Researchers Discover Lipid Link in Inherited Form of Alzheimer’s

Australian researchers have found biochemical changes occurring in the blood, in the rare inherited form of Alzheimer’s disease. Changes in these fat-like substances, may suggest a method to diagnose all forms of Alzheimer’s disease before significant damage to the brain occurs.

In an article published today in the Journal of Alzheimer’s Disease, the Australian team led by Professor Ralph Martins from the CRC for Mental Health and Edith Cowan University, examined the lipid profiles of 20 people who carry a mutation responsible for the rare inherited form of Alzheimer’s, known as familial Alzheimer’s disease.

Using samples from the Dominantly Inherited Alzheimer Network (DIAN) study, the researchers found that people who carried the mutation responsible for this form of Alzheimer’s also had altered levels of specific lipids in their blood plasma compared to the control group. This pilot study, combined with previously published studies on lipids in the most common form of Alzheimer’s disease, suggests that that specific changes in lipid metabolism may be used as a predictive test for Alzheimer’s disease.

Image shows a brain slice from an Alzheimer's patient.
At present, the most common, sporadic form of Alzheimer’s disease is difficult to diagnose until symptoms are readily apparent and significant damage to the brain has occurred. Image is for illustrative purposes only.

At present, the most common, sporadic form of Alzheimer’s disease is difficult to diagnose until symptoms are readily apparent and significant damage to the brain has occurred; findings from this study may provide clues to suitable diagnostic markers. While the results are exciting, the researchers involved urge caution due to the pilot nature of the study.

About this Alzheimer’s disease research

Source: Melanie Carew – IOS Press
Image Source: The image is in the public domain
Original Research: Abstract for “Plasma Phospholipid and Sphingolipid Alterations in Presenilin1 Mutation Carriers: A Pilot Study” by Chatterjee, Pratishtha; Lim, Wei L.F.; Shui, Guanghou; Gupta, Veer B.; James, Ian; Fagan, Anne M.; Xiong, Chengjie; Sohrabi, Hamid R.; Taddei, Kevin; Brown, Belinda M.; Benzinger, Tammie; Masters, Colin; Snowden, Stuart G.; Wenk, Marcus R.; Bateman, Randall J.; Morris, John C.; and Martins, Ralph N. in Journal of Alzheimer’s Disease. Published online February 2 2016 doi:10.3233/JAD-150948


Abstract

Plasma Phospholipid and Sphingolipid Alterations in Presenilin1 Mutation Carriers: A Pilot Study

Background and Objective: Aberrant lipid metabolism has been implicated in sporadic Alzheimer’s disease (AD). The current study investigated plasma phospholipid and sphingolipid profiles in individuals carrying PSEN1 mutations responsible for autosomal dominant AD (ADAD).

Methods: Study participants evaluated were from the Perth and Melbourne sites of the Dominantly Inherited Alzheimer Network (DIAN) study. Plasma phospholipid and sphingolipid profiles were measured using liquid chromatography coupled with mass spectrometry in 20 PSEN1 mutation carriers (MC; eight of whom were symptomatic and twelve asymptomatic, based on Clinical Dementia Rating scores) and compared with six non carriers (NC) using linear mixed models. Further, AD gold standard biomarker data obtained from the DIAN database were correlated with lipid species significantly altered between MC and NC, using Spearman’s correlation coefficient.

Results: One-hundred and thirty-nine plasma phospholipid and sphingolipid species were measured. Significantly altered species in MC compared to NC primarily belonged to choline and ethanolamine containing phospholipid classes and ceramides. Further phosphatidylcholine species (34:6, 36:5, 40:6) correlated with cerebrospinal fluid tau (p <  0.05), and plasmalogen ethanolamine species (34:2, 36:,4) correlated with both cerebrospinal fluid tau and brain amyloid load within the MC group (p <  0.05).

Conclusion: These findings indicate altered phospholipid and sphingolipid metabolism in ADAD and provide insight into the pathomolecular changes occurring with ADAD pathogenesis. Further, findings reported in this study allow comparison of lipid alterations in ADAD with those reported previously in sporadic AD. The findings observed in the current pilot study warrant validation in the larger DIAN cohort.

“Plasma Phospholipid and Sphingolipid Alterations in Presenilin1 Mutation Carriers: A Pilot Study” by Chatterjee, Pratishtha; Lim, Wei L.F.; Shui, Guanghou; Gupta, Veer B.; James, Ian; Fagan, Anne M.; Xiong, Chengjie; Sohrabi, Hamid R.; Taddei, Kevin; Brown, Belinda M.; Benzinger, Tammie; Masters, Colin; Snowden, Stuart G.; Wenk, Marcus R.; Bateman, Randall J.; Morris, John C.; and Martins, Ralph N. in Journal of Alzheimer’s Disease. Published online February 2 2016 doi:10.3233/JAD-150948

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