Gary Gilmour

TL;DR: Key strengths and weaknesses of each of the NMDAR hypofunction hypothesis approaches are described with regard to their ability to recapitulate the deficits seen in patients, and it is surprisingly difficult to identify any single aspect of cognitive function that possesses complete translational integrity.

TL;DR: Evidence supporting the idea of early neuroplastic deficits being prevalent in AD is summarized and substrates of Neuroplasticity represent an emerging complementary class of drug target that would aim to normalize synapse dynamics and restore cognitive function in the AD brain and in other neurodegenerative diseases.

TL;DR: These cross-species studies link a cholinergic response to a prefrontal BOLD activation and indicate that these interrelated mechanisms mediate the integration of external cues with internal representations to initiate and guide behavior.

TL;DR: Results show that coordinated acetylcholine release between the prefrontal cortex and hippocampus is associated with reward and arousal on distinct timescales, providing dual mechanisms to support learned behavior acquisition during cognitive task performance.

TL;DR: Overall, the opportunity to induce a selective cognitive deficit in attention (5CSRT) or working memory (DMTP) in the rat is limited by both the NMDAR antagonist and the dose range used.