TABLE 1.

Pharmacological strategies to mitigate the impact of inflammation on anhedonia

Immunotherapeutic Strategies
mAbs to cytokines, cytokine receptors, cellular adhesion molecules, and chemokine receptors
Inflammatory signaling pathway inhibitors (e.g., TLR4 inhibitors, JAK inhibitors—baricitinib, p38 MAPK inhibitors)
Inflammasome blockade (e.g., P2X7 receptor antagonists)
COX-2/prostaglandin inhibitors (e.g., celecoxib, aspirin)
Inhibitors of microglial activation (e.g., minocycline)
Neuroimmunomodulation [e.g., efferent vagal nerve stimulation; γ frequency light (flicker) exposure]
Neurotransmitter Strategies
Dopamine
Synthesis (e.g., sapropterin, folic acid, l-methylfolate, SAMe, levodopa)
Release (e.g., amphetamine, methamphetamine, lisdexamfetamine)
Reuptake (e.g., bupropion, methylphenidate, modafinil)
Agonists (e.g., aripiprazole, brexpiprazole, pramipexole)
Glutamate
Receptor antagonists (e.g., memantine, ketamine, esketamine, AXS-05)
Reuptake enhancers/glutamate stabilizers (e.g., riluzole)
Immunometabolic Strategies (Systemic and Cellular)
Glycolysis inhibitors (e.g., imatinib, lonidamine, rapamycin, dimethyl fumarate)
Antioxidants (e.g., N-acetyl cysteine)
Insulin sensitizers (e.g., pioglitazone, metformin)
Fatty acid metabolism (e.g., eicosapentaenoic acid, acetyl-l-carnitine)
Kynurenine Pathway Strategies
IDO inhibitors (e.g., indoximod)
Blockade of KYN transport into brain (e.g., leucine)

mAb, monoclonal antibody.