Alzheimer's Disease (AD) is well-known as a disease featuring memory loss and confusion, typically in older patients. Chronic sleep disruption is a risk factor for AD, yet mechanisms underlying this are unknown​. Both CSD and AD impact noradrenergic neurons in the locus coeruleus. Phosphorylation of the protein tau in locus coeruleus neurons (LCn) is one of the first sites of AD neurodegeneration and injury. ​Noradrenaline is metabolized into DOPEGAL by MAO-A, and recent clinical research shows that DOPEGAL is a precursor to AEP Tau buildup and neurofibrillary tangles (NFTs). Clorgyline is a drug that pharmacologically inhibits MAO-A, therefore inhibiting the breakdown of noradrenaline in the brain. Studies focusing on clorgyline are limited, and many to date have focused on clorgyline in other functions. This study focuses on the effects of clorgyline on locus coeruleus morphology and neuronal health, and whether damage due to chronic sleep deprivation can be lessened or prevented by an increase in noradrenaline. Mice were randomized into daily vehicle or clorgyline injections and exposed to CSD for two weeks, performing and analyzing sleep recordings three times during the duration of CSD. Mice were perfused after the two-week period and brains were sectioned, followed by immunohistochemistry and stereology analyzing Cfos+, TH (tyrosine hydroxylase), and AEP Tau. Results indicated that clorgyline failed to protect locus coeruleus neurons, and there was a higher mean AEP Tau content in clorgyline mice. Further studies using larger sample sizes and discussion of norepinephrine neurotoxicity are necessary to fully understand the impacts of clorgyline on LC protection