The Funding section of the Research Article “Neural landscape is associated with functional outcomes in irradiated patients with oropharyngeal squamous cell carcinoma” by S. Islam et al. has been updated to include support for author Sahana Lothumalla from a CPRIT Research Training Award, CPRIT Training Program (RP210028).

TDP-43 aggregate seeds persist in mouse and human skeletal muscle independent of large TDP-43 inclusions.

A wearable osmotic microneedle patch with high loading capacity provides sustained drug delivery for 24 hours in small- and large-animal models.

Kidney stroma and immune cells interact during inflammation in childhood-onset lupus nephritis.

A study of the role of angiogenesis in the human brain aging uncovers sex-specific associations with structural and functional brain outcomes.

cAMP metabolic reprogramming triggers AMPK-dependent autophagy, promoting liver injury during long-term supercooling.

An mRNA-encoded, dominant-negative inhibitor of RUNX1 exhibits preclinical efficacy in models of ocular diseases.

In the Research Article “Nasal tau immunotherapy clears intracellular tau pathology and improves cognitive functions in aged tauopathy mice” by S. Gaikwad et al., an unintentional error was made in Fig. 3E where the synaptophysin bands were duplicated for NeuN bands. The correct NeuN bands have been incorporated in Fig. 3E along with their quantification in Fig. 3H. In the Results section, the text “Consistent with these findings, compared with IgG-ms–treated hTau mice, TTCM2-ms–treated hTau mice showed increased protein levels of neuronal markers, including PSD95, and synaptophysin, and neuronal nuclear protein (NeuN) in the hippocampus—the region associated with memory formation and cognitive functions (Fig. 3, E to H). Immunofluorescence microscopy also showed an increase in the number of NeuN-positive cells in the hippocampi of TTCM2-ms–treated hTau mice (fig. S2, A and B)” was corrected to “Compared with IgG-ms–treated hTau mice, TTCM2-ms–treated hTau mice showed a nonsignificant (PSD95, P = 0.0591) and significant (synaptophysin, P = 0.0054) increase in protein abundance of synaptic markers in the hippocampus—the region associated with memory formation and cognitive functions (Fig. 3, E to G). Neuronal nuclear protein (NeuN, P = 0.3026) protein was not increased (Fig. 3, E and H), but immunofluorescence microscopy showed an increase in the number of NeuN-positive cells in the hippocampi of TTCM2-ms–treated hTau mice (fig. S2, A and B).” The online PDF and HTML (full text) have been updated. These corrections do not affect the overall conclusions of the paper.

In the Research Article “An epoxide hydrolase inhibitor reduces neuroinflammation in a mouse model of Alzheimer’s disease” by A. Ghosh et al., there was a duplication error in Fig. 5C. The N-Tg TPPU images were the same as the N-Tg Veh images. The correct N-Tg TPPU images are now in Fig. 5C, and the conclusions and other data in the paper are not affected.

Low-dose oral ribonucleoside analog is efficacious in guinea pig models of lethal arenavirus disease when administered before and during peak fever.

CDK7 inhibitors reverse inflammatory macrophage phenotypes and show therapeutic promise in rheumatoid arthritis models and patient synovial cells.

Genipin rescues developmental and degenerative phenotypes of the peripheral neuropathy familial dysautonomia and enhances neuron regeneration.

Degradation or depletion of NIT2 drives chemoresistance in gastric cancer by promoting H3K14ac-mediated oxidative phosphorylation.

Blocking Roundabout signaling combats ocular neovascularization by preventing macrophage activation.

Vagal stimulation or inhibition of SUMOylation with TAK-981 ameliorates colitis in mouse models.

The NIH’s RECOVER Initiative aims to ease the suffering of those living with Long Covid.

Diverse mechanisms contribute to persistent symptoms after Lyme disease, and a holistic multidisciplinary approach is needed to optimize care.

Understanding postacute infection syndromes requires sex-specific research approaches.

A research agenda that studies Long Covid in the context of related conditions could transform our understanding of these disabling illnesses.

Understanding the drivers of pediatric Long Covid and MIS-C is essential for developing therapeutic interventions.