Table 2.

Role of ketone bodies involved in neuroinflammation and neurodegeneration.

Biological Activity of KB	Reference
KB compensate mitochondrial respiratory dysfunctions (neurons and glial cells), BHB decrease NAD+/NADH ratio increasing ATP production.	(96)
KB increase mitochondrial function, blocking complex I (CI) involved in etiological mechanism of PD.	(97)
KB is able to prevent neuronal apoptosis via SIRT-1 signalling pathway.	(98)
KB is able to prevent neuronal apoptosis via SIRT-1 signalling pathway, reduce p53 and BAX, up-regulating Bcl-2 and Bcl-xL.	(98)
KB are active as mediators of intracellular signaling, BHB binds to HCA2 regulating homeostasis, inhibiting the production of proinflammatory cytokines and enzymes via NF-κB in microglia.	(101)
Binding of BHB to HCA2 facilitates reduction of endoplasmic reticulum stress, NLRP3 inflammasome activity, and IL-1β and IL-18 levels.	(102)
AcAc inhibits glutamate uptake into presynaptic vesicles, decreasing their excitotoxicity.	(103)
KB improve insulin sensitivity and the glycemic profile, BHB and AcAc slow down insulin glycation.	(104, 105)
KB decrease the accumulation of advanced glycation end products (AGEs).	(106, 107)
KB decreases liposomal lipid peroxidation, preventing microglial apoptosis.	(108–110)