P028 - NEUROPROTECTIVE EFFECTS OF ASTAXANTHIN IN PRECLINICAL MODELS OF ALZHEIMER’S DISEASE (ID 1360)
Abstract
Aims
Alzheimer's disease (AD) is the most common cause of dementia, and it accounts for about 70 % of all dementia cases. The pathological manifestations of Alzheimer's disease include aggregation of misfolded protein fragment beta‐amyloid outside neurons called plaques, hyper-phosphorylation of protein tau inside neurons called tangles, neuronal loss, synaptic degeneration, and neuroinflammation. Until date, there are no disease-modifying therapies available. Astaxanthin, a lipid-soluble xanthophyll beta-carotenoid synthesized by many microorganisms, has been reported to exhibit anti-inflammatory and neuroprotective functions.
Methods
To investigate the neuroprotective effects of astaxanthin, primary mouse hippocampal neurons and organotypic brain slice cultures were treated with either amyloid beta (Aβ1-42) or lipopolysaccharides (LPS) and co-incubated with astaxanthin. Expression levels of relevant markers were examined at protein and mRNA levels by quantitative real time polymerase chain reaction (qRT-PCR), immunofluorescence and immunoblotting techniques. Cytokine release was determined using an immunosorbent assay (Mesoscale discovery, MSD).
Results
Treatment of LPS-stimulated brain slices with astaxanthin significantly reduced the secretion of pro-inflammatory cytokines (TNF-α, IL-6, KC/GRO) into the supernatant. In addition, we observed prevention of both neuronal and synaptic loss as measured by an increased relative signal intensity of neuronal marker NeUN, and post-synaptic marker PSD95 in primary mouse hippocampal neurons treated with Aβ1-42 and co-incubated with astaxanthin.
Conclusions
Our data suggest that astaxanthin may be a therapeutic candidate by ameliorating pathophysiological manifestations associated with Alzheimer’s disease.
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