The inflammatory compound, C-reactive protein, is involved in the development of Alzheimer's disease, other forms of dementia, heart disease, diabetes and most likely cancer and arthritis. A solid study of a large population sample found that people who smoked marijuana at least three times per week had half of the blood levels of C-reactive protein as those who did not use marijuana (Decreased prevalence of diabetes in marijuana users, 2012). This is more evidence that responsible marijuana use benefits human health by preventing disease-friendly internal environments, interrupting disease processes. and triggering repair mechanisms. Neurochem Int. 2012 Feb Promotion of β-amyloid production by C-reactive protein and its implications in the early pathogenesis of Alzheimer's disease. Bi BT, Lin HB, Cheng YF, Zhou H, Lin T, Zhang MZ, Li TJ, Xu JP.SourceDepartment of Pharmacology, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China. Abstract: C-reactive protein CRP and β-amyloid protein Aβ are involved in the development of Alzheimer's disease AD. However, the relationship between CRP and Aβ production is unclear. In vitro and in vivo experiments were performed to investigate the association of CRP with Aβ production. Using the rat adrenal pheochromocytoma cell line PC12 cells to mimic neurons, cytotoxicity was evaluated by cell viability and supernatant lactate dehydrogenase LDH activity. The levels of amyloid precursor protein APP, beta-site APP cleaving enzyme BACE-1, and presenilins PS-1 and PS-2 were investigated using real-time polymerase chain reaction and Western blotting analysis. Aβ1-42 was measured by enzyme-linked immunosorbent assay. The relevance of CRP and Aβ as well as potential mechanisms were studied using APP/PS1 transgenic Tg mice. Treatment with 0.5-4.0 μM CRP for 48 h decreased cell viability and increased LDH leakage in PC12 cells. Incubation with CRP at a sub-toxic concentration of 0.2 μM increased the mRNA levels of APP, BACE-1, PS-1, and PS-2, as well as Aβ1-42 production. CRP inhibitor reversed the CRP-induced upregulations of the mRNA levels of APP, BACE-1, PS-1, and PS-2, and the protein levels of APP, BACE-1, PS-1, and Aβ1-42, but did not reversed Aβ1-42 cytotoxicity. The cerebral levels of CRP and Aβ1-42 in APP/PS1 Tg mice were positively correlated, accompanied with the elevated mRNA expressions of serum amyloid P component SAP, complement component 1q C1q, and tumor necrosis factor-α TNF-α. These results suggest that CRP cytotoxicity is associated with Aβ formation and Aβ-related markers expressions; CRP and Aβ were relevant in early-stage AD; CRP may be an important trigger in AD pathogenesis.