Lavender essential oil (LO) is a traditional medicine used for the treatment of Alzheimer’s disease (AD). It was extracted from Lavandula angustifolia Mill. This study was designed to investigate the effects of lavender essential oil (LO) and its active component, linalool (LI), against cognitive impairment induced by D‐galactose (D‐gal) and AlCl₃ in mice and to explore the related mechanisms. Our results revealed that LO (100 mg/kg) or LI (100 mg/kg) significantly protected the cognitive impairments as assessed by the Morris water maze test and step‐though test. The mechanisms study demonstrated that LO and LI significantly protected the decreased activity of superoxide dismutase (SOD), glutathione peroxidase (GPX), and protected the increased activity of acetylcholinesterase (AChE) and content of malondialdehyde (MDA). Besides, they protected the suppressed nuclear factor‐erythroid 2‐related factor 2 (Nrf2) and heme oxygenase‐1 (HO‐1) expression significantly. Moreover, the decreased expression of synapse plasticity‐related proteins, calcium‐calmodulin‐dependent protein kinase II (CaMKII), p‐CaMKII, brain‐derived neurotrophic factor (BDNF), and TrkB in the hippocampus were increased with drug treatment. In conclusion, LO and its active component LI have protected the oxidative stress, activity of cholinergic function and expression of proteins of Nrf2/HO‐1 pathway, and synaptic plasticity. It suggest that LO, especially LI, could be a potential agent for improving cognitive impairment in AD.

Even symptomatic Mecp2 -null mice can develop motor skills, which improve behavior and extend life span by 20%.

The medial prefrontal cortex (mPFC), a critical hub for social regulation, is highly vulnerable to stress. While mPFC dysfunction underlies stress-induced social alterations, the precise circuit mechanisms underlying remain elusive. Given mPFC’s integration of stress signals from key nodes like the basolateral amygdala (BLA) and paraventricular hypothalamus (PVN), we hypothesized that enhanced BLA and PVN inputs disrupts mPFC’s circuit dynamics, mediating social alterations after stress exposure. Here, using longitudinal in vivo Ca²⁺ imaging during repeated restraint stress, we observed post-stress mPFC hypoactivity, impaired pattern decorrelation and disrupted population coding for social discrimination following both acute and chronic stress. Further combining circuit-specific optogenetics, we revealed that the mPFC dysfunction arise from convergent potentiation of dual inhibitory circuits, including the BLA glutamatergic inputs activating GABAergic neurons and the PVN oxytocinergic projections activating OXTR⁺ GABAergic interneurons. Critically, suppressing either circuit rescued mPFC hypoactivity, restored its encoding for social discrimination, and normalized social performance in stressed mice. Together, these findings establish a unified circuit pathology wherein BLA and PVN hyperactivity converts environmental stress into social alterations, by disrupting the downstream mPFC’s activity dynamics, coactivity pattern, and population coding essential for social discrimination.