Diseased blood vessels in the brain itself may contribute more significantly to Alzheimer’s disease dementia than was previously believed, according to new study results published in The Lancet Neurology.
“Cerebral vessel pathology might be an under-recognised risk factor for Alzheimer’s disease dementia,” the researchers write.
The study—by researchers from the Rush Alzheimer’s Disease Center (Chicago, USA)—analysed medical and pathological data on 1,143 older individuals who had donated their brains for research upon their deaths, including 478 (42%) with Alzheimer’s disease dementia. Analyses of the brains showed that 445 (39%) of study participants had moderate to severe atherosclerosis—plaques in the larger arteries at the base of the brain obstructing blood flow — and 401 (35%) had brain arteriolosclerosis.
The study found that the worse the brain vessel diseases, the higher the chance of having dementia, which is usually attributed to Alzheimer’s disease. The increase was 20% to 30% for each level of worsening severity. The study also found that atherosclerosis and arteriolosclerosis are associated with lower levels of cognitive ability—associations that were present in persons with and without dementia.
“Both large and small vessel diseases have effects on dementia and thinking abilities, independently of one another, and independently of the common causes of dementia such as Alzheimer’s pathology and strokes,” says Zoe Arvanitakis. A neurologist and researcher at the Rush Alzheimer’s Disease Center, Arvanitakis led the study, which was funded by the US National Institutes of Health.
The study was not designed to determine causation of Alzheimer’s dementia, or even whether vascular disease or Alzheimer’s developed first; “but, it does suggest that vessel disease plays a role in dementia,” Arvanitakis says. “We found that blood vessel diseases are very common in the brain, and are associated with dementia that is typically attributed to Alzheimer’s disease during life.”
The study examined which cognitive difficulties are caused by vessel diseases and whether vessel disease and Alzheimer’s are more destructive in tandem than they would be alone. An editorial in The Lancet Neurology that accompanied the study findings noted that while other studies have indicated that proactive measures like eating a selective diet and getting regular exercise might protect people against getting Alzheimer’s, those interventions might actually be acting on non-Alzheimer’s disease processes, such as cerebrovascular disease.
Arvanitakis says that they do not know yet. “They may decrease actual Alzheimer’s, and possibly even work by yet other pathways,” Arvanitakis says. “We hope to better distinguish how the clinical expression of vessel diseases in the brain differ from those of Alzheimer’s, so that we may eventually use earlier and more targeted treatments for dementia.”