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BREAKING NEWS
Source: SARS-CoV-2 Research  May 24, 2021  2 years, 10 months, 3 weeks, 4 days, 18 hours, 31 minutes ago

BREAKING! University of Oklahoma Study Indicates That SARS-CoV-2 Might Cause Serum Amyloid A (SAA) Amyloidosis And Even Alzheimer Ultimately!

BREAKING! University of Oklahoma Study Indicates That SARS-CoV-2 Might Cause Serum Amyloid A (SAA) Amyloidosis And Even Alzheimer Ultimately!
Source: SARS-CoV-2 Research  May 24, 2021  2 years, 10 months, 3 weeks, 4 days, 18 hours, 31 minutes ago
A new study by researchers from University of Oklahoma has found that the SARS-CoV-2 coronavirus could be causing a secondary medical condition known as Serum Amyloid A (SAA)  Amyloidosis.


 
The proteins Serum amyloid A (SAA) are a family of apolipoproteins associated with high-density lipoprotein (HDL) in plasma. Different isoforms of SAA are expressed constitutively (constitutive SAAs) at different levels or in response to inflammatory stimuli (acute phase SAAs). These proteins are produced predominantly by the liver.
 
It is already known that acute-phase serum amyloid A proteins (A-SAAs) are secreted during the acute phase of inflammation. These proteins have several roles, including the transport of cholesterol to the liver for secretion into the bile, the recruitment of immune cells to inflammatory sites, and the induction of enzymes that degrade extracellular matrix.
 
A-SAAs are implicated in several chronic inflammatory diseases, such as amyloidosis, atherosclerosis, and rheumatoid arthritis. Three acute-phase SAA isoforms have been reported in mice, called SAA1, SAA2, and SAA3. During inflammation, SAA1 and SAA2 are expressed and induced principally in the liver, whereas SAA3 is induced in many distinct tissues. SAA1 and SAA2 genes are regulated in liver cells by the proinflammatory cytokines IL-1, IL-6, and TNF-α. Both SAA1 and SAA2 are induced up to a 1000-fold in mice under acute inflammatory conditions following exposure to bacterial lipopolysaccharide (LPS). Three A-SAA genes have also been identified in humans, although the third gene, SAA3, is believed to represent a pseudogene that does not generate messenger RNA or protein.
 
Serum amyloid A (SAA) is also an acute phase marker tha