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Cognitive dysfunction, which occurs in 80% of people with traumatic brain injury (TBI), is associated with upregulation of phosphodiesterase 4B2 (PDE4B2). In an animal study, researchers examined the potential usefulness of the PDE4B inhibitor A33 for cognitive manifestations of artificially induced TBI.
Rats underwent surgery for sham or experimental TBI. Experimental but not sham TBI caused learning and working-memory deficits, which were associated with depressed basal hippocampal synaptic transmission; impaired long-term potentiation; postinjury elevation in brain tumor necrosis factor-α (TNF-α), a proinflammatory cytokine; cortical atrophy with accumulation of microglia; and decreased phosphorylation (activation) of cAMP-response elemen…