Proteins — tools of living cells — can’t do their job if they’re not in shape. Literally.
And a new study is the first to image the various stages of a protein’s undoing, which will lend valuable insight to treatment of diseases such as Alzheimer’s and Parkinson’s.
Those are just two of the diseases caused by proteins that are misfolded — their amino acid chains are not arranged correctly, resulting in a misshapen three-dimensional structure. When misfolded, these proteins don’t work and, in the case of diseases such as Alzheimer’s, gunk up the brain and eventually destroy nerve cells.
Understanding how proteins fold is crucial to developing ways to prevent and treat these diseases. Previous attempts to document the process have involved heat or chemicals, creating conditions under which the proteins quickly unraveled and thus limiting observation of the in-between states.
Thanks to NASA and emerging commercial space flight companies, there will likely be more astronauts in the future, and they’ll be traveling farther and more frequently into space. Space travel has known risks for bones, eyesight and other bodily systems, but a new study is the first to show that space travel could lead to Alzheimer’s disease l
ater in life.
Outside the protection of the Earth’s magnetic field, astronauts are exposed to cosmic radiation. These high-mass, highly-charged particles can penetrate solid objects—spaceships, astronauts and brains included.
Amyloid beta deposits in brain of Alzheimer’s patient.
What’s the News: A drug used to cure skin cancer is also a possible treatment for Alzheimer’s, according to a new study in Science. The drug not only reduced levels of amyloid beta—a protein whose elevated levels are a hallmark of the disease—but also reversed cognitive decline. In mice, dramatic effects were evident after just 72 hours.
A protein tangle in an Alzheimer’s-afflicted neuron
Exactly how Alzheimer’s disease proliferates through the brain, overtaking one region after another, has eluded scientists. As the disease progresses, tau—a malformed protein that forms snarls and tangles inside neurons—shows up in more and more brain areas. Researchers have wondered whether tau, and the disease, are working their way out from a single area of origin or mounting numerous, distinct attacks on vulnerable parts of the brain. Two new studies in mice provide strong support for the first idea: Tau seems to pass from affected cells to their neighbors, spreading much the same way a virus or bacteria infection would.
Artist’s rendering of a mitochondrian, the energy-producing
cellular structure affected by ARSACS
Scientists have pinpointed the cause of a rare, fatal neurodegenerative disorder called ARSACS, or autosomal recessive spastic ataxia of Charlevoix-Saguenay. The disease is due to defects in neuron’s mitochondria, the bit of biological machinery that generates energy for the cell—a structure known to be affected in Parkinson’s, Alzheimer’s, and other neurological diseases, as well.
ARSACS was first observed in the descendants of a small group of 17th century French settlers who made their homes near the Charlevoix and Saguenay rivers in what is now Quebec, and has since been seen worldwide. But its incidence remains unusually high in that particular French Canadian community, with 1 in 1,500 to 2,000 people developing ARSACS and 1 in 23 people unaffected genetic carriers of the disease.