A TrkB and TrkC partial agonist restores deficits in synaptic function and promotes activity-dependent synaptic and microglial transcriptomic changes in a late-stage Alzheimer's mouse model

Amira Latif-Hernandez, Tao Yang, Robert R Butler, Patricia Moran Losada, Paras S Minhas, Halle White, Kevin C Tran, Harry Liu, Danielle A Simmons, Vanessa Langness, Katrin I Andreasson, Tony Wyss-Coray, Frank M Longo

INTRODUCTION: Tropomyosin related kinase B (TrkB) and C (TrkC) receptor signaling promotes synaptic plasticity and interacts with pathways affected by amyloid beta (Aβ) toxicity. Upregulating TrkB/C signaling could reduce Alzheimer''s disease (AD)-related degenerative signaling, memory loss, and synaptic dysfunction.'