Here's an article that discusses the study I just posted. Someone else can provide more insight.
https://www.medlink.com/news/could-targeting-...se-therapy
..."For years, canonical amino acid-sensing pathways — such as Sestrin2-mediated leucine sensing — have dominated the field of mTORC1 biology. These studies have been largely conducted in HEK293 cells. However, the researchers highlight growing evidence that in neurons and glial cells, as well as numerous other cell types, leucine-derived acetyl-coenzyme A (AcCoA) may play a more prominent regulatory role.
In this pathway, AcCoA activates the acetyltransferase p300, leading to acetylation of the mTORC1 component Raptor and subsequent activation of mTORC1 signaling"...
..."[color=rgb(0, 0, 0)]Importantly, chronic overactivation of mTORC1 has been linked to impaired autophagy and toxic protein accumulation across multiple neurodegenerative diseases, including Alzheimer disease, Parkinson disease, [/color] Huntington disease [color=rgb(0, 0, 0)], and ALS"...[/color]
[color=rgb(0, 0, 0)]..."[/color][color=rgb(0, 0, 0)]In this review, researchers also summarize evidence that metabolic and inflammatory pathways may converge on neuronal mTORC1 regulation. For example, abnormal AcCoA accumulation and inflammatory signaling through[/color][color=rgb(50, 109, 164)]CCR5[/color][color=rgb(0, 0, 0)]represent two different mechanisms that have been implicated in pathological mTORC1 activation and autophagy defects in neurodegenerative disease models.[/color]
"These findings suggest that neuronal nutrient sensing may have differences to what is seen in HEK293 cells, which have been used extensively in the previous literature," the researchers note. "Understanding these specialized metabolic control mechanisms could help identify new therapeutic opportunities upstream of mTORC1."..
https://www.medlink.com/news/could-targeting-...se-therapy
..."For years, canonical amino acid-sensing pathways — such as Sestrin2-mediated leucine sensing — have dominated the field of mTORC1 biology. These studies have been largely conducted in HEK293 cells. However, the researchers highlight growing evidence that in neurons and glial cells, as well as numerous other cell types, leucine-derived acetyl-coenzyme A (AcCoA) may play a more prominent regulatory role.
In this pathway, AcCoA activates the acetyltransferase p300, leading to acetylation of the mTORC1 component Raptor and subsequent activation of mTORC1 signaling"...
..."[color=rgb(0, 0, 0)]Importantly, chronic overactivation of mTORC1 has been linked to impaired autophagy and toxic protein accumulation across multiple neurodegenerative diseases, including Alzheimer disease, Parkinson disease, [/color] Huntington disease [color=rgb(0, 0, 0)], and ALS"...[/color]
[color=rgb(0, 0, 0)]..."[/color][color=rgb(0, 0, 0)]In this review, researchers also summarize evidence that metabolic and inflammatory pathways may converge on neuronal mTORC1 regulation. For example, abnormal AcCoA accumulation and inflammatory signaling through[/color][color=rgb(50, 109, 164)]CCR5[/color][color=rgb(0, 0, 0)]represent two different mechanisms that have been implicated in pathological mTORC1 activation and autophagy defects in neurodegenerative disease models.[/color]
"These findings suggest that neuronal nutrient sensing may have differences to what is seen in HEK293 cells, which have been used extensively in the previous literature," the researchers note. "Understanding these specialized metabolic control mechanisms could help identify new therapeutic opportunities upstream of mTORC1."..
