Sentences with phrase «beta plaques form»

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After the night with disrupted sleep, the researchers found people had higher levels of beta - amyloid proteins, the proteins that clump together and form the plaque found in Alzheimer's - afflicted brains, in the volunteers» spinal fluid.

IRON overload may accelerate Alzheimer's disease, according to research that also reveals the role of beta - amyloid precursor protein (APP), which forms plaques in affected brains.

In rats and tissue cultures of human nerve cells, these «beta sheet breakers» not only prevent amyloid plaques from forming, but also dissolve existing plaques.

The UCLA researchers, led by David Eisenberg, director of the UCLA - Department of Energy Institute of Genomics and Proteomics and a Howard Hughes Medical Institute investigator, report the first application of this technique in the search for molecular compounds that bind to and inhibit the activity of the amyloid - beta protein responsible for forming dangerous plaques in the brain of patients with Alzheimer's and other degenerative diseases.

These plaques, which are believed to cause the dementia associated with the disease, are made up of tangles of amyloid beta (Aβ), a protein that is found in soluble form in healthy individuals.

In Alzheimer's disease, an abnormal protein called amyloid beta begin s to appear on the neurons, forming plaques and compromising brain activity.

We don't fully understand what it means, but it may combine with other forms of amyloid - beta to stimulate plaque formation.»

They may pave the way for better diagnosis of neurodegenerative diseases, such as Alzheimer's disease, in which plaque forms from the amyloid beta or tau proteins.

A definitive diagnosis of Alzheimer's includes dementia and two distortions in the brain: amyloid plaques, sticky accumulations of misfolded pieces of protein known as amyloid beta peptides; and neurofibrillary tangles, formed when proteins called tau clump into long filaments that twist around each other like ribbons.

Previously, researchers have shown that treating cells with neuregulin - 1, for example, dampens levels of amyloid precursor protein, a molecule that generates amyloid beta, which aggregate and form plaques in the brains of Alzheimer's patients.

The disease is largely attributed to an abnormal buildup of proteins, which can form amyloid beta plaques and tangles in the brain that trigger inflammation and result in the loss of brain connections called synapses, the effect most strongly associated with cognitive decline.

To better explain this finding, the team turned to yet another protein, amyloid beta — which in its soluble form, before building up and hardening into plaques, has already been found to be toxic to the synapses.

The drug also appeared to reduce the amount of the protein amyloid beta (which forms toxic plaques in the brains of Alzheimer's patients) by decreasing the levels of metals such as zinc and copper.

But recent research indicates that smaller, soluble forms of amyloid - beta — rather than the solid plaques — are responsible for the death of nerve cells that leads to cognitive decline.

The plaques are aggregations of fibers that form when individual amyloid - beta peptides begin sticking together abnormally.

The test measures the relative amounts of different forms of beta - amyloid in blood to see whether plaques are likely to be building in the brain.

It binds to the beta - amyloid plaques that characterize Alzheimer's disease, helping to measure the extent to which plaques have formed in different brain regions.

And more direct evidence for its role in making plaques is the fact that cells produced more beta amyloid if they contained certain mutated forms of nicastrin, the researchers report in the 7 September issue of Nature.

Amyloid beta compounds clump together and form the brain plaques that characterize Alzheimer's disease.

Jankowsky and her colleagues have previously shown that combining two complementary treatments to reduce amyloid - beta not only curbs further plaque growth, but also helps to clear plaques that have already formed.

Beta - amyloid peptide 1 - 42 and beta - amyloid peptide 1 - 40 are the two main forms that appear in senile plaqBeta - amyloid peptide 1 - 42 and beta - amyloid peptide 1 - 40 are the two main forms that appear in senile plaqbeta - amyloid peptide 1 - 40 are the two main forms that appear in senile plaques.

Elongated fibres (fibrils) of the beta - amyloid protein form the typical senile plaques present in the brains of patients with Alzheimer's disease.

The nature of those plaques finally came into focus in 1984, when George Glenner, a research scientist at the University of California, San Diego, identified the peptide called amyloid - beta and hypothesized that Alzheimer's was caused by «amyloidosis» of the brain, a process in which insoluble forms of an amyloid protein accumulate.

Glenner's research eventually morphed into the «amyloid cascade hypothesis,» which says that the formation of amyloid - beta plaques leads to tangled forms of another protein, tau, and ultimately to inflammation in the brain.

Golde notes that while normal concentrations of amyloid - beta in human brains can aggregate to form plaques, that doesn't happen in the lab without help.

The next step, he says, will be to use his team's three - dimensional «Alzheimer's in a dish» model to see whether microbes can induce amyloid - beta plaques to form in human brain tissue, and then whether those plaques lead to tau tangles and inflammation.

Amyloid - beta then forms plaques to fight off the invaders, and that triggers the rest of the disease process.

The mutations take place on a protein that serves as the precursor for amyloid beta, a different protein that forms plaques in the brains of individuals afflicted by Alzheimer's disease.

But if additional studies confirm amyloid - beta's antimicrobial function — and the role of infections in causing amyloid - beta plaques to form — this model might open up new ways of thinking about Alzheimer's therapies.

Alzheimer's disease, the most common form of dementia, is characterized by the accumulation of plaques (composed of amyloid - beta protein) and fibrous tangles (composed of abnormal tau) in brain cells called neurons.

Beta amyloid plaques can form when particular fragments of the amyloid precursor protein (APP), cleaved by the enzyme gamma secretase, clump together.

Researchers have shown that clearance of the substance amyloid - beta that forms plaques is impaired in individuals with Alzheimer's.

Researchers feel that the most damaging form of amyloid beta may be groups of a few pieces that block these nerve synapses rather than the large plaques.

Amelyoid beta is a plaque forming protein thought to be a result of brain inflammation and neuronal death.

Studies have indicated that lithium may inhibit the build up of beta - amyloid and tau proteins, the main components of the plaques and tangles that form in the brain with Alzheimer's disease.