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A new study from the Monell Center, the U.S. Department of Agriculture (USDA), and collaborating institutions reports a uniquely identifiable odor signature from mouse models of Alzheimer's disease. The odor signature appears in urine before significant development of Alzheimer-related brain pathology, suggesting that it may be possible to develop a non-invasive tool for early diagnosis of Alzheimer's disease.

For Collinge, this led to a worrying conclusion: that the plaques might have been transmitted, alongside the prions, in the injections of growth hormone-the first evidence that Alzheimer's could be transmitted from one person to another. If true, that could have far-reaching implications: the possibility that 'seeds' of the amyloid-β protein involved in Alzheimer's could be transferred during other procedures in which fluid or tissues from one person are introduced into another, such as blood transfusions, organ transplants and other common medical procedures.

Could it be that Alzheimer's disease stems from the toxic remnants of the brain's attempt to fight off infection? Provocative new research by a team of investigators at Harvard leads to this startling hypothesis, which could explain the origins of plaque, the mysterious hard little balls that pockmark the brains of people with Alzheimer's.

Some tiny clusters of brain cells grown in a lab dish are making big news at this week's Society for Neuroscience meeting in San Diego. Known as "minibrains," these rudimentary networks of cells are small enough to fit on the head of a pin, but already are providing researchers with insights into everything from early brain development to Down syndrome, Alzheimer's and Zika.

The research suggests that in mice with Alzheimer's disease certain immune cells that normally protect the brain begin abnormally to consume an important nutrient called arginine. By blocking this process using the drug difluoromethylornithine (DFMO), memory loss and a buildup of sticky proteins known as brain plaques were prevented.

By then, researchers had identified three genetic mutations that can be inherited and, if they are, cause a form of Alzheimer's called early onset because it strikes before age 65 and sometimes far earlier. Since 2004, Hornstein and all five of her siblings have been tested. Hornstein is the only one who doesn't carry PSEN1, one of the mutations.

"Now we have evidence that urinary odor signatures can be altered by changes in the brain characteristic of Alzheimer's disease," said Dr. Bruce Kimball, a chemical ecologist at the USDA National Wildlife Research Center, in a news release. "This finding may also have implications for other neurologic diseases."

For the second time in four months, researchers have reported autopsy results that suggest Alzheimer's disease might occasionally be transmitted to people during certain medical treatments-although scientists say that neither set of findings is conclusive. The latest autopsies, described in the Swiss Medical Weekly on January 26, were conducted on the brains of seven people who died of the rare, brain-wasting Creutzfeldt-Jakob disease (CJD). Decades before their deaths, the individuals had all received surgical grafts of dura mater-the membrane that covers the brain and spinal cord. These grafts had been prepared from human cadavers and were contaminated with the prion protein that causes CJD.

Researchers have pinpointed a catalytic trigger for the onset of Alzheimer's disease - when the fundamental structure of a protein molecule changes to cause a chain reaction that leads to the death of neurons in the brain.

More than 40 million people worldwide suffer from Alzheimer's disease, and that number is expected to increase drastically in the coming years. But no real progress has been made in the fight against the disease since its classification more than 100 years ago. Scientist Samuel Cohen shares a new breakthrough in Alzheimer's research from his lab as well as a message of hope. "Alzheimer's is a disease," Cohen says, "and we can cure it."

A promising new natural treatment for Alzheimer's disease is moving toward clinical trials. This will be a major step forward as there is nothing on the market that slows the progression of Alzheimer's; natural products chemist has patented a botanical compound, withanamides.

Researchers at the University of Melbourne in Australia followed 144 older people who had mild cognitive impairment for seven years. To gauge how much iron was in their brains, they measured ferritin, a protein that binds to the metal, in their cerebrospinal fluid. For every nanogram per millilitre people had at the start of the study, they were diagnosed with Alzheimer's on average three months earlier. The team also found that the biggest risk gene for Alzheimer's, ApoE4, was strongly linked with higher iron, suggesting this is why carrying the gene makes you more vulnerable.

In the war against aging, Alzheimer's disease is one of our biggest foes. But while we seem to be losing the battle, we may finally have found some chinks in its armor. The most common form of dementia already affects an estimated 5.2 million Americans and 45 million others worldwide, and these numbers are projected to triple by the year 2050 as the baby boomer generation reaches retirement.