Fagotti, JulianeTarga, Adriano D SRodrigues, Lais SNoseda, Ana Carolina DDorieux, Flávia W CScarante, Franciele FIlkiw, Jessica LLouzada, Fernando MChowdhury, Namrata Rvan der Veen, Daan RMiddleton, BenitaPennings, Jeroen L ASwann, Jonathan RSkene, Debra JLima, Marcelo M S2019-03-222019-03-222019-02-132045-23223076078610.1038/s41598-018-37657-6http://hdl.handle.net/10029/622947Parkinson's disease (PD) is a chronic disorder that presents a range of premotor signs, such as sleep disturbances and cognitive decline, which are key non-motor features of the disease. Increasing evidence of a possible association between sleep disruption and the neurodegenerative process suggests that sleep impairment could produce a detectable metabolic signature on the disease. In order to integrate neurocognitive and metabolic parameters, we performed untargeted and targeted metabolic profiling of the rotenone PD model in a chronic sleep restriction (SR) (6 h/day for 21 days) condition. We found that SR combined with PD altered several behavioural (reversal of locomotor activity impairment; cognitive impairment; delay of rest-activity rhythm) and metabolic parameters (branched-chain amino acids, tryptophan pathway, phenylalanine, and lipoproteins, pointing to mitochondrial impairment). If combined, our results bring a plethora of parameters that represents reliable early-phase PD biomarkers which can easily be measured and could be translated to human studies.enArticleSci Rep 2019; 9(1):1898