Blood lipids promising identifiers of Alzheimer’s disease

Latest research form UNSW Sydney’s Centre for Healthy Brain Ageing (CHeBA) reveals new insight into the underlying mechanisms of Alzheimer’s disease.

Published in Translational Psychiatry, the study looked at the differences between the plasma lipidome of people with Alzheimer’s disease and compared that to the plasma lipidome of ‘healthy’ individuals.

Participants were from CHeBA’s Sydney Memory and Ageing Study and were aged between 75 and 97 years.

According to senior author and leader of CHeBA’s Brain Ageing Research Laboratory Dr Nady Braidy, blood lipids are emerging as promising identifiers of Alzheimer’s disease.

“Although there have been numerous studies on the association between lipids and the biological pathology of Alzheimer’s disease, few studies have look at the plasma lipidome,” says Dr Braidy.

“This research looked to determine whether lipid profiles are associated with genetic risk of Alzheimer’s disease.”

Reportedly, the benefit of lipidomics in biomarker research is that it simultaneously identifies and quantifies hundreds of lipids, acting as a powerful tool for mapping global biochemical changes in disease and treatment.

However, the separation of the brain from the periphery is a major challenge when examining the biological significance of plasma lipids in Alzheimer’s disease, since not all lipids can be transported across the blood-brain barrier.

“This separation may likely be compromised by age-related changes in the blood brain barrier, affecting lipid and amyloid beta – the main component of the amyloid plaques found in the brains of people with Alzheimer’s disease,” says Dr Braidy.

The research team developed a classification model, using plasma cholesterol esters, sphingomyelin and triglycerides, to discriminate Alzheimer’s disease from controls with 80% accuracy.

The study also highlighted that genes related to Alzheimer’s disease play a role in influencing lipids that are associated with Alzheimer’s disease, reinforcing the consequence of physiological factors, such as inflammation, on brain ageing.

“The results in the cellular lipidome support findings that certain genes play a contributory if not causal role in bringing about changes in lipid profiles of people with Alzheimer’s disease,” continues Dr Braidy.

Co-Director of CHeBA and co-author Professor Perminder Sachdev says “quantifying these plasma lipids using mass spectrometry provides renewed insight in the underlying mechanisms of Alzheimer’s disease”.

“It also directs us to additional drug targets and may have prognostic benefits in the clinic. It is possible that new nutritional interventions can be developed,” he says.

For more information and to read the study, visit: nature.com/articles/s41398-021-01362-2