Sentences with phrase «of human amyloid»

Overexpression of human amyloid - β protein precursor (AβPP) within the gut was assessed by qPCR and IHC; fecal microbiome analysis was conducted by 16SrRNA quantitation of selected phyla and species.

Young mice that expressed high levels of human amyloid - β (but did not have pathological plaques) infected in the brain with Salmonella typhimurium were more likely to survive the infection compared to wild - type mice that did not express the peptide, Tanzi, Moir, and their colleagues found.

C. elegans expressing a modified form of human amyloid - β survived three or four more days following infection in the gut with Candida albicans, compared to wild - type worms that did not express the peptide.

Not exact matches

Four clones were isolated from an adult human brain complementary DNA library with an oligonucleotide probe corresponding to the first 20 amino acids of the beta peptide of brain amyloid from Alzheimer's disease.

Beta - amyloid protein is found in the brains of mice and humans.

The newly identified gene affects accumulation of amyloid - beta, a protein believed to be one of the main causes of the damage that underpins this brain disease in humans.

Specifically, rodents genetically modified to express human amyloid precursor protein (hAPP), which can lead to the debilitating plaques that form in the brains of Alzheimer's patients, seem to struggle to find the hidden platform relative to their healthy peers.

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.

Scientists attribute more than 20 human diseases to the formation of amyloid fibrils.

The sequences of amyloid - β and tau proteins are identical in humans and chimps.

The result, says Flajolet, is a brain that is hard and transparent, almost «like glass,» which allowed the researchers to see the amyloid plaques in full detail and in 3D, in a full mouse brain hemisphere, as well as in small blocks of human brain tissue.

It not only prevented the buildup of amyloid beta (Aß), a sticky protein linked to Alzheimer's, but it also does not appear to produce the dangerous side effects of earlier versions tested in humans.

First, the researchers used mice that had been genetically modified to produce excess amounts of the human version of ß amyloid — a common Alzheimer's disease model.

AMYLOID plaques are a sign of Alzheimer's disease, and bad news for humans.

But with the human cells, Young - Pearse and her team, including postdoctoral fellow and study first author, Christina Muratore, could demonstrate that preventing amyloid - beta imbalances reduced levels of distorted tau.

UBC Psychiatry Professor Dr. Weihong Song and Neurology Professor Yan - Jiang Wang at Third Military Medical University in Chongqing attached normal mice, which don't naturally develop Alzheimer's disease, to mice modified to carry a mutant human gene that produces high levels of a protein called amyloid - beta.

To corroborate the findings, the researchers also developed a novel mouse model that was deficient for autophagy specifically in beta cells with expression of the human form of islet amyloid polypeptide.

Caleb Finch, a neurobiologist who studies Alzheimer's at the University of Southern California in Los Angeles, points out that in human brains, amyloid plaques are associated with neuron death, which wasn't measured in the new study.

While acute sleep deprivation is known to elevate brain beta - amyloid levels in mice, less is known about the impact of sleep deprivation on beta - amyloid accumulation in the human brain.

Similar to humans, increasingly larger volumes of amyloid beta plaques and blood vessels were found with greater age.

«The presence of amyloid and tau pathology in aged chimpanzees indicates these Alzheimer's disease lesions are not specific to the human brain as generally believed,» Hof continued.

In a key memory experiment in the study, mice brains were injected with beta - amyloid, whose increase is one hallmark of Alzheimer's in humans.

A team of scientists at Sweden's Linköping University have developed a molecular probe that can detect an array of different amyloid deposits in several human tissues.

«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.

Importantly, intraperitoneal inoculation of pancreatic homogenates containing IAPP aggregates into transgenic mice expressing human IAPP dramatically accelerates IAPP amyloid deposition, which was accompanied by clinical abnormalities typical of T2D, including hyperglycemia, impaired glucose tolerance, and a substantial reduction on β cell number and mass.

Autopsy studies in humans suggest that islet amyloid is associated with the loss of β cells mass (Clark et al., 1988).

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).

IT TURNS OUT THAT the sequence of amino acids that makes up the amyloid - beta protein isn't unique to humans.

His laboratory and their collaborators have also identified human amyloid fibrils in semen that enhance the ability of HIV to infect new cells — a discovery that one day could help stem the global spread of this deadly pathogen.

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.

By 2008, when Moir stumbled on the parallels between amyloid - beta and LL - 37, Tanzi had discovered additional genes associated with Alzheimer's that were also related to innate immunity, the part of the human immune system that is shared with worms, flies, spiders and other primitive creatures.

Amyloid fibers are best known as the plaque that gunks up neurons in people with neurodegenerative illnesses such as Alzheimer's and Creutzfeldt - Jacob disease — the human analog of mad cow disease.

CAMBRIDGE, Mass. (June 8, 2005)-- Amyloid fibers are best known as the plaque that gunks up neurons in people with neurodegenerative illnesses such as Alzheimer's and Creutzfeldt - Jacob disease — the human analog of mad cow disease.

One of the hallmarks of Parkinson's disease is amyloid formation of a particular human protein, called alpha - synuclein.

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

Other theories and lines of research have begun to prosper due to the lack of tangible human results for anti-amyloid immunotherapies, in particular that neurofibrillary tangles of misfolded tau protein are just as much a target for clearance as is amyloid - β, and that perhaps it is time to focus on the decline of known clearance mechanisms rather than the amyloid itself.

Health improvement (allowing to post - pone / escape the diseases and thus live, healthier / disease - free longer, but not above human MLSP of around 122 years; thus these therapies do not affect epigenetic aging whatsoever, they are degenerative aging problems not regular healthy aging problem (except OncoSENS - only when you Already Have Cancer - which cancer increases epigenetic aging, but cancer removal thus does not change anything / makes no difference about what happens in the other cells / about what happens in the normal epigenetic «aging» course in Normal non-cancerous healthy cells) Although there is not such thing as «healthy aging» all aging in «unhealthy» (as seen from elders who are «healthy enough» who show much damage), it's just «tolerable / liveable» enough (in terms of damage accumulating) that it does not affect their quality of life (enough yet), that is «healthy aging»: ApoptoSENS - Clearing Senescent Cells (this will have great impact to reduce diseases, the largest one, since it's all inflammation fueled by the inflammation secretory phenotype (SASP) of these senescent cells) AmyloSENS - Dissolving the Plaques (this will allow humans to evade Alzheimer's, Parkinsons and general brain degenerescence, allowing quite a boost; making people much more easily reach the big 100 - since the brain is causal to how long we live; keeping brain amyloid - free and keeping our memories / neuron sharp / means longer LongTerm Potentiation - means longer brain function means longer heavy brain mass (gray matter / white matter retention seen in «sharp - witted» Centenarians who show are younger brain for their age), and both are correlated to MLSP).

The good safety profile of Aducanumab in patients may well be attributed to the antibody's specific capacity to bond with the abnormally folded beta - amyloid protein fragment as well as the fact that the antibody is of human origin.

Therapies applying this paradigm to clear β - amyloid protein (Aβ) plaques and soluble aggregates from patients with Alzheimer's disease (AD) is an extremely active field of research, with multiple active and passive Aβ vaccines currently in human clinical trials.

Telomere length predicts both cellular health and disease in rodent models and humans.8 Shorter telomeres predict onset of cardiometabolic diseases of aging.9 Chronic stress is associated with higher inflammation, shorter telomeres, and lower activity levels of telomerase, the cellular enzyme that elongates telomeric DNA.10, 11 Levels of amyloid beta (Aβ) proteins circulating in the blood appear to be stress - related in rodent models12 and may be affected by stress reduction, and greater Aβ42 / Aβ40 ratios are associated with lower risk of dementia.13

Using blood collected from elderly persons aged up to one hundred and demonstrating no cognitive impairment, the researchers isolated precisely those immune cells whose antibodies are able to identify toxic beta - amyloid plaques but not the amyloid precursor protein that is present throughout the human body and that presumably plays an important role in the growth of nerve cells.

Given the lack of definitive AD biomarkers in humans, transgenic animal models of the amyloid pathology continue to be valuable tools to examine molecular changes preceding the deposition of amyloid plaques and associated pathology (i.e. late inflammation, neuritic dystrophy, etc.).

There exist several dozen lines of transgenic mice that express human amyloid - β protein precursor (AβPP) with Alzheimer's disease (AD)- linked mutations.

«Our results support the increasingly accepted notion that amyloids may not always be harmful and markers of disease, but, instead, may carry out important functions in the human body.»

Administration of this reagent into mice bearing human AL tumors or those with systemic AA deposits resulted in marked reduction in amyloid burden with no evidence of toxicity in the animals.

These reagents, prepared against human light chain - related fibrils, recognize an epitope common to the beta - pleated structure of AL and other types of amyloid proteins and can effect rapid amyloidolysis when administered to mice injected with human AL amyloid extracts.

The results revealed robust expression of the human APP transgene in the retinas of transgenic mice, but a lack of identifiable retinal pathology during the period when amyloid deposits were dramatically escalating in the brain.

Amyloidosis involves the extracellular deposition of proteinaceous amyloid fibrils and accessory molecules in organ (s) and / or tissue (s), and is associated with a host of human diseases, including Alzheimer disease, diabetes, and heart disease.

Adhesion of exogenous human microglia and THP - 1 cells to amyloid plaques of postmortem Alzheimer's disease brain.

Background: Studies conducted in animal models and humans suggest the presence of a dynamic equilibrium of amyloid - β (Aβ) peptide between cerebrospinal fluid (CSF) and plasma compartments.