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In science, as in fashion, it pays to have a healthy irreverence for the trends. John Hardy has helped outfit clashing views about the origins of Alzheimer disease, but has always managed to steer clear of cliché.
As antidepressants come under scrutiny for their suspected link to suicide, skeptics question how safe and effective the 'miracle drugs' really are. But as Apoorva Mandavilli discovers, the prospects for a better alternative are downright depressing.
Vascular endothelial growth factor (VEGF), known as a mediator of blood vessel formation and permeability, now gains an essential position in allergic lung responses (pages 1095–1103).
Clinical transplants of hematopoietic stem cells have a large spectrum of therapeutic applications, but these can be limited by insufficient stem cell numbers and the current inability to expand them in vitro. Inactivation of an enzyme that impedes stem-cell homing to the bone marrow may offer a simple alternative.
The reduction in blood flow to the brain that causes a stroke triggers a deadly cascade of events that can lead to brain death. Studies in mice show that activation of an adenosine receptor on neutrophils invading the brain from the blood contribute to the damage (pages 1081–1087).
After primary Leishmania major infection, two populations of CD4+ T cells, termed 'effector' and 'central memory' T cells, are generated. Work in mice shows that both populations can mediate protection against subsequent infection, and that persistent infection keeps the effector response robust (pages 1104–1110).
Antibodies that stimulate T-cell costimulatory receptors block progression of established rheumatoid arthritis in a mouse model. No existing therapy arrests disease to such an extent (pages 1088–1094).
Overeating can lead to the development of insulin resistance and diabetes. A component of the mTOR nutrient signaling pathway now bridges the mechanistic gap between obesity and insulin resistance.
The inability of axons to regenerate in the injured spinal cord leads to permanent paralysis. The discovery and cloning of Nogo, one of the axon growth inhibitors in myelin, was a major step in understanding the failure of axon regeneration. Subsequent work identifying the Nogo receptor and associated signaling factors has renewed optimism for the development of treatments to ease the brakes on axon regeneration after spinal cord trauma.