PVALB and Alzheimer disease: In a knock-in mouse model of AD expressing a mutant form of human Aβ precursor protein, cells in LEC show loss of parvalbumin containing interneurons that regulate excitability, leading to hyperexcitability of principle neuron and increases in EPSPs, and the disruption of parvalbumin neurons was observed earliest in the LEC (Petrache et al., 2019).