amyloid beta tagged posts

What is the earliest spark that ignites the memory-robbing march of Alzheimer’s disease? Why do some people with Alzheimer’s-like changes in the brain never go on to develop dementia? These questions have bedeviled neuroscientists for decades.

Now, a team of researchers at Harvard Medical School may have found an answer: lithium deficiency in the brain.

The work, published in Nature, shows for the first time that lithium occurs naturally in the brain, shields it from ...

The therapy—developed at the University of Nebraska Medical Center (UNMC)—relies on both the immune system to fight key aspects of Alzheimer’s, plus modified cells that zero in on the brain protein plaques that are a hallmark of the disease.

In patients with Alzheimer’s, amyloid-beta protein forms plaques that prevent nerve cells from signaling each other. One theory is that this might cause irreversible memory loss and behavior changes characteristic of Alzheimer’s disease.

The new study was recently published in the journal Molecular Neurodegeneration. Researchers used genetically modified immune-controlling cells called Tregs to target amyloid-beta.

When the UNMC te...

Cholesterol manufactured in the brain appears to play a key role in the development of Alzheimer’s disease, new research indicates.

Scientists from the University of Virginia School of Medicine and their collaborators found that cholesterol produced by astrocytes is required for controlling the production of amyloid beta, a sticky protein that builds up in the brains of patients with Alzheimer’s. The protein accumulates into insoluble plaques that are a hallmark of the disease. Many efforts have targeted these plaques in the hope that removing or preventing them could treat or prevent Alzheimer’s.

The new findings offer important insights into how and why the plaques for...

Researchers have developed synthetic peptides that target and inhibit the small, toxic protein aggregates that are thought to trigger Alzheimer’s disease. Neurons in the human brain make a protein called amyloid beta. Such proteins on their own, called monomers of amyloid beta, perform important tasks for neurons. But in the brains of people with Alzheimer’s disease, amyloid beta monomers have abandoned their jobs and joined together. First, they form oligomers – small clumps of up to a dozen proteins – then longer strands and finally large deposits called plaques...