#1

I hope the title of my post is an accurate summary of this article that came up in my feed today. I recall reading that larger doses of Rapamycin are thought to enable crossing of blood, brain, barrier. Has that been proven or is that still in the realm of speculation? And if proven, does anyone know just how much we should take to rapify our brains?

Here’s the link to the paper:
[Enhanced mTORC1 signaling and protein synthesis in pathologic α-synuclein cellular and animal models of Parkinson’s disease | Science Translational Medicine](https://www.science.org/doi/10.1126/scitranslmed.add0499)

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#2

Dr. Kaeberlein and Sabatini were debating the dose to cross the BBB, but they did not give any other hints other than a ‘large dose’. So, we don’t have much to go on other than that. How big is large? I have no idea. I’m pretty sure it’s above a 9 mg equivalent. Maybe a 20 mg equivalent might make it?

MTOR rebound (overexpression) above 20 mg is a possible danger. We know this has about a 50% chance of happening at 40 mg (human study) and about a 0% of this happening at 20 mg and below. 20-40 mg is a grey zone where we’re not quite sure what the odds are. I keep my doses below 20 mg and usually at 6-9 mg. I use GFJ as a 3X multiplier so 2-3 mg of Rapa + GFJ = 6-9 mg equivalence.

If you want to risk a large dose, I’d say 20 mg equivalence with a 2-3 week break between doses will get you the safest and largest dose.

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#3

You can measure Mtor in brain noninvasive.

Posted this back in February, 2022

All it takes is re$ource.

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#4

Wouldn’t it be great if mTor overexpression were to be recognized as a disease, enabling doctors to treat aging as a disease?

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#5

The study also identified other proteins that interact with alpha-synuclein, potentially leading to brain cell death. The researchers found approximately 100 candidates, most of which played roles in cellular processes related to protein production. Specifically, when the pathological form of alpha-synuclein interacted with a protein called tuberous sclerosis complex 2 (TSC2), it allowed another protein called mTOR to become overactive, resulting in the death of brain cells.

Remarkably, the researchers found that administering a drug called rapamycin, which targets mTOR, halted excessive protein production in mice with a Parkinson’s-like condition. As a result, the mice also experienced improvements in their motor skills, as the slow and halting movements characteristic of Parkinson’s disease diminished.

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