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Re: Bourbon_on_my_cornflakes post# 117042

Thursday, 08/24/2017 3:55:09 PM

Thursday, August 24, 2017 3:55:09 PM

Post# of 471363
I am by no means an expert on this. Wayyyy out of my league. But I found this explanation online:

"Locus coeruleus cells are not dying, but are more likely losing their fully mature phenotype, since no apoptotic neurons in the pons were detected.

Researchers have concluded that "Because these neurons are a pivotal source of norepinephrine throughout the brainstem and forebrain and are involved in the regulation of diverse functions disrupted in Rett syndrome, such as respiration and cognition, we hypothesize that the locus coeruleus is a critical site at which loss of MECP2 results in CNS dysfunction." The restoration of normal locus coeruleus function may therefore be of potential therapeutic value in the treatment of Rett syndrome."

Reading this I surmise that what seems to be happening is that the genetic flaw is causing a breakdown in the working of the neurons in a very specific place in the brain. This flaw is not DIRECTLY involved in the dysfunction. It is one step removed. If you can alert the cells to the problem happening upstream they might be able to compensate and restore homeostasis.
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