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On page 835, Loukas and colleagues show that individuals resistant to schistosomal infection make immune responses to the schistosomal tetraspanin TSP2. In mice, the authors show that TSP2 is a promising antischistosomal vaccine candidate, reducing adult worm burdens and liver and fecal egg counts. The cover image shows paired adult-stage Schistosoma mansoni blood flukes. The larger male worm is carrying the female worm in his gynecophoral canal. This is a permanent state of mating and is how adult worms are usually found in vivo. Photo courtesy of Malcolm Jones, Queensland Institute of Medical Research, Australia.
An untested herbal product in South Africa is being touted as an effective AIDS treatment—with the full support of a local scientist. Natasha Bolognesi investigates.
Young children are particularly susceptible to seizures induced by high fever. Experiments in rats suggest that changes in brain pH might be to blame (pages 817–823).
Fungal cell-wall polymers are potent stimulators of immune responses. New findings reveal that fungi shield inflammatory cell-wall polysaccharides from immune recognition, a process that is disrupted by an antifungal compound.
Findings in mice suggest that treatment with VEGF inhibitors prompts the upregulation of erythropoietin (Epo), a powerful cytokine and regulator of blood cell development. Could Epo be dulling the therapeutic effects of VEGF inhibition?
Animal models of schizophrenia are incomplete, and human brain tissue has been difficult to study. Results from postmortem human tissue begin to overcome these hurdles and find a role for modulation of NMDA type glutamate receptors (pages 824–828).
A metagenomic analysis of the microbes in the human gut reveals their diversity and just how interdependent we are on them. Together with our microbes we are a human-bacterial superorganism with immense metabolic diversity and capacity.
Is there a conspiracy afoot to keep one theory dominant in Alzheimer disease research? Maybe not, but as Apoorva Mandavilli discovers, it may still be high time for new ideas.
Between lively banter and public debates, Virginia Lee and John Trojanowski have challenged Alzheimer disease researchers to look beyond the usual suspects. What's the secret of their success?
The promise of disease-modifying treatments for Alzheimer disease calls for biomarkers that enable early diagnosis. A new discovery shows how to visualize amyloid pathology in living Alzheimer patients.
Mobilizing the immune system may be a promising strategy to fight Alzheimer disease. A clinical trial has shed light on the therapeutic potential—and the pitfalls—of Aβ immunization.
How do Aβ levels increase in individuals with Alzheimer disease? Recent work suggests that some forms of neuronal activity can drive Aβ accumulation in the brain.
Plaques and tangles populate the brains of people with Alzheimer disease. A mouse model that contains both of these lesions is providing insights into how the proteins that make up these hallmarks of the disease interact.
Tau aggregates into insoluble tangles in the brains of individuals with Alzheimer disease. Recent work suggests that these tangles do not cause the cognitive decline that typifies the disease.
Aβ generation requires γ-secretase activity. Inhibition of γ-secretase may now be easier due to the recent identification of the four proteins that make up the γ-secretase complex.
In the same spirit as our metabolic syndrome focus, a close look at the papers that have had the most influence on the Alzheimer community, and an analysis of the relevant drug market and funding priorities.