Chemokine Receptor Antagonists Prevent and Reverse Cofilin-Actin Rod Pathology and Protect Synapses in Cultured Rodent and Human iPSC-Derived Neurons.

Synapse loss is the principal cause of cognitive decline in Alzheimer's disease (AD) and related disorders (ADRD). Synapse development depends on the intricate dynamics of the neuronal cytoskeleton. Cofilin, the major protein regulating actin dynamics, can be sequestered into cofilactin rods, intra-neurite bundles of cofilin-saturated actin filaments that can disrupt vesicular trafficking and cause synaptic loss.

Short-term outcomes after pure bone marrow aspirate injection for severe knee osteoarthritis: a case series.

Bone marrow aspiration (BMA) is among a group of autologous cell-based therapies currently being explored to treat osteoarthritis (OA). This retrospective case study observed ten patients (13 knees) with severe knee OA who failed extensive conservative treatment and were treated with BMA injection using a novel, pure bone marrow aspiration (pBMA) technique. No adverse events were reported.

Surgical Outcomes of Os Trigonum Syndrome in Dancers: A Case Series.

Background: Management of ankle pain in dancers can be challenging because of the repetitive stress and complex demands placed on this region. Despite the prevalence of ankle injuries in this population, literature on surgical outcomes and return to dance is limited.

Purpose: To retrospectively evaluate the efficacy and functional outcomes after surgical excision of a symptomatic os trigonum in dancers.

Cellular prion protein: A co-receptor mediating neuronal cofilin-actin rod formation induced by β-amyloid and proinflammatory cytokines.

Increasing evidence suggests that proteins exhibiting "prion-like" behavior cause distinct neurodegenerative diseases, including inherited, sporadic and acquired types. The conversion of cellular prion protein (PrP(C)) to its infectious protease resistant counterpart (PrP(Res)) is the essential feature of prion diseases. However, PrP(C) also performs important functions in transmembrane signaling, especially in neurodegenerative processes.

Amyloid-β and proinflammatory cytokines utilize a prion protein-dependent pathway to activate NADPH oxidase and induce cofilin-actin rods in hippocampal neurons.

Neurites of neurons under acute or chronic stress form bundles of filaments (rods) containing 1∶1 cofilin∶actin, which impair transport and synaptic function. Rods contain disulfide cross-linked cofilin and are induced by treatments resulting in oxidative stress. Rods form rapidly (5-30 min) in >80% of cultured hippocampal or cortical neurons treated with excitotoxic levels of glutamate or energy depleted (hypoxia/ischemia or mitochondrial inhibitors).

A genetically encoded reporter for real-time imaging of cofilin-actin rods in living neurons.

Filament bundles (rods) of cofilin and actin (1:1) form in neurites of stressed neurons where they inhibit synaptic function. Live-cell imaging of rod formation is hampered by the fact that overexpression of a chimera of wild type cofilin with a fluorescent protein causes formation of spontaneous and persistent rods, which is exacerbated by the photostress of imaging. The study of rod induction in living cells calls for a rod reporter that does not cause spontaneous rods.