Action |
|
They reduce βA production |
atorvastatin*a, bis‑tacrine, cerebrolysine*, fenretinide, flurbiprofen*, GSK 188909, huperzine Aa, ibuprofen*b, ladostigil, leuprorelin*b, LY450139b, memoquin, imatinib*, neuropeptide PACAP, simvastatin*b
|
They inhibit βA aggregation |
AZD-103, β-sheet-brakers, colostrinin, curcumin, lipocrine, memoquin, PBT-2a, tramiprosate |
They enhance βA elimination |
PAI-1 or TGB-β1 antagonists, curcumin, active immunotherapy (ACC‑001, CAD‑106), passive immunotherapy (bapineuzumabb), intranasal insulin, rosiglitazone*b
|
They reduce neurofibrillary degeneration |
aloisines, indirubin derivatives, hymenialdisine, anti-phospho-τ immunotherapy, lithium*, lovastatin*, memantine*, memoquin, nicotinamide*, paullones, thiadiazolidinones |
They decrease excitotoxicity and oxidative stress |
docosahexaenoic acid*b, ω3 fatty acids* + lipoic acid*, bis‑tacrine, colostrinin, curcumin, dihydroepiandrosterone*, dimebonb, tacrine-melatonin hybrids, huperzine Aa, ladostigil, lipocrine, melatonin*, memantine*, memoquin, neramexaneb, PBT‑2a, rosiglitazone*b, vitamins E+C*
|