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Attention for friends working in shifts with nocturnal tendencies : Never compromise sleep
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Extended Wakefulness -> Compromised Metabolics -> Degeneration of Locus Ceruleus Neurons -> genetic and idiopathic Parkinson’s disease, progressive supranuclear palsy, Pick’s disease or Alzheimer’s disease.
Btw, this was common sense in our culture until few generations back, shared between generations by sayings and folk-songs.
In fact, in Ayurveda, sleep is considered foster-mother(भूतधात्री)
रात्रिस्वभावप्रभवा मता याताँ भूतधत्रीं प्रवदन्ति निद्राम्॥
अर्थात्- रात्रि स्वभाव के कारण उत्पन्न होने वाली जो रात्रि की निद्रा होती है, विशेषज्ञ उसको भूतधात्री कहते हैं। भूतानि प्राणिनी दधाति पुष्णाति इसलि भूतधात्री (चक्रपाणि) अर्थात् रात्रि निद्रा में सर्वाधिक लाभ होने से भूतधात्री। धात्री जिस प्रकार बालकों का पालन-पोषण करती है, निद्रा भी ठीक इसी प्रकार प्राणियों का पोषण करती है।
It is different thing that, we have responded to this common sense wisdom with disgusting subnormal intelligence by carelessly ignoring importance of sleep.
Take care, at least when our pet modern science is accepting our culture’s common sense 
🙂. And yes, grand-pa was not wrong when he advised to sleep early and wake up early 
Research
Extended Wakefulness: Compromised Metabolics in and Degeneration of Locus Ceruleus Neurons
http://www.jneurosci.org/content/34/12/4418
Abstract
Modern society enables a shortening of sleep times, yet long-term consequences of extended wakefulness on the brain are largely unknown. Essential for optimal alertness, locus ceruleus neurons (LCns) are metabolically active neurons that fire at increased rates across sustained wakefulness. We hypothesized that wakefulness is a metabolic stressor to LCns and that, with extended wakefulness, adaptive mitochondrial metabolic responses fail and injury ensues. The nicotinamide adenine dinucleotide-dependent deacetylase sirtuin type 3 (SirT3) coordinates mitochondrial energy production and redox homeostasis. We find that brief wakefulness upregulates SirT3 and antioxidants in LCns, protecting metabolic homeostasis. Strikingly, mice lacking SirT3 lose the adaptive antioxidant response and incur oxidative injury in LCns across brief wakefulness. When wakefulness is extended for longer durations in wild-type mice, SirT3 protein declines in LCns, while oxidative stress and acetylation of mitochondrial proteins, including electron transport chain complex I proteins, increase. In parallel with metabolic dyshomeostasis, apoptosis is activated and LCns are lost. This work identifies mitochondrial stress in LCns upon wakefulness, highlights an essential role for SirT3 activation in maintaining metabolic homeostasis in LCns across wakefulness, and demonstrates that extended wakefulness results in reduced SirT3 activity and, ultimately, degeneration of LCns.
