Alzheimer's researchers at Harvard for the first time are scanning the brains of healthy patients for the presence of a hallmark protein called tau, which forms toxic tangles of nerve fibers associated with the fatal disease.

The new scans are part of a large clinical trial called Anti-Amyloid Treatment in Asymptomatic Alzheimer's or A4, the first designed to identify and treat patients in the earliest stages of Alzheimer's, before memory loss begins.

Scientists are unraveling a mystery behind a fairly common disease that leads to heart failure: Why do some people with a key mutated gene fall ill while others stay healthy?

Researchers tested more than 5,200 people to tease apart when mutations really are harmful or are just bystanders. The work could help in screening families prone to heart failure but also has broader implications as more people undergo genetic tests that can turn up unnecessarily worrying results.

For the first time, and to the astonishment of many of their colleagues, researchers created what they call Alzheimer’s in a Dish — a petri dish with human brain cells that develop the telltale structures of Alzheimer’s disease. In doing so, they resolved a longstanding problem of how to study Alzheimer’s and search for drugs to treat it; the best they had until now were mice that developed an imperfect form of the disease.

The discovery of the first chemical to prevent the death of brain tissue in a neurodegenerative disease has been hailed as the "turning point" in the fight against Alzheimer's disease.

More work is needed to develop a drug that could be taken by patients.

But scientists say a resulting medicine could treat Alzheimer's, Parkinson's, Huntington's and other diseases.

In tests on mice, the Medical Research Council showed all brain cell death from prion disease could be prevented.

Based on early studies in animals and humans, researchers report Wednesday that there may be reason to think that mental illnesses such as depression could be treated with gene therapy.

Severe depression afflicts at least one in 15 adults nationwide. The Science Translational Medicine journal study in mice and human brain cells finds a deficit of a protein called "p11" may play a role in depression and that fixing the genes that produce those proteins could affect the course of depression.

"Psychological disorders, such as depression, are increasingly viewed as brain disorders," says study author Michael Kaplitt of the Weill Cornell Medical College in New York. "If true, we may be able to help some patients by bringing levels of this protein back to normal."

Genetic markers that could help highlight who is at risk of developing Alzheimer's disease have been identified by US scientists.

The research in Neuron identifies mutations that affect the build-up of certain proteins in the brain.

High levels of these tau proteins increase the chance of having the disease.

UK experts said the study could help understand the changes that occur in the brains of Alzheimer's patients.

In a leap forward in understanding the basic science of one of the most lethal cancers, two groups of researchers have found mutations in most melanomas that are unlike any they have seen before in cancer. The changes are in regions that control genes, not in the genes themselves. The mutations are exactly the type caused by exposure to ultraviolet light, indicating they might be among the first DNA changes in a cell’s path to melanoma.

A gene that helps the body convert that big plate of holiday cookies you just polished off into fat could provide a new target for potential treatments for fatty liver disease, diabetes and obesity.

Researchers at the University of California, Berkeley, are unlocking the molecular mechanisms of how our body converts dietary carbohydrates into fat, and as part of that research, they found that a gene with the catchy name BAF60c contributes to fatty liver, or steatosis.

In the study, to be published online Dec. 6 in the journal Molecular Cell, the researchers found that mice that have had the BAF60c gene disabled did not convert carbohydrates to fat, despite eating a high-carb diet.

Herpesviruses are master manipulators. Once inside the body, they can turn healthy cells into virus factories within a few short hours.

“These tiny organisms come with few of their own resources, yet they’re exquisitely adept at taking control of their far more powerful host,” says Britt Glaunsinger.