Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
The first examination of a brain from a patient enrolled in a halted clinical trial for an Alzheimer disease (AD) vaccine reveals striking—and potentially dangerous—effects.
“The disease leads to death, and it does so within a short period of two to three years...The disease must, from our present experience, be considered from the onset not only as incurable but also as deadly.”—Moritz Kaposi, 1872
Research on an inherited form of cardiac arrhythmia has now homed in on the elusive trigger of electrical instability in the heart. Aberrant calcium regulation emerges as a strong candidate.
Two studies link signaling of the anticoagulant thrombomodulin–protein C pathway to successful implantation during pregnancy and protection from ischemic brain injury. The data call for a reassessment of the causes of pre-eclampsia, and also provide hope for a new type of stroke therapy (pages 331–337 and 338–342).
Feedback from differentiated cells may keep precursor cells in check, controlling proliferation and differentiation. One such mechanism is now shown to control neuron numbers in the olfactory epithelium.
The power of small RNAs to shut down specific gene activities has now been brought to bear on an animal model of hepatitis. Mice infused with an siRNA against a cell death receptor recover liver function after experimentally induced injury (pages 347–351).
Coaxing T cells into attacking tumors is an intelligent approach to cancer therapy that has met with limited success. A new study applies some very persuasive techniques (pages 279–286).
Kaposi sarcoma herpesvirus (KSHV) seems to exploit almost every known cancer pathway to promote tumorigenesis. Activation of the canonical Wnt–β-catenin pathway can now be added to its list of conquests (pages 300–306).
Nervous system cells surrounding insulin-producing cells in the pancreas are destroyed early in the development type 1 diabetes, reveals a new study. The findings broaden our ideas of the disease process and may lead to new prediagnostic markers and therapies (pages 198–205).
As the major activator of HIV transcription, Tat drives viral gene expression. Now, it seems that in dendritic cells Tat also regulates the expression of chemokines that promote lymphocyte and monocyte migration. By recruiting susceptible host cells to infected dendritic cells, Tat may facilitate HIV dissemination (pages 191–197).
Efficiently defending a host from repeat invasions by the same pathogen requires a lasting B-cell response. The identification of a molecule that keeps B cells prepared may help to explain some immune disorders and lead to improved vaccines.
Mixing lymph and blood in the vascular system can have dramatic effects on health, but how these two systems remain separate has been unclear. Now, it seems that two signaling molecules expressed mainly in hematopoietic cells segregate lymphatic and blood vessels during development and tissue revascularization.
Staying awake and alert requires hypothalamic neurons that secrete the neurotransmitter hypocretin, also called orexin. A new study shows that feedback loops of hypocretin and glutamate neurons orchestrate the neuronal output that regulates arousal.
New data implicate the LXRs, a class of nuclear hormone receptors, in reducing inflammation. When activated, these receptors ease inflammation in three mouse models. The results are relevant to atherosclerosis, Alzheimer disease, sepsis and other inflammatory disorders (pages 213–219).
A vaccine that is able to work as a treatment for HIV-infected patients has been an elusive goal. Now experiments on macaques suggest that injections of modified dendritic cells might boost immunity to hold back disease progression (pages 27–32).
