Tau proteins are microtubule-associated proteins found in neurons in the brain.
Researchers at Gladstone Institutes have discovered that a rare genetic variant known as the "Christchurch mutation" can block detrimental effects of apolipoprotein E4, the best-established risk factor for the most common form of Alzheimer's disease.
If you've ever belly-flopped into a pool, then you know: water can be surprisingly hard if you hit it at the wrong angle. But many species of kingfishers dive headfirst into water to catch their fishy prey.
Alternative splicing, a clever way a cell generates many different variations of messenger RNAs -; single-stranded RNAs involved in protein synthesis -; and proteins from the same stretch of DNA, plays an important role in molecular biology.
Dr Catherine Mummery, a consultant neurologist at UCL Queen Square Institute of Neurology & the National Hospital for Neurology and Neurosurgery, has led a trial. The trial signifies for the first time that a “gene silencing” method has been taken in Alzheimer’s and dementia disease.
MIT neuroscientists have found a way to reverse neurodegeneration and other symptoms of Alzheimer's disease by interfering with an enzyme that is typically overactive in the brains of Alzheimer's patients.
Of all the known genetic risk factors for late-onset Alzheimer's disease, the strongest is a gene for the protein called ApoE4.
Scientists are not yet clear on how the tau protein changes from a benign protein essential for normal function in our brains into the toxic neurofibrillary tangles that are a signature of Alzheimer's and other neurodegenerative diseases.
The loss of functional neurons in the brain is a characteristic of Alzheimer’s disease. What, on the other hand, is the source of this loss?
Take a cell-deep tour of a brain afflicted with Alzheimer's disease, and you will find minuscule clumps of protein that seem suspicious. Ever since the 1980s, when neuroscientists began identifying these protein tangles, researchers have discovered that other brain diseases have their own tangled-protein signatures.
According to a recent research, enhancing the expression of one gene in cells that help the brain’s neurons, shields neurons in mouse models of Alzheimer’s disease.
Scientists from the Icahn School of Medicine at Mount Sinai published the first of its kind research in the field of addiction genetics employing a multi-omics method to offer a huge list of causal candidate genes linked with alcohol consumption and alcohol use disorder (AUD).
Scientists have found that a particular chemical feature of a crucial protein may cause it to build up in the brain and lead to various disorders.
Studies conducted on patients’ tissue as well as mini-brains created from stem cells have provided a better insight into Alzheimer’s disease.
A genetic engineering approach has helped scientists to drastically decrease the levels of tau protein.
Research into Alzheimer's disease has long focused on understanding the role of two key proteins, beta amyloid and the tau protein. Found in tangles in patients' brain tissue, a pathological form of the tau protein contributes to propagating the disease in the brain.
A new, rare genetic form of dementia has been discovered by a team of Penn Medicine researchers. This discovery also sheds light on a new pathway that leads to protein build up in the brain -- which causes this newly discovered disease, as well as related neurodegenerative diseases like Alzheimer's Disease -- that could be targeted for new therapies. The study was published today in Science.