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September 16-17, 2019 | Paris, France

Dementia and Alzheimer's Disease

13

th

World Congress on

Journal of Clinical Psychiatry and Cognitive Psychology | Volume: 03

Lipid oxidation and Carotenoid supplementation

Stella Ademowo, Irundika Dias

1

, Silke De Spirt

2

, Wilhelm Stahl

2

, Helen R Griffiths

3

University of Cambridge, UK;

1

Aston University Birmingham, UK;

2

Heinrich-Heine-Universität Düsseldorf, Germany;

3

University of Surrey, UK

O

xidative stress has been considered as important in

the pathogenesis of Alzheimer’s disease, AD. Post-

mortem investigations of affected brain regions in AD

have shown the accumulation of oxidative damage to

protein, DNA and lipids. Carotenoids have the ability to

quench singlet oxygen and scavenge other reactive oxygen

species (ROS) without being consumed in the process. We

have previously shown increased concentrations of the

novel oxidized phospholipid biomarker, 1-palmitoyl-2(5-

oxo-valeroyl)-sn-glycero-3-phosphocholine (POVPC) and

lower carotenoid plasma concentrations in AD. POVPC

was analysed using electrospray ionisation tandem mass

spectrometry (MS) with multiple reaction monitoring

(MRM), 8-isoprostane (IsoP) was measured by ELISA and

ferric reducing antioxidant potential (FRAP) was measured

by a colorimetric assay in AD patients and healthy age-

matched control subjects. The developed MRM-MS

method was used to analyse POVPC as a measure of

peroxidative damage to phospholipids in serum. Using

this method, the peroxidised phospholipid POVPC was

found to be higher in AD patients and was correlated with

cognitive performance but not reduced by carotenoid

supplementation. We also investigated the protective role

for carotenoids against mitochondrial dysfunction induced

by POVPC (1-20µM) in differentiated (d)SH-SY5Y neuronal

cells. POVPC, lutein (0.1-1µM) and zeaxanthin (0.05-

5µM) were recovered in dSH-SY5Y cells after 24 hours of

treatment. Glutathione (GSH) levels, mitosox oxidation

and mitochondrial function were analysed in cells treated

with POVPC (1-20µM) and co-incubation with carotenoids

(lutein and zeaxanthin). We found pathophysiological

concentration-induced damage can be protected with

appropriate dose of carotenoid.

The talk will highlight some of our main findings on the

effects of carotenoid supplementation on lipid oxidation.

e:

osa25@cam.ac.uk