainly male groups, Kantarci and colleagues analyzed members of a cohort of recently menopausal women enrolled in a randomized trial of hormone therapy to slow the progression of atherosclerosis.
Women taking part in the main study were asked to take part in the substudy, in which MRI was used to measure changes in WMH before randomization and at 18, 36, and 48 months afterward.
At baseline, the researchers measured conventional cardiovascular risk factors, carotid intima-media thickness, coronary arterial calcification, plasma lipids, markers of platelet activation, and numbers of thrombogenic microvesicles.
They correlated those with changes in WMH volume, adjusting for age, months past menopause, and whether or not participants had the APOE e4 gene, which is associated with Alzheimer’s risk.
All told, 95 women (average age 53) were included in the analysis. All had at least some WMH at baseline, with an average of 0.88% of the total white matter volume, Kantarci and colleagues reported.
On average, the volume of WMH rose by 63 mm3 at 18 months, 122 mm3 at 36 months, and 155 mm3 at 48 months, but only the 36- and 48-month levels were significantly different from baseline, Kantarci and colleagues found.
Nevertheless, the 36- and 48-month levels were significantly correlated (P=0.03) with the numbers of platelet-derived and total thrombogenic microvesicles observed at baseline, although not with most other measured risk factors.
“Neither smoking status nor the history of medication-controlled migraines modified the WMH load and longitudinal change in WMH volume at the specified time points (P>0.05),” the authors explained.
The associations “suggest that in vivo platelet activation may contribute to a cascade of events leading to development of WMH in recently menopausal women,” the researchers concluded.
But they cautioned that there might be several unexamined mechanisms, such as genetic variation, underlying the progression of WMH. They also noted that the study population consists of healthy, well-educated and mostly nonsmoking women, so the results may not reflect the general postmenopausal population.
By Michael Smith
