Lipid Metabolism in Late-Onset Alzheimer’s Disease Differs from Patients Presenting with Other Dementia Phenotypes

Syena Sarrafpour, Cora Ormseth, Abby Chiang, Xianghong Arakaki, Michael Harrington and Alfred Fonteh
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Syena Sarrafpour: Huntington Medical Research Institutes, Pasadena, CA 91105, USA
Cora Ormseth: Huntington Medical Research Institutes, Pasadena, CA 91105, USA
Abby Chiang: Huntington Medical Research Institutes, Pasadena, CA 91105, USA
Xianghong Arakaki: Huntington Medical Research Institutes, Pasadena, CA 91105, USA
Michael Harrington: Huntington Medical Research Institutes, Pasadena, CA 91105, USA
Alfred Fonteh: Huntington Medical Research Institutes, Pasadena, CA 91105, USA

IJERPH, 2019, vol. 16, issue 11, 1-15

Abstract: Abnormal cerebrospinal fluid (CSF) levels of β-amyloid peptides (Aβ 42 ) and Tau and cognitive decline are typical characteristics of Alzheimer’s disease (AD). Since dysregulation in lipid metabolism accompanies abnormal amyloid formation, we quantified glycerophospholipids (GP) and sphingolipids (SP) in CSF fractions from participants with late-onset AD (LOAD, n = 29) or with Other Dementia (OD, n = 10) to determine if alterations in lipid metabolism account for pathological differences. Aβ 42 and total Tau levels were determined using a sandwich ELISA. Liposomal-based fluorescent assays were used to measure phospholipase A 2 (PLA 2 ) and acid or neutral sphingomyelinase (aSMase, nSMase) activities. Supernatant fluid (SF) and nanoparticle (NP) lipids were quantified using LC-MS/MS. Although CSF Aβ 42 and Tau levels are similar, phosphatidylserine (PS) in SF and ceramide (CM) levels in NP are significantly higher in OD compared with LOAD. The aSMase but not the nSMase activity is higher in OD. PLA 2 activity in CSF from OD subjects positively correlates with several GP classes in SF and NP fractions but not in LOAD fractions. Our data indicate differences in CSF lipid metabolism between dementia variants. Higher levels of inflammatory and apoptotic lipids may induce faster neuronal death, resulting in the earlier cognitive decline in patients with OD phenotypes.

Keywords: amyloid; ceramide; cerebrospinal fluid; late-onset Alzheimer’s disease; lysophosphatidylcholine; other dementia; phosphatidylserine; phospholipase A 2; sphingomyelinase; Tau proteins (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2019
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