Unraveling the complexities of cognitive decline in obstructive sleep apnea, new research sheds light on the TDP43/HDAC6/Prdx1 signaling pathway’s pivotal role in inflammation and oxidative stress.
– by Marv
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TDP43/HDAC6/Prdx1 signaling pathway participated in the cognitive impairment of obstructive sleep apnea via regulating inflammation and oxidative stress.
Ou et al., Int Immunopharmacol 2023
DOI: 10.1016/j.intimp.2023.111350
Oh, what a joyous day for science! We’ve discovered that if you can’t breathe properly while sleeping, your brain might not be in tip-top shape. Who would’ve thought, right? In this groundbreaking study, researchers played peekaboo with the obvious: obstructive sleep apnea (OSA) can lead to cognitive dysfunction. But wait, there’s more! They’ve roped in some fancy proteins—TAR DNA-binding protein 43 (TDP-43), histone deacetylase 6 (HDAC6), and peroxiredoxin 1 (Prdx1)—because why not make it sound more complicated?
First, they threw a sleepover and used polysomnography (a fancy word for watching you sleep with wires) to diagnose OSA. Then, they handed out the Montreal Cognitive Assessment (MoCA)—no, not a coffee drink, but a test to see how well your brain is doing. Blood was drawn because, of course, what’s a study without a little vampire action?
They split the participants into three groups: the lucky ones who sleep like babies, the mild-to-moderate snorers, and the severe “I might stop breathing in my sleep” group. Surprise, surprise, the more you struggle to breathe at night, the worse you did on the MoCA. But fear not, the mighty continuous positive airway pressure (CPAP) therapy swooped in to save the day for those with severe OSA.
In a shocking twist, they found that TDP-43 and HDAC6 were partying too hard in the OSA crowd, while Prdx1 was feeling left out. After 12 weeks of CPAP therapy, the party calmed down a bit. They even played with some cells in a dish, treating them with lipopolysaccharide (LPS) to mimic inflammation because, why simulate a bar fight when you can have a controlled brawl in a petri dish?
Turns out, TDP-43 is the ringleader, influencing Prdx1 by bossing around HDAC6, and this whole shindig is linked to inflammation and oxidative stress. Throw in an HDAC6 inhibitor, and voilà, the inflammation and oxidative stress take a chill pill.
In conclusion, the researchers suggest that messing with TDP-43 and HDAC6 could be the key to helping OSA patients remember where they left their car keys. Potential therapeutic targets, they say—because nothing says “we’re not done here” like ending with the promise of more research.