A new study published this month in Nature marks a key milestone in Alzheimer's research. It demonstrates the first complete model of a tau filament, a protein structure found in the brain cells of Alzheimer's patients and thought to be the cause of the neurodegenerative disease. Many scientists believe that tau proteins are the molecular building blocks of Alzheimer's disease. These tangles are thought to inhibit cell communication, form lesions, and eventually cause the memory loss associated with Alzheimer's. Different arrangements of tau proteins, or "morphologies," can accompany different neurodegenerative diseases such Parkinson's.
Can you catch Alzheimer's disease? Fear has been growing that the illness might be capable of spreading via blood transfusions and surgical equipment, but it has been hard to find any evidence of this happening. Now a study has found that an Alzheimer's protein can spread between mice that share a blood supply, causing brain degeneration, and suggesting that the disease may transmissible in a similar way to Creutzfeldt-Jacob Disease (CJD). We already know from CJD that misfolded proteins can spread brain diseases. Variant CJD can spread through meat products or blood transfusions infected with so-called prion proteins, for example.
Alzheimer's disease may be prevented by stopping a crucial brain protein from turning rogue, a study in mice suggests. Tau protein has long been suspected to play a role in causing the condition. In healthy brains, tau is essential for normal cell functioning. But during Alzheimer's disease, the protein goes haywire, clumping together and becoming toxic. Eventually, tau forms large, twisted tangles, but it is thought that it is smaller clumps of this protein that damage the brain.
Certain antibodies may be able to remove Alzheimer's plaques from the brain, according to new research carried about in mice. As much as 20 years before the symptoms of Alzheimer's set in, people with the disease begin to develop amyloid beta plaques that build up in the brain and, scientists believe, interfere with neural signals to cause cognitive and memory losses. But researchers at Washington University School of Medicine have developed an antibody that can remove the proteins these plaques are made of altogether, according to their new research. Several recent clinical trials have tried to use antibodies to target the plaques, but none have gotten past these trial phases, and many treatments have come with unsustainable side effects. The new approach may offer a way around these side effects and stop Alzheimer's plaques before its heart-breaking symptoms begin, the researchers hope.
The root cause of Alzheimer's, a progressive disease that as of 2013 affects some 5 million Americans, is still not completely understood. Researchers know that hallmarks of the disease are tiny balls of plaque that accumulate in Alzheimer's patients' brains. But how and why they form was still pretty much a mystery. Now, researchers at Harvard University, made a surprising finding: Proteins in the brain leftover from fighting off common infections like from a virus or a bacteria, clump together and create the plaque that is ubiquitously found in Alzheimer's patients. The new research, published yesterday in the journal Science, could pave the way to more precise research on how to stop or prevent the disease.