Abstract
Lipidomics is strategic in the discovery of biomarkers of neurodegenerative diseases (NDDs). The skin surface lipidome bears the potential to provide biomarker candidates in the detection of pathological processes occurring in distal organs. We investigated the sebum composition to search diagnostic and, possibly, prognostic, biomarkers of Alzheimer’s disease (AD) and Parkinson’s disease (PD). The observational study included 64 subjects: 20 characterized as “probable AD with documented decline”, 20 as “clinically established PD”, and 24 healthy subjects (HS) of comparable age. The analysis of sebum by GCMS and TLC retrieved the amounts (µg) of 41 free fatty acids (FFAs), 7 fatty alcohols (FOHs), vitamin E, cholesterol, squalene, and total triglycerides (TGs) and wax esters (WEs). Distributions of sebum lipids in NDDs and healthy conditions were investigated with multivariate ANOVA-simultaneous component analysis (ASCA). The deranged sebum composition associated with the PD group showed incretion of most composing lipids compared to HS, whereas only two lipid species (vitamin E and FOH14:0) were discriminant of AD samples and presented lower levels than HS sebum. Thus, sebum lipid biosynthetic pathways are differently affected in PD and AD. The characteristic sebum bio-signatures detected support the value of sebum lipidomics in the biomarkers search in NDDs.
Highlights
The sebometric analysis showed that sebum weight and Sebum excretion rates (SER)
Consistent with the literature, Parkinson’s disease (PD) was associated with hyper-seborrhea [26], which may account for the high incidence of seborrheic dermatitis in this Neurodegenerative diseases (NDDs) [27]
We found differences in SER between males and females compatible with the different rates of decrement with aging, even if significant differences in SER between males and females were found only in the healthy subjects (HS) group
Summary
The prevalence of the two NDDs is predicted to increase in the future [1,2,3]. Both pathologies are extremely elusive in their onset and development. It is clear that when the neurodegeneration becomes clinically manifest, brain damage has reached an advanced stage. In preclinical AD, individuals have measurable biomarkers of brain changes, but they have not developed symptoms yet [4]; in PD, classic motor symptoms appear only when more than a half of neurons in the substantia nigra (SN) undergo overt degeneration [5]. It is crucial to make an early diagnosis to adopt appropriate strategies in the prevention of neuronal death
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