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. 2015 Mar 18;10(3):e0116092. doi: 10.1371/journal.pone.0116092

Table 6. Summary of previous studies showing changes in acute phase proteins in Alzheimer’s disease.

Name Site of effect Function Modification Reference
Alpha-2-macroglobulin plasma Inhibitor of coagulation; inhibitor of fibrinolysis Increased in MCI and AD [5,47]
Complement C3 plasma Most abundant protein of the complement system, enhances response Increased in AD [101104]
Complement C4 plasma Protein involved in the complement system and undergoes cleavage Increased in AD [5,105]
C4b-binding protein plasma Inhibits C4 and binds necrotic cells Decreased in MCI and AD [47]
Complement C5 plasma Fifth component of the complement pathway Increased in MCI [47]
Complement C9 mRNA and protein levels, vascular amyloid deposits Involved in MAC formation Increased in AD brain areas, increased deposition in vascular plaques [101,102,106]
Complement factor H plasma Regulation of alternative pathway of the complement system, ensuring no damage to host tissue Increased in AD [5,107]
Fibrinogen plasma Involved in blood clotting Decreased in AD [47,104,108,109]
Haptogloblin Plasma, CSF Binds free haemoglobin thereby reducing its oxidative activity Increased in AD plasma, decreased in CSF of MCI and AD patients. Other studies show increase in CSF of AD [110,111]
Hemopexin plasma and CSF Binds heme, preserves iron levels in the body Increased in AD [105,112,113]
Thrombin Brain tissue, amyloid plaques, neurofibrillary tangles Coagulation protein that converts fibrinogen into fibrin, also catalyses other coagulation related reactions Increased in AD [114116]
Transthyretin Plasma, CSF Carrier of the thyroid hormone thyroxine Decreased in AD [47,112,117,118]