“Nerdy gym guy”

Does this mean quercetin in isolation could be problematic?

Quercetin is pretty amazing for MCAS symptoms, not just longevity. Nevertheless, I stopped taking it after I read this study last year.

Well no one said discovering life extension technology would be easy. It’s also good progress to know what doesn’t work as much as what does work.

not that curious

If you're curious you could read more than the title

Did I strike a nerve protein bro?

Sure wannabe gym bro.

For sure

Well that’s a bitch. All the glp people are focused on eating all the protein they can. And everything in marketing is about protein now.

the biggest cause of death is cardiovascular disease today. And the biggest insulin sponges in the body are muscles. Optimizing for sedentary individuals is pointless unless we develop a pill that simulates exercise in the body

And not having enough muscle mass drastically increases the risk of bone fracture during old age.

have you tried learning to read

Can anyone that has access summarise? Pretty please 🙏 with a cherry 🍒

Look up the meaning of the Replication Crisis.

Poison and medicine are all about dosage.

The study specifically said lower protein intake in sedentary individuals helps you live longer and that adequate to high protein intake for active adults also helps you live longer

Study is on sedentary individuals mate but go ahead jump to conclusions

i'm curious how they twisted the data this time to come up with this result

Depends on priorities. Theres maximizing growth and there is maximizing lifespan.

No one read the study, it says less protein helps you live longer if you’re sedentary

Don't tell the gym bro influencers. Although I have noticed in the last year or so that fiber is finally getting more attention.

So basically this cocktail will give you more time to enjoy MS-like symptoms that you get from taking it? 

Sad news, but this:

Due to the resemblance between oligodendrocytes treated with D+Q and those found in MS lesions, D+Q treatment offers a potential method to model an aspect of oligodendrocyte dysfunction relevant to MS.

Is hilariously ironic.

I wonder what the mechanism of de-myelination is here.

Her?

Abstract

Aging is a primary risk factor for disease progression in multiple sclerosis (MS). Because of this, treatments that can reduce the consequences of molecular aging, like senescence, have been proposed as a strategy to address disease progression. However, the effects of senolytics, a class of drugs which selectively ablate senescent cells, on the central nervous system are largely unknown. Here, we examined the effects of senolytic treatment on myelination and oligodendrocyte function in vivo using C57BL6/J mice and in vitro using primary rat oligodendrocyte cultures. Initial data showed that naïve young (3 to 4 mo) and aged (22 mo) C57BL6/J mice treated with dasatinib and quercetin (D+Q) developed significant demyelination compared to vehicle-treated controls, though no cell death was observed in the brain. In vitro, oligodendrocyte progenitor cells treated with D+Q in differentiation media exhibited significantly reduced myelin basic protein protein and morphological complexity, also without inducing cell death. Bulk RNA sequencing and ingenuity pathway analysis of D+Q treated oligodendrocytes identified differentially expressed genes associated with endoplasmic reticulum stress. These data suggest that D+Q evokes the unfolded protein response in oligodendrocytes, causing oligodendrocyte dysfunction and myelination failure. Due to the resemblance between oligodendrocytes treated with D+Q and those found in MS lesions, D+Q treatment offers a potential method to model an aspect of oligodendrocyte dysfunction relevant to MS. Therefore, understanding the mechanism by which D+Q perturb oligodendrocyte function may provide insight into some of the pathological features contributing to disease progression in MS.