Aspirin and nonsteroidal anti-inflammatory drugs inhibit amyloid-beta aggregation

Aspirin and many other nonsteroidal anti-inflammatory drugs (NSAIDs), (eg, ibuprofen, naproxen, indomethacin, and ketorolac) are carboxylic acids [ 1 ]. Their pKa values range from (aspirin) to (ibuprofen). As such, they are not ionized at the acidic pH found in the gastric lumen and thus can be absorbed across the gastric mucosa. Once these drugs move from the acidic environment of the gastric lumen into the pH–neutral mucosa, the drugs ionize and are trapped temporarily in epithelial cells where it may damage these cells.

Some conclude the benefits are greater than the risks due to bleeding in those at average risk. [53] Others are unclear if the benefits are greater than the risk. [59] [60] Given this uncertainty, the 2007 United States Preventive Services Task Force guidelines on this topic recommended against the use of aspirin for prevention of CRC in people with average risk. [61] Nine years later however, the USPSTF issued a grade B recommendation for the use of low-dose aspirin (75 to 100 mg/day) “for the primary prevention of CVD and CRC in adults 50 to 59 years of age who have a 10% or greater 10-year CVD risk, are not at increased risk for bleeding, have a life expectancy of at least 10 years, and are willing to take low-dose aspirin daily for at least 10 years”. [62]

Aspirin and nonsteroidal anti-inflammatory drugs inhibit amyloid-beta aggregation

aspirin and nonsteroidal anti-inflammatory drugs inhibit amyloid-beta aggregation

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