📊 Key Statistics
🔬 Introduction
How Sleep Deprivation Drives Alzheimer's Risk
What is Alzheimer's Disease?
A brain disorder that destroys memory and the ability to complete daily tasks. Amyloid-beta plaques disrupt neuron communication and ultimately cause cell death.
Why Drosophila melanogaster?
- Well-established model for studying neurodegeneration
- Provides insights into mechanisms of Alzheimer's disease
- Allows testing of risk factors on disease phenotypes
- Short lifespan enables rapid longitudinal observation
📚 Review of Literature
Sügün et al. (2025)
- ~15% of AD cases due to sleep disruption
- Aβ-42 levels increase when sleep is impaired
- Sleep is a target for early detection & prevention
Baril et al. (2024)
- Longer sleep duration associated with AD development
- Daytime napping linked to worse cognition
- Both processes may trigger neuroinflammation
Emerson et al. (2020)
- Used Tau mutant Drosophila as model
- Did not measure effects over time
- Sleep deprivation does affect locomotion in Tau mutant
🎯 Purpose
To determine if sleep deprivation in Aβ-42 transgenic Drosophila melanogaster can increase the risk of developing Alzheimer-like symptoms in a shorter period of time than non-sleep-deprived mutants.
💡 Hypothesis
The sleep-deprived Aβ-42 transgenic Drosophila melanogaster mutants will develop locomotor deficits in a shorter period of time than the non-sleep-deprived mutants.
🧪 Intended Methodology
Model Organism
Aβ-42 Transgenic Drosophila melanogaster
UAS "Arctic" Aβ-42 × Neuronal GAL4
Controlled Conditions
12h / 12h
Light/Dark
22°C
Temperature
Cornmeal
Diet
Variables
| Type | Variable |
|---|---|
| Independent | Sleep deprivation in Drosophila |
| Dependent | Locomotor ability of Drosophila |
| Controlled | Light cycle, temperature, diet |
📅 Assay Timeline — Negative Geotaxis
Demonstrating Sleep Deprivation
Tracking Locomotor Decline
📈 Related Results
High AD polygenic risk is not associated with daytime sleepiness but is associated with reduced nighttime sleep duration. Clinical AD diagnosis amplifies both associations.
Aβ accumulation is significantly higher in flies deprived of sleep at night vs. during the day, confirming a bidirectional link between sleep timing and amyloid-beta deposition.
🔍 Analysis & Discussion
Take Aways From Figure 1
Expected Results
When nighttime sleep duration is disrupted, there will be a locomotor decline in flies — likely due to increased amyloid-beta deposition in the brain.
Take Aways From Figure 2
Expected Results
Sleep deprivation will cause Alzheimer-like symptoms to occur in sleep-deprived flies earlier than in non-sleep-deprived flies.
✅ Conclusion
This study aims to determine whether sleep deprivation in Aβ-42 transgenic Drosophila melanogaster will cause the flies to experience decreased locomotor ability.
It is expected that the sleep-deprived transgenic flies will show decreased locomotor abilities earlier than the non-sleep-deprived flies — providing evidence that sleep deprivation accelerates Alzheimer-like disease progression.
Predicted Causal Chain
🔭 Application & Future Focus
🌍 Application
- Raise awareness about the adverse consequences of sleep deprivation on brain health
- Support evidence from human studies that lack of sleep accelerates AD risk
- Inform prevention strategies targeting sleep as a modifiable risk factor
🔬 Future Focus
Track amyloid-beta plaques directly in fly brains — measure deposition over time to confirm accumulation rates between groups.
Test a sleep-deprivation remedy to see if it can prevent or delay Alzheimer-like symptoms in the same transgenic flies.