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Mycobacterium leprae, the bacterium that causes leprosy, causes the breakdown of myelin. This breakdown is now shown to occur through the ErbB2 receptor, a process that can be blocked by Herceptin and kinase inhibitors (pages 961–966).
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.
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).
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.
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.