Modulation of mitochondrial functions contributes to the protection of lamotrigine against Alzheimer's disease.

Background: Our previous studies have established that the broad-spectrum anti-epileptic drug lamotrigine (LTG) confers protection against cognitive impairments, synapse and nerve cell damage, as well as characteristic neuropathologies in APP/PS1 mice, a mouse model of Alzheimer's disease (AD). However, the precise molecular mechanisms responsible for this protective effect induced by LTG remain largely elusive.

Objective: In this study, we aimed to investigate the mechanisms underlying the beneficial effects of LTG against AD.

Early infarct growth rate is associated with symptomatic intracranial hemorrhage after endovascular thrombectomy.

Background: Time elapsed from stroke onset and baseline infarct volume is influential on endovascular thrombectomy (EVT) outcomes.

Objectives: This study aimed to explore the utility of early infarct growth rate (EIGR) measured by apparent diffusion coefficient (ADC) in predicting symptomatic intracranial hemorrhage (sICH) of ischemic stroke patients after EVT.

Methods: We retrospectively analyzed patients from the prospectively maintained stroke registry admitted between January 2019 and March 2023, presenting with large vessel occlusive stroke in the anterior circulation.

Mo-Pb redox triggers self-enhanced removal and recovery of Pb with superselectivity.

Membrane-based electrodeposition (MED) has emerged as a promising approach for reversible removal-recovery of toxic but valuable Pb. However, limited by the low specificity of membrane deposition toward various heavy metal ions in MED, the selective removal of Pb remains an obstacle. Inspired by the soft-hard acid-base theory, here we developed a Pb-affinity electroactive membrane by incorporating MoS with the cation exchange membrane (CEM) to achieve a tandem Pb selective adsorption-deposition process.

Knockdown of Alleviates Neuropathological Hallmarks and Cognitive Deficiency in a Model of Sporadic Alzheimer's Disease.

Objective: Recently, we revealed that triggering receptor expressed on myeloid cells-like 2 (TREML2) modulated inflammation by regulating microglial polarization and NLRP3 inflammasome activation. However, the role of TREML2 in Alzheimer's disease (AD) pathogenesis remains poorly understood. In this study, we tried to observe the impact of TREML2 on neuropathological hallmarks (including amyloid-β (Aβ) pathology, hyperphosphorylated tau and neuroinflammation) and cognitive deficiency in senescence-accelerated mouse prone substrain 8 (SAMP8) mice, an animal model of sporadic AD.