Concepedia

Publication | Closed Access

Fatty acid composition of brain phospholipids in aging and in Alzheimer’s disease

660

Citations

20

References

1991

Year

TLDR

It is unclear whether the observed fatty‑acid changes are specific to Alzheimer’s disease, but alterations in the saturated/polyunsaturated ratio could affect cellular function and contribute to neural deficits. The study examined phosphatidylethanolamine and phosphatidylcholine fatty‑acid composition in frontal gray and white matter, hippocampus, and pons. The fatty‑acid profiles of PE and PC were region‑specific, with PC dominated by saturated and 18:1 fatty acids and PE rich in polyunsaturated species; aging did not alter these patterns, but in Alzheimer’s disease PE was altered across all regions, showing increased saturated fatty acids and decreased polyunsaturated fatty acids while 18:1 remained unchanged, indicating that AD is not simply an accelerated aging process.

Abstract

The two major phospholipid classes, namely, phosphatidylethanolamines (PE) and phosphatidylcholines (PC), were studied in four different regions of human brain, i.e., in frontal gray matter, frontal white matter, hippocampus and in pons. The fatty acid (FA) compositions of these phospholipids were found to be specific for the different regions. PC contains mostly saturated and 18:1 FA, while PE is rich in polyunsaturated FA. Aging has no influence on the FA compositions, while in Alzheimer's disease (AD) PE is modified in all four regions, particularly in frontal gray matter and in hippocampus. The abundance of the major monounsaturated FA of PE, 18:1, is not significantly altered in Alzheimer's disease, but there is a substantial increase in the relative amounts of the saturated components 14:0, 16:0 and 18:0. This is paralleled by a decrease in the polyunsaturated FA 20:4, 22:4 and 22:6. It is not clear whether the changes observed are specific for AD. Changes in saturated/polyunsaturated FA ratio are likely to influence cellular function, which in turn may cause certain neural deficiencies. The findings do not support the hypothesis that AD reflects an accelerated aging process.

References

YearCitations

Page 1