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In more severe damage, PARPs can completely deplete the cellular NAD+ pool and the cell dies (paradoxically, from lack of energy)

Improved regulation of CBF in response to both transient hyper- and hypotension subsequently protects cerebral microvasculature from hyperperfusive injury and damage as well as ensuring cerebral perfusion is able to match metabolic demand during periods of reduced driving pressures (i.e., orthostatic stress) (Claassen et al., 2021)

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trials for long-acting injectable combination treatments and next-generation oral medications, escalating competition

A., Kuwajima, S., Duncan, S

doi:10.1007/BF02977612 5