Reported by Dr. Venkat S Karra, Ph.D.
A series of proteins in blood could form the basis of a test for Alzheimer’s disease in the future, say scientists in the US. They employed proteomics to identify proteins that were expressed at different levels in the blood of patients with Alzheimer’s disease or mild cognitiive impairment compared with those of healthy control patients. The results are described in Neurology.
Four plasma analytes remained after cross-checking against the findings of the Alzheimer’s Disease Neuroimaging Initiative (ADNI). They are apolipoprotein E, B-type natriuretic peptide, C-reactive protein and pancreatic polypeptide. Their levels also correlated with the cerebrospinal fluid contents of beta-amyloid proteins, which have been associated with the onset of Alzheimer’s disease. It is still too early to say for sure that a blood test based on these proteins would work. One of the next steps should be to confirm the link between the biomarkers in blood and cerebrospinal fluid.
source: spectroscopynow
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I’ll hold my breath on this. b-type natriuretic peptide reaches high levels in patients with CHF. It is secreted by the heart as a propeptide, the amino terminal proBNP, but it is degraded mostly by the vascular endothelium, unlike the NT-proBNP, which is entirely excreted by the kidney. This accounts for the greater prognostic power in the NT-proBNP, a subject best treated by Robert Christenson, but the treatment of the test for adjusting for the eGFR is still not done as I had suggested and have a growing number of requests to publish more on. If there is any correlation, it is with the same population that they have in common.
As to the C-Reactive Protein, it is a very important measure of inflammatory disease, reaching fairly typical elevations of 70 to over 100 mg/dl in pneumonia and sepsis, among the 10 most common causes of death in the ICU, and in the 6 months after discharge from ICU. The most remarkable finding by the Braunwald Professor of Cardiology at Harvard maybe 15 years ago from the Framingham specimens was that CRP is a risk factor for a future coronary event, which was not taken so seriously until the Jupiter study determined that use of a lipid-lowering agent has a separate anti-inflammatory effect, and its use for treatment reduced the risk. The CRP might not be a surprise in the light of a concept that there is a significant inflammatory component in Alzheimer’s ds, as we know is the case for type 2 DM. This could be the tie between the process and the development of beta amyloid as an end product.
Apo-Lp E has been investigated for a long time and is not entirely a surprise. This is also tied to a gene sequence.
Pancreatic polypeptide leaves me blankly staring at the wall. Why? What possible role? Is the formation of amyloid in the pancreas the burns out the islet cells related to hyalinization of this protein?
This is half-baked science.
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