[Tupelo3]

Defective nucleoli (small nuclei) have been implicated in a number of rare hereditary conditions, as well as in neurodegenerative diseases like Huntington’s and Alzheimer’s. Nucleolus is the term for the microscopic structure inside the nucleus. In this structure inside the nucleus, proteins and RNA molecules are assembled, forming ribosomes, the cells’ protein factories.

Neurons that produce dopamine inside the brain of individuals with Parkinson’s were microscopically examined. This kind of cell malfunctions and dies in Parkinson’s, resulting in the typical palsy symptoms. Most nucleoli were in fact discovered to be defective inside these cells.

http://www.ahealthblog.com/scientist...s-disease.html

[lurkingforacure]

Originally Posted by Tupelo3

http://www.ahealthblog.com/scientist...s-disease.html

I find this confusing, but confess I don't have a scientific background. I read this article to say that reduced Mtor activity is bad, but from outside reading, reduced Mtor activity is good and actually has been shown to increase lifespan. Conversely, increased Mtor activity is linked to several conditions:

" ...MTOR integrates the input from upstream pathways, including insulin, growth factors (such as IGF-1 and IGF-2), and amino acids.[3] mTOR also senses cellular nutrient, oxygen, and energy levels.[11] The mTOR pathway is dysregulated in human diseases, such as diabetes, obesity, depression, and certain cancers.[12] Rapamycin inhibits mTOR by associating with its intracellular receptor FKBP12.[13][14] The FKBP12-rapamycin complex binds directly to the FKBP12-Rapamycin Binding (FRB) domain of mTOR, inhibiting its activity....

MTOR is implicated in the failure of a 'pruning' mechanism of the excitatory synapses in autism spectrum disorders......

Decreased TOR activity has been found to increase life span in S. cerevisiae, C. elegans, and D. melanogaster.[34][35][36][37] The mTOR inhibitor rapamycin has been confirmed to increase lifespan in mice by independent groups at the Jackson Laboratory, University of Texas Health Science Center, and the University of Michigan....."

The above is from: http://en.wikipedia.org/wiki/Mechani...t_of_rapamycin

Wiki has a really good diagram of Mtor which might be worth a look. I find it interesting that there is a glucose and autism link here, as many PWP have a much stronger "startle" reaction than nonPWP.

[Tupelo3]

Originally Posted by lurkingforacure

I find this confusing, but confess I don't have a scientific background. I read this article to say that reduced Mtor activity is bad, but from outside reading, reduced Mtor activity is good and actually has been shown to increase lifespan. Conversely, increased Mtor activity is linked to several conditions:

" ...MTOR integrates the input from upstream pathways, including insulin, growth factors (such as IGF-1 and IGF-2), and amino acids.[3] mTOR also senses cellular nutrient, oxygen, and energy levels.[11] The mTOR pathway is dysregulated in human diseases, such as diabetes, obesity, depression, and certain cancers.[12] Rapamycin inhibits mTOR by associating with its intracellular receptor FKBP12.[13][14] The FKBP12-rapamycin complex binds directly to the FKBP12-Rapamycin Binding (FRB) domain of mTOR, inhibiting its activity....

MTOR is implicated in the failure of a 'pruning' mechanism of the excitatory synapses in autism spectrum disorders......

Decreased TOR activity has been found to increase life span in S. cerevisiae, C. elegans, and D. melanogaster.[34][35][36][37] The mTOR inhibitor rapamycin has been confirmed to increase lifespan in mice by independent groups at the Jackson Laboratory, University of Texas Health Science Center, and the University of Michigan....."

The above is from: http://en.wikipedia.org/wiki/Mechani...t_of_rapamycin

Wiki has a really good diagram of Mtor which might be worth a look. I find it interesting that there is a glucose and autism link here, as many PWP have a much stronger "startle" reaction than nonPWP.

Great question. It certainly seems to be inconsistent with all of the research on mTOR inhibitors on various diseases. Yet we do know that mTORC1 inhibits autophagy, an essential protein degradation and recycling system, which cells employ to sustain their viability. Recent studies have highlighted the fact that autophagy plays crucial roles in many aspects of human health including cancer development, and neurodegenerative diseases.

As you said, confusing.