Blood-brain barrier Permeable nanoparticles for Alzheimer's disease treatment by selective mitophagy of microglia.

Current treatments for Alzheimer's disease (AD) that focus on inhibition of Aβ aggregation failed to show effectiveness in people who already had Alzheimer's symptoms. Strategies that synergistically exert neuroprotection and alleviation of oxidative stress could be a promising approach to correct the pathological brain microenvironment. Based on the key roles of microglia in modulation of AD microenvironment, we describe here the development of Prussian blue/polyamidoamine (PAMAM) dendrimer/Angiopep-2 (PPA) nanoparticles that can regulate the mitophagy of microglia as a potential AD treatment.

Oxoglaucine mediates Ca influx and activates autophagy to alleviate osteoarthritis through the TRPV5/calmodulin/CAMK-II pathway.

Background And Purpose: Stimulation of calcium influx and suppression of autophagy play important roles in the pathogenesis of osteoarthritis (OA). In this study, we used a novel inhibitor of TRPV5 cation channels - oxoglaucine to attenuate progression of deterioration and pathological changes in OA patient-derived chondrocytes and OA animal model, by activating autophagy.

Experimental Approach: Inhibition by oxoglaucine of calcium influx was assessed in cells.

Nifedipine inhibits oxidative stress and ameliorates osteoarthritis by activating the nuclear factor erythroid-2-related factor 2 pathway.

Nifedipine is a voltage-gated calcium channel inhibitor widely used in the treatment of hypertension. Nifedipine has been reported to have antioxidant and anti-apoptotic effects and promotes cell proliferation. However, the effects of nifedipine on oxidative stress and apoptosis in osteoarthritic (OA) chondrocytes are still unclear.

Correction: Dopamine-melanin nanoparticles scavenge reactive oxygen and nitrogen species and activate autophagy for osteoarthritis therapy.

Correction for 'Dopamine-melanin nanoparticles scavenge reactive oxygen and nitrogen species and activate autophagy for osteoarthritis therapy' by Gang Zhong et al., Nanoscale, 2019, 11, 11605-11616.

Correction to: TREM2 Attenuates Aβ1-42-Mediated Neuroinflammation in BV-2 Cells by Downregulating TLR Signaling.

The article titled "TREM2 Attenuates Aβ1‑42‑Mediated Neuroinflammation in BV‑2 Cells by Downregulating TLR Signaling", written by Huiping Long, Gang Zhong, Chengzhi Wang, Jian Zhang, Yueling Zhang, Jinglian Luo, Shengliang Shi, was originally published electronically on the publisher's internet portal (currently SpringerLink) on 27 May 2019 with open access.

Dopamine-melanin nanoparticles scavenge reactive oxygen and nitrogen species and activate autophagy for osteoarthritis therapy.

Anti-oxidative agents hold great potential in osteoarthritis (OA) therapy. However, most radical scavengers have poor biocompatibility and potential cytotoxicity, which limit their applications. Herein we explore dopamine melanin (DM) nanoparticles as a novel scavenger of reactive oxygen species (ROS) and reactive nitrogen species (RNS).

TREM2 Attenuates Aβ1-42-Mediated Neuroinflammation in BV-2 Cells by Downregulating TLR Signaling.

The pathogenesis of late-onset Alzheimer's disease (LOAD) mainly involves abnormal accumulation of extracellular β-amyloid (Aβ) and the consequent neurotoxic effects. The triggering receptor expressed on myeloid cells 2 (TREM2) gene is associated with the pathogenesis of LOAD and plays important roles in mediating the phagocytosis of Aβ by microglia and regulating inflammation in central nervous system. However, the exact mechanisms of these processes have not yet been clarified.

miRNA-335-5p relieves chondrocyte inflammation by activating autophagy in osteoarthritis.

Aims: Osteoarthritis (OA) is a chronic and degenerative joint disease prevalent in the elderly, which is characterized by hypertrophy and reactive hyperplasia of articular cartilage. Autophagy has been reported to inhibit inflammation and reduce chondrocyte apoptosis in OA. As the microRNA (miRNA)-335-5p has been linked to both inflammation and autophagy, this study aimed to investigate its potential role in regulating autophagy during the pathogenesis of OA.

Artemisinin Ameliorates Osteoarthritis by Inhibiting the Wnt/β-Catenin Signaling Pathway.

Background/aims: Current drug therapies for osteoarthritis (OA) are not practical because of the cytotoxicity and severe side-effects associated with most of them. Artemisinin (ART), an antimalarial agent, is well known for its safety and selectivity to kill injured cells. Based on its anti-inflammatory activity and role in the inhibition of OA-associated Wnt/β-catenin signaling pathway, which is crucial in the pathogenesis of OA, we hypothesized that ART might have an effect on OA.