Abstract
Decreased concentration of phospholipids were observed in brain tissue from individuals with dementia compared with controls, indicating phospholipids might be a key variable in development of age-related cognitive impairment. The reflection of these phospholipid changes in blood might provide both reference for diagnosis/monitoring and potential targets for intervention through peripheral circulation. Using a full-scale targeted phospholipidomic approach, 229 molecular species of plasma phospholipid were identified and quantified among 626 senile residents; the association of plasma phospholipids with MoCA score was also comprehensively discussed. Significant association was confirmed between phospholipid matrix and MoCA score by a distance-based linear model. Additionally, the network analysis further observed that two modules containing PEs were positively associated with MoCA score, and one module containing LPLs had a trend of negative correlation with MoCA score. Furthermore, 23 phospholipid molecular species were found to be significantly associated with MoCA score independent of fasting glucose, lipidemia, lipoproteins, inflammatory variables and homocysteine. Thus, the decreased levels of pPEs containing LC-PUFA and the augmented levels of LPLs were the most prominent plasma phospholipid changes correlated with the cognitive decline, while alterations in plasma PC, PS and SM levels accompanying cognitive decline might be due to variation of lipidemia and inflammatory levels.
Highlights
Age-related cognitive impairment, characterized clinically by gradual progressive intellectual deterioration, and pathologically by neurofibrillary tangles, senile plaques, neuropil threads or neuron loss, is becoming a serious problem among aging societies around the world [1,2]
Plasma phospholipid profile and biochemical parameters related with lipid metabolism and cognitive impairment were further analyzed in laboratory
The variables related with lipid metabolism includes fasting glucose, lipidemia and lipoproteins
Summary
Age-related cognitive impairment, characterized clinically by gradual progressive intellectual deterioration, and pathologically by neurofibrillary tangles, senile plaques, neuropil threads or neuron loss, is becoming a serious problem among aging societies around the world [1,2]. The pathophysiological changes associated with cognitive impairment were found to begin years before the emergence of clinical symptoms. Identification of metabolic changes associated with cognitive decline is critical for both understanding the underlying pathogenesis and early diagnosis/intervention of cognitive impairment. Phospholipid is a complicated lipid family containing phosphorus. Diverse permutations of head groups, backbones and fatty acyl chains generate hundreds of phospholipid molecular species in biosamples, generally classified as phosphatidylcholine (PC), phosphatidylethanolamines (PE), phosphatidylserine (PS), phosphatidylinositol (PI), phosphatidylglycerol (PG), phosphatidic acid (PA), sphingomyelin (SM) and their lyso-type (Lysophospholipids, LPLs). Accounting for a quarter of brain’s dry mass, phospholipids provide structural and functional variety for membrane of neural cells [4,5], and participate in conduction of neurotransmitter and electrical signals [6]
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