Abstract
Alzheimer's Disease The hippocampus serves a critical role in memory formation and cognition. Hippocampal lesions are among the earliest changes in Alzheimer's disease (AD); however, the molecular mechanisms responsible for these alterations remain unclear. Using autoptic brain samples from patients with AD and a mouse model of AD, Tian et al. show that in the hippocampus, pathologic β-amyloid directly binds and inhibits the receptor for the “hunger hormone” ghrelin (GHSR1α). In the animal model, the binding blocked the GHSR1α-mediated dopamine receptor D1 (DRD1) activation, leading to synaptic plasticity impairments and memory loss. Simultaneous pharmacological activation of GHSR1α and DRD1 rescued synaptic plasticity and spatial memory in AD mice. Sci. Transl. Med. 11 , eaav6278 (2019).
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