A study, performed in mice and utilizing post-mortem samples of brains from patients with Alzheimer’s disease, found that a single event of a moderate-to-severe traumatic brain injury (TBI) can disrupt proteins that regulate an enzyme associated with Alzheimer’s. The paper, published in The Journal of Neuroscience, identifies the complex mechanisms that result in a rapid and robust post-injury elevation of the enzyme, BACE1, in the brain. These results may lead to the development of a drug treatment that targets this mechanism to slow the progression of Alzheimer’s disease.
A previously unrecognized system that drains waste from the brain at a rapid clip has been discovered by neuroscientists at the University of Rochester Medical Center and dubbed the glymphatic system.
Researchers discovered a way to stimulate the brain's natural defense mechanisms in mice with Alzheimer's disease symptoms. This major breakthrough opens the door to the development of a treatment for Alzheimer's disease and a vaccine to prevent the illness.
Using transgenic mice with specially designed gene fragments derived from bacteria and human cells, researchers were able to control the production of amyloid beta peptide using antibiotics.
Researchers have developed an experimental drug, NitroMemantine, to boost brain synapses lost in Alzheimer's disease. The drug stops the destructive cascade of brain changes which destroy connections between neurons that leads to memory loss and cognitive decline.
Researchers discover by looking at amyloid-beta and tau independently that the interaction between the proteins could be the key to the cognitive decline associated with Alzheimer's disease. As the interaction between the two proteins increased, the progression of Alzheimer's worsened.
Researchers discover a way to traverse the blood-brain barrier and retinal-blood barrier to deliver a molecule which degrades the main component of Alzheimer's plaques.
Researchers transform iPSCs into neurons to test the efficacy of drugs to treat Alzheimer's disease.
Researchers have discovered a potential drug which can force BACE into different parts of a cell, reducing its ability to produce amyloid beta.