HTR5A and Alzheimer disease: Specifically, reduced 5-HT/5-HT3AR and 5-HT/5-HT1AR signaling in the downstream synaptic terminals contribute to the hyperexcitability of CA1 pyramidal neurons in hAPP-J20 mice, suggesting that hippocampal serotonergic sprouting may compensate for 5-HT/5-HT3AR and 5-HT/5-HT1AR-induced hyperexcitability of excitatory neurons in early AD [49].