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.
Targeting tangles of tau protein in mice with Alzheimer's-like symptoms has reversed their brain damage, halting memory loss and extending their lives. Clumps of two types of sticky protein build up in the brains of people with Alzheimer's disease: beta-amyloid plaques, and tangles of tau. While many attempts to develop drugs to treat Alzheimer's have targeted beta-amyloid, tau protein tangles have long been suspected to play a role in memory loss. "Tau is what correlates with memory problems, so one hypothesis is that lowering tau could be beneficial," says Tim Miller of Washington University in St Louis, Missouri. Now Miller's team has purged tau tangles from the brains of Alzheimer's-like mice for the first time.
Signs of Alzheimer's disease have been found in the brains of chimpanzees for the first time. Researchers say it is unclear whether the characteristic'plaques and tangles' they found cause dementia in the animals. The team says the Alzheimer's signs were more prominent in older chimps, just like in humans, and that their findings could help develop new drugs for the disease. Signs of Alzheimer's disease have been found in the brains of chimpanzees (file photo) for the first time. Researchers say it is unclear whether the characteristic'plaques and tangles' they found cause dementia in the animals Alzheimer's disease is the most common cause of dementia.
RESISTANCE isn't futile, especially when it comes to Alzheimer's. Some people's brains can withstand the ravages of the disease by elongating the connections between brain cells – a process that seems to counter mental decline. Now we need to understand why some brains can respond to the disease in this way and to see if the effect can be enhanced with medicines or lifestyle changes. Alzheimer's disease, which causes memory loss and confusion, is the most common form of dementia. The condition is characterised by a build-up of a protein called beta-amyloid, which forms plaques between brain cells, and tangles of another protein called tau inside the cells.
Scientists have discovered a way of counteracting the proteins that cause Alzheimer's-like symptoms including memory loss. Whereas other treatments have focused on beta-amyloid clumps (which the University of Michigan recently discovered how to "fingerprint"), researchers at Washington University in St. Louis, Missouri focus on tau protein tangles. Specifically, the genes that produce them. By injecting mice with bits of antisense oligonucleotides -- RNA -- four times a month, tau levels dropped, existing tangles were seemingly obliterated and the protein stopped spreading through the brains of older mice. It's worth noting that the rodents had been genetically engineered to have Alzheimer's-like symptoms at the experiment's outset.