Comments
derphurr t1_jdpuyrw wrote
The transmission of OXPHOS disease and methods to prevent this ( 2005)
>Despite extensive studies on use of various pharmacological agents and vitamin supplements, there is still no cure for OXPHOS disease. Pharmacological therapy mainly relies on the administration of artificial electron acceptors, metabolites and cofactors or oxygen radical scavengers (Dimauro et al., 2004).
>Physical exercise can also be important to prevent disease manifestations. Most patients with mitochondrial disease are inactive because of exercise intolerance or fear for muscle damage, in spite of the fact that aerobic training increases work and oxidation capacity in these patients (Taivassalo et al., 2001; Taivassalo and Haller, 2004).
elegance78 t1_jdq28kr wrote
Anyone qualified would like to comment? Seems like a big deal with regards to root causes of Alzheimer's disease.
Inner-Cress9727 t1_jdqrnz7 wrote
Can’t read b/c paywall. Sounds very interesting. My educated hunch is that there is no single cause of AD, but rather it is a syndrome of failed cellular metabolism, which can be caused by a number of means.
[deleted] t1_jdt1tpc wrote
[removed]
indimedia t1_jdtuxen wrote
We can email the authors and they will reply with the article for free and are said to be happy to!
AutoModerator t1_jdpr9hy wrote
Welcome to r/science! This is a heavily moderated subreddit in order to keep the discussion on science. However, we recognize that many people want to discuss how they feel the research relates to their own personal lives, so to give people a space to do that, personal anecdotes are allowed as responses to this comment. Any anecdotal comments elsewhere in the discussion will be removed and our normal comment rules apply to all other comments.
I am a bot, and this action was performed automatically. Please contact the moderators of this subreddit if you have any questions or concerns.
[deleted] t1_jdsthsl wrote
[removed]
basmwklz OP t1_jdprb76 wrote
Abstract: >Astrocytes provide key neuronal support, and their phenotypic transformation is implicated in neurodegenerative diseases. Metabolically, astrocytes possess low mitochondrial oxidative phosphorylation (OxPhos) activity, but its pathophysiological role in neurodegeneration remains unclear. Here, we show that the brain critically depends on astrocytic OxPhos to degrade fatty acids (FAs) and maintain lipid homeostasis. Aberrant astrocytic OxPhos induces lipid droplet (LD) accumulation followed by neurodegeneration that recapitulates key features of Alzheimer’s disease (AD), including synaptic loss, neuroinflammation, demyelination and cognitive impairment. Mechanistically, when FA load overwhelms astrocytic OxPhos capacity, elevated acetyl-CoA levels induce astrocyte reactivity by enhancing STAT3 acetylation and activation. Intercellularly, lipid-laden reactive astrocytes stimulate neuronal FA oxidation and oxidative stress, activate microglia through IL-3 signalling, and inhibit the biosynthesis of FAs and phospholipids required for myelin replenishment. Along with LD accumulation and impaired FA degradation manifested in an AD mouse model, we reveal a lipid-centric, AD-resembling mechanism by which astrocytic mitochondrial dysfunction progressively induces neuroinflammation and neurodegeneration.