Table 1.

Potential anti-inflammatory medications for alcohol use disorder and Alzheimer’s disease.

Drug	Mechanism of action	Preclinical studies	Clinical trials
Minocycline	Inhibition of microglia activation (Regen et al., 2015; Clemens et al., 2018)	Reduces ethanol drinking in C57BL/6J mice (Agrawal et al., 2011) Reduces levels of IL-1β, TNF-α, IL-4, and IL-10 in mouse models of familial AD (Garcez et al., 2017) Improved spatial memory in radial arm maze in Aβ (1–42) administered mice (Garcez et al., 2017) Protects against oxidative damage/regulates energy metabolism in specific brain areas in model of chronic stress (Réus et al., 2015) Attenuated neuronal cell death and improved learning and memory in Aβ peptide1#x02013;42-infused rats (Choi et al., 2007)	544 participants of both sexes with mild AD were given 400 mg, 200 mg, and placebo over 2 years and found no delay in progress of cognitive or functional impairment (Howard et al., 2020)
Ibudilast, Mesopram, Rolipram, CDP 480	Phosphodiesterase 4 inhibitors	Reduced ethanol intake in in C57BL/6J mice (Blednov et al., 2014) Reduced ethanol intake in alcohol-preferring rats (Bell et al., 2015) Prevented Aβ1–42 induced memory impairments in morris water maze and attenuated neuroinflammatory and apoptotic responses (Wang et al., 2014)	Ibudilast 100 mg/kg in progressive multiple sclerosis (MS) patients did not reduce serum nor cerebrospinal fluid neurofilament light chain levels (Fox et al., 2021) Ibudilast did not attenuate focal inflammation pathology in progressive MS but had neuroprotective effect (Goodman et al., 2021)
Non-steroidal anti-inflammatory drugs (NSAIDs)	Cyclooxygenase-2 inhibitors (Zarghi and Arfaei, 2011)	Ibuprofen, naproxen, and MF-tricyclic rescued memory function in Aβ 42 overexpressing Tg2576 mice which was inversely associated with prostaglandin E2 levels (Kotilinek et al., 2008) In Amyloid precursor protein (APP) females, ibuprofen treatment reduced caspase activation per plaque and reduced Aβ levels (Lim et al., 2001) In APP mice, ibuprofen reduced cytokine levels, GFAP levels, and Aβ deposits (Lim et al., 2000)	Chronic use of NSAIDs prior to MCI or AD may be beneficial while use after Aβ deposition has already started may not be effective (Imbimbo et al., 2010)