Description
The study shows glutamatergic terminals are preferentially lost while GABAergic terminals are spared in Aβ-treated mice, but the underlying mechanisms explaining this differential vulnerability are unknown. Understanding this selectivity could reveal therapeutic targets for preserving synaptic function in AD.
Gap type: unexplained_observation Source paper: Predominant loss of glutamatergic terminal markers in a β-amyloid peptide model of Alzheimer’s disease. (None, None, PMID:24029236)