Toward a dissection of β-Amyloid localized effects on glutamatergic hippocampal repertoire: An Editorial Highlight for "Amyloid-beta1-42 induced glutamatergic receptor and transporter expression changes in the mouse hippocampus"on https://doi.org/10.1111/jnc.15099

Abstract

Hippocampal excitatory glutamatergic transmission is critically involved in cognitive functions such as learning and memory. A severe impairment of spatial memory is associated with the Alzheimer's disease characteristic augmentation of soluble Amyloid-beta_1-42 which in turn leads to glutamatergic neurotransmission dysfunction. As the molecular basis of such correlations has not been completely understood, this Editorial highlights a study in the current issue of the Journal of Neurochemistry in which Yeung and coworkers provide an elegant anatomical study that sheds light into this problematic. Through a rigorous immunohistochemical approach, a sub-regional expression pattern of ionotropic glutamate receptors and vesicular transporters was determined in control and beta amyloid-injected mouse hippocampus. The selected areas participate in information processing and thus, in memory formation. Furthermore, the authors discuss their findings in the context of cognitive deficits present in Alzheimer's disease patients delivering an intuitive analysis of plausible molecular events that disturb proper glutamate signaling. This study takes an important step toward a better understanding of the complexity of Amyloid-beta_1-42 and glutamatergic neurotransmission interactions.

Keywords: Alzheimer's disease; Amyloid-beta1-42; hippocampus; ionotropic glutamate receptors; vesicular glutamate transporters.