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Achieving the optimal therapeutic dose for combating secondary injury in TBI will likely depend on CBD's bioavailability (123) which varies as a function of consumption method [for a detailed review of CBD's pharmacokinetics in humans, see Millar et al. (123)]. Cannabidiol (CBD) is a non-intoxicating, non-psychedelic phytocannabinoid that has over 65 known ECS and non-ECS targets in the brain and body that are influenced dose-dependently [for a detailed review of relevant molecular targets, see (14)]. Further mechanistic investigation is needed to determine the ECS and non-ECS receptor contributions to neuroprotection in TBI. One potential non-ECS receptor target could be δ-subunit containing GABAA receptors (115) that are found extrasynaptically and mediate a tonic-inhibitory current (116). Many AD patients become more agitated and confused in the evening (“sundowning”), and it is plausible that poor sleep and network dysfunction in AD are likely contributors [30, 31]. 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