Sentences with phrase «of alpha synuclein»
Propagation and aggregation of alpha synuclein in murine models K. R. WALKER, W. ARIAS, J. BERGER, N. CHIRICHELLA, B. S. NUNEZ, R. SPRINGER, K. CIRILLO, J. SANCHEZ - PADILA, G. TOMBAUGH, A. GHAVAMI, S. RAMBOZ... Abstract / Posters
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Propagation and aggregation of alpha synuclein in murine models S RAMBOZ WASHINGTON A, RAYNEL S, JASON B, NICOLE C, SHEILYN N, KIMBERLY C, KIM C, KENDALL W... Abstract / Posters
The researchers hypothesize that these chaperone proteins may assist in the proper folding of alpha synuclein, which could prevent it from forming clumps.
Not exact matches
This drug is designed to reduce the build up of a neural protein in the brain called alpha - synuclein that is associated with the disease.
Although one of the mutations has no effect, the other, which switches one nucleotide from an A to a G, slightly but significantly boosts alpha - synuclein production.
For example, in sporadic PD, multiple GWAS point to the alpha - synuclein gene (SNCA) as one of the strongest risk loci in patients» genomes, yet GWAS contain little information regarding the mechanism of how this gene is dysregulated in sporadic PD patients.
When compared to the enhanced alpha - synuclein production in the familial form of the disease, the modest effect created by the A to G mutation would be sufficient over a lifetime to increase the risk of PD, according to Soldner.
though the exact cause of Parkinson's is unknown, evidence points to an accumulation of alpha - synuclein, which has been found to be common to all people with the disorder.
The study, published in the October edition of the journal Neurotherapeutics, found that the drug, AT2101, which has also been studied for Gaucher disease, improved motor function, stopped inflammation in the brain and reduced levels of alpha - synuclein, a protein critically involved in Parkinson's.
«More light means an increased level of alpha - synuclein, which would be considered a diseased state.»
The team said research will focus on what aspects of the alpha - synuclein protein kill neurons during Parkinson's disease.
«Among them were multiple genes known to predispose individuals to Parkinson's — so we show that various genetic forms of Parkinson's are directly related to alpha - synuclein.
Whether in a yeast cell or in a neuron, alpha synuclein directly interfered with the rate of production of proteins in the cell, and the transport of proteins between cellular compartments.
To start, they created two ways to systematically map the footprint of alpha - synuclein within living cells.
«In the second paper, we created a spatial map of alpha - synuclein, cataloging all the proteins in living neurons that were in close proximity to the protein,» explained Chee Yeun Chung, former Whitehead Institute Senior Research Scientist, who co-led both studies with Khurana.
(To do the experiment in a blinded, unbiased manner, the Loyola researchers did not know which types of alpha - synuclein were which.)
Moreover, the results showed that many effects of alpha - synuclein have been conserved across a billion years of evolution from yeast to human,» said Khurana, former Visiting Scientist at the Whitehead Institute.
Melki, a protein researcher at the Paris - Saclay Institute of Neuroscience, is known for his ability to generate distinct types of alpha - synuclein.
So they asked collaborator Ronald Melki, PhD, to send them samples of different types of alpha - synuclein.
The mapping was achieved without disturbing the native environment of the neuron, by tagging alpha - synuclein with an enzyme — APEX — that allowed proteins less than 10 nanometers away from synuclein to be marked with a trackable fingerprint.
Arising from the abnormal buildup of a protein known as alpha - synuclein in the brain, such conditions damage the nerves that control blood pressure and heart rate.
To investigate, scientists at the University of California at San Diego ran supercomputer simulations using 962,757 processor hours to explore myriad possible shapes that alpha - synuclein molecules can take.
«Activation of these cell receptors appear to prevent brain cells from cleaning out the trash — the toxic buildup of proteins, such as alpha - synuclein, tau and amyloid, common in neurodegenerative diseases,» says the study's senior author, neurologist Charbel Moussa, MBBS, PhD, director of Georgetown's Laboratory for Dementia and Parkinsonism, and scientific and clinical research director of the GUMC Translational Neurotherapeutics Program.
Researchers at the University of Pittsburgh School of Medicine have uncovered a major reason why the Parkinson's - related protein alpha - synuclein, a major constituent of the Lewy bodies that are the pathological hallmark of Parkinson's disease (PD), is toxic to neurons in the brain.
People whose cells make too much alpha - synuclein or make a mutated form of the protein are at high risk of developing PD because of the protein's toxicity, researchers found.
They found that by attaching to a mitochondrial protein called TOM20, alpha - synuclein prevented the mitochondria from functioning optimally, which resulted in the production of less energy and more damaging cellular waste.
In the new study, Dr. Greenamyre and his team — led by coauthors Roberto Di Maio, Ph.D., and Paul Barrett, Ph.D., both of PIND — used a well - established rodent model of PD to show exactly how alpha - synuclein disrupts mitochondrial function.
In mice infected with the H5N1 virus, deposits of phosphorylated alpha - synuclein (arrows) in dopamine neurons may be a sign of neurodegeneration.
Degenerating neurons contain large clumps of a protein called alpha - synuclein.
«The effects of alpha - synuclein on mitochondria are like making a perfectly good coal - fueled power plant extremely inefficient, so it not only fails to make enough electricity, but also creates too much toxic pollution,» said Dr. Greenamyre.
Yet if you look at people who develop the clinical syndrome of dementia, especially later in life, yes, they have amyloid in the brain but they also have other pathologic entities — vascular disease; synucleinopathies [insoluble fibrils of the normally soluble protein, alpha - synuclein]; a tauopathy [which is marked by disease - inducing, insoluble tangles of another protein, tau].
The pathological hallmark of this disease is the accumulation of alpha - synuclein, which in turn leads to cell death and consequently to problems in neurotransmission.
As published this week in Nucleic Acids Research, they have discovered a mechanism that regulates the expression of alpha - synuclein, a protein linked to Parkinson's disease and multiple system atrophy (MSA).
The Penn team also found that patients with this genetic variation had a slower rate of Parkinson's disease progression, and lower amounts of alpha - synuclein in the brain.
The human alpha - synuclein protein is made of 140 amino acids and is encoded by the SNCA gene.
Alpha - synuclein is a protein that experts know plays a role in the development of Parkinson's disease.
Alpha - synuclein is the primary structural component of Lewy bodies, which are clumps of protein that develop inside nerve cells in Parkinson's disease and some other disorders.
Scientists have been investigating treatments that could prevent alpha - synuclein from becoming malformed, but much of the research is still in its early stages, Liddle said.
New leads on alpha - synuclein could also aid the development of therapies targeting the protein.
Inside these cells is a protein called alpha - synuclein, which is known to go awry and lead to damaging clumps in the brains of Parkinson's patients, as well as those with Alzheimer's disease.
Clinical and experimental evidence suggests however that alpha - synuclein — or abnormal forms of it — could «jump» from one neuron to another and thus spread between anatomically interconnected regions.
«Protein associated with Parkinson's travels from brain to gut: New laboratory study provides clues on a particular pathway of «alpha - synuclein» diffusion.»
«Some forms of Parkinson's disease are associated with an overproduction of alpha - synuclein.
The study also reveals a preferential route of alpha - synuclein transmission via the vagus nerve.
«It shows that transmission of alpha - synuclein is not just a matter of anatomical connections.
Fibers of the vagus nerve connect the brain to a variety of internal organs; travelling within these fibers, human alpha - synuclein was ultimately able to reach the gastric wall about six months after its initial midbrain expression.
Alpha - synuclein lesions have also been observed within neurons of the peripheral nervous system, such as those in the gastric wall.
«Our present approach was to look at this long - distance transmission of alpha - synuclein from the opposite perspective, investigating the possibility that alpha - synuclein may travel from the brain to the gut.»
With the help of a tailor - made viral vector they triggered production of human alpha - synuclein in rats.
The virus transferred the blueprint of the human alpha - synuclein gene specifically into neurons of the midbrain, which then began producing large quantities of the foreign protein.