Role of amyloids in HIV and XMRV transmission and pathogenesis

[DysautonomiaXMRV]

http://www.ncbi.nlm.nih.gov/pubmed/...d_DefaultReportPanel.Pubmed_RVDocSumNeurochem

Res. 2004 Mar;29(3):493-504.

Mitochondrial dysfunction in neurodegenerative diseases associated with copper imbalance.

Rossi L, Lombardo MF, Ciriolo MR, Rotilio G.

Department of Biology, "Tor Vergata" University of Rome, Via della Ricerca Scientifica, 00133 Rome, Italy.

Abstract

Copper is an essential transition metal ion for the function of key metabolic enzymes, but its uncontrolled redox reactivity is source of reactive oxygen species. Therefore a network of transporters strictly controls the trafficking of copper in living systems. Deficit, excess, or aberrant coordination of copper are conditions that may be detrimental, especially for neuronal cells, which are particularly sensitive to oxidative stress. Indeed, the genetic disturbances of copper homeostasis, Menkes' and Wilson's diseases, are associated with neurodegeneration. Furthermore, copper interacts with the proteins that are the hallmarks of neurodegenerative disorders, such as Alzheimer's disease, Parkinson's disease, prion diseases, and familial amyotrophic lateral sclerosis. In all cases, copper-mediated oxidative stress is linked to mitochondrial dysfunction, which is a common feature of neurodegeneration. In particular we recently demonstrated that in copper deficiency, mitochondrial function is impaired due to decreased activity of cytochrome c oxidase, leading to production of reactive oxygen species, which in turn triggers mitochondria-mediated apoptotic neurodegeneration.

This caught my eye as people with ME are known to have intermittent excess urine copper. (Urine is filtered blood).
Copper could be elevated if Red Blood Cells die off. Of note, Red Blood Cell 'mass' in ME CFS is not normal in some patients. If this were to happen VEGF-1 could rise to compensate (to make more oxygen).

We know mitochondria is affected in ME CFS. (Cellular ATP dysregulation).
VEGF-1 has also shown to be elevated in ME CFS, presumably as a compensatory measure.
Interestingly, XMRV is hemopoietic, (it can affect the production of Red Blood Cells).
Lastly, Red Blood Cell shape has been shown to be altered in ME CFS by New Zealand researcher Dr Les Simpson. (Now retired) and Copper can affect this.
(Altered shape of RBC could affect oxygen transport, circulation).

 

[Rosemary]

http://www.biomedcentral.com/1471-2350/9/31

Cathepsin D SNP associated with increased risk of variant Creutzfeldt-Jakob disease

This study looked at a polymorphism in the cathepsin D gene (refSNP ID: rs17571) previously examined in Alzheimer's disease (AD).

Conclusion
This mutation event has been observed to alter the protease activity of the cathepsin D protein and has been linked to an increase in amyloid beta plaque formation in AD. vCJD neuropathology is characterised by the presence of amyloid plaques, formed from the prion protein, and therefore alterations in the amyloid processing activity of cathepsin D may affect the neuropathogenesis of this disease.

 

[fairlight]

Serum Amyloid A recently linked to sarcoidosis by John Hopkins doctors. I wonder if there's a connection? I also have sarcoidosis.


A CENTURY-OLD PUZZLE COMES TOGETHER: SCIENTISTS ID POTENTIAL PROTEIN TRIGGER IN LUNG DISEASE SARCOIDOSIS
http://www.hopkinsmedicine.org/Press_releases/2010/05_03_10.html