Sentences with phrase «of amyloid»

The study noted increased levels of amyloid beta in a large group of patients with no hereditary risk gene.

It also showed that their immune cells were increasing noticeably in both size and activity, suggesting that these cells were cleaning up the high levels of amyloid proteins.

The researchers built a protein structure, called «alpha sheet,» that complements the toxic structure of amyloid proteins that they discovered in computer simulations.

This accumulation of amyloid beta causes the neurons to die, but until now the underlying mechanism remained a mystery.

This work may also help identify which form of amyloid - beta is the most toxic.

The compound failed to reduce the amount of amyloid in the mice's brains.

Regardless, simply through the demonstrated clearance of amyloid in human patients this is a big step forward for the field.

On one front, they worked with a mouse model genetically engineered to stop the production of amyloid - beta.

Medical or surgical treatment of the underlying chronic infection or inflammatory disease can slow or stop the progression of this type of amyloid.

The molecular structure of an amyloid protein can be only slightly different from a normal protein and can transform to a toxic state fairly easily, which is why amyloid diseases are so prevalent.

Only one patient, he said, did not have any signs of amyloid.

For drug companies, it means that the effects of amyloid - reducing drugs, of which there are many, can finally be studied in living patients: do they really work?

For researchers, it means that the core question of how the quantity of amyloid relates to cognitive impairment can finally begin to be answered.

But billions of dollars have poured into large - scale clinical trials of amyloid - lowering therapies that so far have failed.

The paper builds upon techniques used in an earlier study of amyloid beta proteins.

Those with the memory dementia had the same amount of amyloid on the left and right side of the brain.

The nature of amyloid disease makes it difficult to qualify for most life insurance policies because amyloid disease can affect so many different parts of the body in may «unpredictable» ways.

The use of amyloid - reactive antibodies would represent a novel approach in the treatment of individuals with this invariably fatal disorder.

The researchers conducted a series of experiments to see if they could replicate the phenomenon of amyloid beta clearance absent brain inflammation.

They have devised a test that measures the manufacture and disposal of amyloid - beta in the brain.

The study also reveals that an accumulation of amyloid beta inside neurons is toxic for the cells.

One study noted that mice fed diets high in aluminum showed increased levels of amyloid.

PET imaging can quantify the amount of amyloid and also show where it is in a person's brain.

IN BRIEF Scientists have new evidence that suggests that THC inhibits the formation of amyloid plaques by blocking the enzyme in the brain that produces them.

In persons with the disease, the formation of amyloid plaque aggregates, a process known to cause the onset of Alzheimer's disease, prevents the Crtc1 protein from functioning correctly.

Amyloid beta (Aβ) is a small peptide molecule generated from cleavage of amyloid precursor protein (APP).

The presence of amyloid plaque in the brain precedes Alzheimer's and can be detected by costly positron emission tomography (PET) scans, which are not usually covered by insurance.

Alzheimer's disease results from the deposition of amyloid plaques in the brain.

To determine the occurrence of Aβ peptides in the rat CSF we resorted to Aβ immunoprecipiation followed by MALDI - MS analysis, before and after the formation of amyloid deposits.

Alzheimer's is sometimes called Diabetes type 3 because insulin resistance may also cause the build up of amyloid plaques.

Recent research also has illuminated how the deadly cascade that leads to brain atrophy is set in motion: The buildup of amyloid plaques, working in tandem with certain gene mutations, sparks the formation of the renegade tau proteins.

The method is proven to detect the large clumps of amyloid beta in Alzheimer's disease patients» brains but less is known about whether it is an accurate label for the smaller clumps that can occur in healthy people.

In a 2016 study from JAMA Psychiatry, senior citizens whose brain scans showed the development of amyloid protein clusters were 7.5 times more likely to be classified as lonely than those whose scans were negative.

A role for Aβ - mediated toxicity is further supported by the fact that cognitive deficits progressed according with the incremental accumulation of the amyloid pathology, in particular, increased levels of soluble Aβ42 (Figure 8a).

Fat soluble antioxidants such as vitamin E's and A's may help prevent lipid membrane oxidation and methoxylated flavonoids (flavonoids [plant antioxidants] with free hydroxyl groups are much more easily disposed of by the liver and kidneys and have trouble entering the brain, and usually have very little biological effect) may also prevent damage and prevent the toxic aggregation of amyloid beta peptides.

«It is the best source of fresh human brain tissue available at the moment,» says Jucker, who plans to scrutinize it carefully under the microscope for anything that might resemble tiny clumps or seeds of amyloid - β.

Like humans with AD, hAPP mice have elevated levels of amyloid β (Aβ) peptides in the brain, network and synaptic dysfunction, and amyloid plaques (9).

Aggregates of amyloid proteins form and deposit in different tissues which can affect the normal function.

Aβ peptides, initially discovered extracellularly, are the core component of amyloid plaques in AD and DS brains [54, 55].

This work confirms what Tanzi and Moir proposed few years about antimicrobial activity of amyloid β.

Researchers have determined how omega - 3 fatty acids and vitamin D3 can boost the immune system's capability to remove the brain of amyloid plaques, a hallmark of Alzheimer's disease.

As notable was the relative absence of amyloid plaques in these spots.

InAlzheimer's disease, however, a biochemical «switch» associated withthe cleavage of the amyloid peptide seems to lock Alzheimer's brains into areverse gear of forgetting alone.

The study sheds light on the metabolism of amyloid beta, and its role in neurodegeneration and memory loss.

«This discovery is very important, as the elimination of amyloid plaques by the brain cells themselves is one of the key strategies under development as a cure for Alzheimer's disease.