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A\u03b2 is cleared from the brain by enzymatic degradation and by transport out of the brain. More than 20 A\u03b2\u2010degrading enzymes have been described. Increasing the degradation of A\u03b2 offers an opportunity to decrease brain A\u03b2 levels in AD patients. This review discusses the direct and indirect approaches which have been used in experimental systems to alter the expression and\/or activity of A\u03b2\u2010degrading enzymes. Also discussed are the enzymes' regulatory mechanisms, the conformations of A\u03b2 they degrade, where in the scheme of A\u03b2 production, extracellular release, cellular uptake, and intracellular degradation they exert their activities, and changes in their expression and\/or activity in AD and its animal models. Most of the experimental approaches require further confirmation. Based upon each enzyme's effects on A\u03b2 (some of the enzymes also possess \u03b2\u2010secretase activity and may therefore promote A\u03b2 production), its direction of change in AD and\/or its animal models, and the A\u03b2 conformation(s) it degrades, investigating the effects of increasing the expression of neprilysin in AD patients would be of particular interest. Increasing the expression of insulin\u2010degrading enzyme<jats:italic>,<\/jats:italic>endothelin\u2010converting enzyme\u20101<jats:italic>,<\/jats:italic>endothelin\u2010converting enzyme\u20102<jats:italic>,<\/jats:italic>tissue plasminogen activator<jats:italic>,<\/jats:italic>angiotensin\u2010converting enzyme<jats:italic>,<\/jats:italic>and presequence peptidase would also be of interest. Increasing matrix metalloproteinase\u20102, matrix metalloproteinase\u20109, cathepsin\u2010B, and cathepsin\u2010D expression would be problematic because of possible damage by the metalloproteinases to the blood brain barrier and the cathepsins' \u03b2\u2010secretase activity. Many interventions which increase the enzymatic degradation of A\u03b2 have been shown to decrease AD\u2010type pathology in experimental models. If a safe approach can be found to increase the expression or activity of selected A\u03b2\u2010degrading enzymes in human subjects, then the possibility that this approach could slow the AD progression should be examined in clinical trials.<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc15762-fig-0002-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text><\/jats:p>","DOI":"10.1111\/jnc.15762","type":"journal-article","created":{"date-parts":[[2023,1,12]],"date-time":"2023-01-12T10:30:35Z","timestamp":1673519435000},"page":"725-763","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Experimental approaches for altering the expression of Abeta\u2010degrading 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