AI Article Synopsis
- The study investigates how saturated, monounsaturated, and polyunsaturated fatty acids are metabolized differently in Alzheimer's disease compared to cognitively healthy individuals and those with mild cognitive impairment, highlighting a potential link between fat metabolism and the disease.
- Gas chromatography-mass spectrometry was used to analyze fatty acid levels in cerebrospinal fluid fractions, revealing that levels of certain fatty acids like docosahexaenoic acid (DHA) are lower in Alzheimer's patients, while some other fatty acids were found in higher concentrations in those with Alzheimer’s.
- The findings suggest that altered fatty acid levels and metabolism may play a crucial role in Alzheimer's pathology, indicating possible biomarkers for the disease and shedding light on the dysfunction of
Article Abstract
Background: Although saturated (SAFA), monounsaturated (MUFA), and polyunsaturated (PUFA) fatty acids are important structural components of neuronal membranes and precursors of signaling molecules, knowledge of their metabolism in Alzheimer's disease (AD) is limited. Based on recent discovery that lipids in cerebrospinal fluid (CSF) are distributed in both brain-derived nanoparticles (NP) and supernatant fluid (SF), we hypothesized that fatty acid (FA) abundance and distribution into these compartments is altered in early AD pathology.
Methodology And Findings: We assayed the FA composition and abundance in CSF fractions from cognitively healthy (CH), mild cognitive impairment (MCI), and AD study participants using gas chromatography-mass spectrometry. In the SF fraction, concentration of docosahexaenoic acid [DHA, (C22:6n-3)] was less in AD compared with CH, while alpha linolenic acid [α-LNA, (C18:3n-3)] was lower in MCI compared with CH. In the NP fraction, levels of SAFAs (C15:0, C16:0) and a MUFA (C15:1) differentiated CH from MCI, while two MUFAs (C15:1, C19:1) and four PUFAs (C20:2n-6, C20:3n-3, C22:4n-6, C22:5n-3) were higher in AD compared with CH. Levels of even-chain free SAFA and total free FA levels were higher in AD, levels of odd-chain free SAFAs, MUFAs, n-3 PUFAs, and total PUFA, were lower in AD compared with CH. Free n-6 PUFA levels were similar in all three groups.
Conclusions And Significance: FA metabolism is compartmentalized differently in NP versus SF fractions of CSF, and altered FA levels reflect the importance of abnormal metabolism and oxidative pathways in AD. Depleted DHA in CSF fractions in AD is consistent with the importance of n-3 PUFAs in cognitive function, and suggests that disturbed PUFA metabolism contributes to AD pathology. This study of FA levels in CSF fractions from different cognitive stages shows potential AD biomarkers, and provides further insight into cell membrane dysfunctions, including mechanisms leading to amyloid production.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4067345 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0100519 | PLOS |
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