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NIH Begins Gene Therapy Trial for Parkinson's Disease - Scientific American (blog)

NIH Begins Gene Therapy Trial for Parkinson's Disease - Scientific American (blog) | Neurology | Scoop.it
Scientific American (blog)
NIH Begins Gene Therapy Trial for Parkinson's Disease
Scientific American (blog)
When Cohen learned he had Parkinson's disease 17 years ago his symptoms were subtle.
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Neurodegenerative Disorders Part I - Dementia, Alzheimer's, MND, MS

A very introduction to the Pathophysiology of some Neurodegenerative disorder. Song by: Angus and Julia stone - Devils tears WATCH PART II on FACEBOOK!! ::::...
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King's College London: Brain Disease Research - Keeping You You

Have you ever wondered how scientists research the brain? Have you wondered who digs through that beautiful mass of grey matter between our ears to understan...
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Former TV reporter campaigns to bring Huntington's disease out of the shadows - Washington Post

Former TV reporter campaigns to bring Huntington's disease out of the shadows - Washington Post | Neurology | Scoop.it
Former TV reporter campaigns to bring Huntington's disease out of the shadows
Washington Post
Huntington's disease has particularly cruel features.
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Charles Sabine

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Anemia Increases Risk Of Dementia By 41%: What's The Connection? - Medical Daily

Anemia Increases Risk Of Dementia By 41%: What's The Connection? - Medical Daily | Neurology | Scoop.it
Anemia Increases Risk Of Dementia By 41%: What's The Connection?
Medical Daily
Reductions in oxygen to the brain have been shown to reduce memory and thinking abilities and may contribute to damage to neurons," said Yaffe.
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Tells you about the different types of dementia

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Murray loses battle with motor neurone disease

RTÉ broadcaster Colm Murray has passed away at the age of 61.
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Huntington's disease: The fight for the right to die - BBC News

Huntington's disease: The fight for the right to die - BBC News | Neurology | Scoop.it
BBC News
Huntington's disease: The fight for the right to die
BBC News
Newsbeat's been speaking to 22-year-old Josh Cook, a semi-professional rugby player from Huddersfield who says he should have the right to die when he chooses.
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Misfolded protein transmits Parkinson’s from cell to cell

Misfolded protein transmits Parkinson’s from cell to cell | Neurology | Scoop.it
Link between cell death and protein clumps opens pathway to possible treatment.

 

The catastrophic damage wreaked by a rogue protein involved in Parkinsons' disease has been tracked by researchers, in work that might help to reinvigorate an old treatment strategy to slow the condition.

 

A team led by Virginia Lee, a neurobiologist at the University of Pennsylvania in Philadelphia, injected a misfolded synthetic version of the protein α-synuclein into the brains of normal mice and saw the key characteristics of Parkinson’s disease develop and progressively worsen. The study suggests that the disease is spread from one nerve cell to another by the malformed protein, rather than arising spontaneously in the cells.

 

The finding raises the possibility that an antibody that binds the misfolded α-synuclein could be used to intercept the protein as it passes between nerve cells. “It’s very hard to ask antibodies not only to get inside the brain, but to get inside cells,” says Lee. “But now you have the possibility of stopping the spreading. And if you stop the spreading, perhaps you can slow the progression of the disease.” The idea that Parkinson’s might be spread from neuron to neuron by a rogue protein took off in 2008, when transplants of fetal nerve tissue given to patients with the disease developed the characteristic clumps associated with the condition. This indicated that the nearby diseased cells had somehow infected the transplanted tissue. Subsequent studies showed that misfolded α-synuclein can spread between neighbouring cells and can cause cell death.

 

But the question remained as to whether the misfolded α-synuclein was responsible for the cascade of damage seen in Parkinson’s. Lee says that her team has now captured the full consequences of runaway α-synuclein in the brain.

 

Parkinson’s disease has two distinct features: clumps of protein called Lewy bodies and a dramatic loss of nerve cells that produce the chemical messenger dopamine. When Lee’s team injected the misfolded α-synuclein into a part of the mouse brain rich in dopamine-producing cells, Lewy bodies began to form. This was followed by the death of dopamine neurons. Nerve cells that linked to those near the injection site also developed Lewy bodies, a sign that cell-to-cell transmission was taking place, say the researchers.

 

“It’s really pretty extraordinary,” says Eliezer Masliah, a neuroscientist at the University of California, San Diego. “We have been trying that experiment for a long time in the lab and we have not seen such dramatic effects.” The study lends theoretical support to the handful of biotechnology companies that are sponsoring clinical trials of α-synuclein antibodies for Parksinson’s, Masliah says. It should also spur research on how the protein gets in and out of cells, he adds.

 

At least one mystery still remains: why do the Lewy bodies appear in the first place? “Parkinson’s disease is not a disorder in which somebody injects synuclein into your brain,” notes Ted Dawson, director of the Institute for Cell Engineering at Johns Hopkins University in Baltimore, Maryland. “So what sets it in motion?”


Via Dr. Stefan Gruenwald
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Sangamo tries to use engineered zinc finger transcriptional repressors to cure Huntington’s disease

Sangamo tries to use engineered zinc finger transcriptional repressors to cure Huntington’s disease | Neurology | Scoop.it
At the root of Huntington’s disease is a specific type of mutation, called a trinucleotide repeat expansion, in the Huntingtin (Htt) gene. The normal Htt gene contains up to 28 copies of the nucleotide sequence CAG, but this expands to more than 40 copies in the disease-causing allele. As a result of the expanded repeat, insoluble clumps of the Huntingtin protein accumulate inside neurons, causing cell death that leads to uncontrollable movements, dementia and, ultimately, death. Patients with between 28 and 35 repeats are unaffected, while those with between 36 and 40 have a form of the disease with reduced penetrance.

 

In animal models, reducing mutant Htt protein levels prevents disease progression and reverses some symptoms. However, most therapeutic approaches in development lower both versions of the huntingtin protein (the one produced by the normal gene, and the one made by the mutated gene). This has raised concerns about their safety for human use, because the normal protein has important, albeit as yet unknown, cellular function. To overcome this, Sangamo researchers have developed zinc finger transcriptional repressors that specifically target the mutant Htt allele and block its expression while preserving near-normal expression levels of the normal allele. Zinc fingers are naturally occurring protein segments that recognize and bind to specific DNA sequences, typically regulating the output of a given gene. Using genetic engineering, the Sangamo researchers designed zinc finger proteins containing a DNA-binding site that recognizes the prolonged tricnucleotide repeat found in the mutant Htt gene. They then fused this binding site to a protein domain that recruits other molecules that zip closed the chromosomal region containing the Htt gene with the expanded repeat—thus hindering production of mutated huntingtin protein.

 

In a recent experiment in a lab dish, the group added the engineered zinc fingers to fibroblast cells obtained from six people with Huntington’s disease. This lowered production of the mutant protein by more than 90%, while reducing the amount of the normal protein by just 10% or less, the researchers reported at the annual meeting of the Society for Neuroscience, held here this week. “There was very potent discrimination between the mutant and normal alleles in cells from all six patients, even though each contained mutant alleles of different lengths,” explains Phillip Gregory*, chief scientific officer at Sangamo BioSciences. “The next step is to make that sure they operate at a broad range of doses, and then we need to move into animal studies of efficacy and safety.”

 

This is the first attempt to apply the zinc finger approach to Huntington’s disease, and the researchers eventually aim to deliver genes for the zinc finger proteins directly into the brain using adeno-associated viral vectors*, which are already being used to successfully deliver therapeutic genes into the brains of people with Parkinson’s disease in clinical trials.

 

“This is very promising and exciting work,” says Sarah Tabrizi, a professor at the Institute of Neurology in London, who was not involved in the study, “but it’s still at a very early and exploratory stage, and it’s a big jump going from cells in culture to the human brain.” One challenge is that targeting viral vectors to specified brain areas and then ensuring their proper distribution is difficult, and this is further complicated by the fact that Huntington’s disease begins in deep brain structures before spreading to the cerebral cortex. “Distributing the vector will be a challenge,” Tabrizi says, “but I don’t think it’s insurmountable.”

 

Read more about ZFN and TALENs ("Editing the genome, here, there and everywhere"): http://tinyurl.com/ccdhao5


Via Dr. Stefan Gruenwald
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What is worse Alzheimer's or Dementia? | Alzheimer's Reading Room

What is worse Alzheimer's or Dementia? | Alzheimer's Reading Room | Neurology | Scoop.it
What is worse, Alzheimer's or Dementia?

Via Bob DeMarco
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Dementia=symptom. AD= cause

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Bob DeMarco's curator insight, July 20, 2013 9:38 AM

Communicating in Alzheimer's World

http://bit.ly/ck5Yon

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I Am Breathing – review

I Am Breathing – review | Neurology | Scoop.it
A documentary about one man's experience of motor neurone disease is sobering and moving, if not as much as his own writing This sobering documentary stands as a memorial to Neil Platt, a Harrogate-based architect and new father who, at 33, was...

Via Jane Young
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Mutated gene tie to motor neurone disease › News in Science (ABC Science)

Mutated gene tie to motor neurone disease › News in Science (ABC Science) | Neurology | Scoop.it
New insights into the cause of motor neurone disease have been uncovered with a study showing mutations in a specific gene lead to the death of the nerve cells responsible for powering our muscles.

Via TEAM Mike Lopez Memorial Foundation |Find us on Twitter:@TEAMCUREALS
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CREST gene

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Scientists find more clues to Parkinson's disease | La Jolla Light

Scientists find more clues to Parkinson's disease | La Jolla Light | Neurology | Scoop.it
Parkinson's disease is a degenerative disorder affecting nerve cells that produce dopamine, a brain chemical that helps control muscle movement. When neuron death occurs, the result is tremors, muscle rigidity, and slowed ...
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Anemia Tied to Dementia Risk - NYTimes.com

Anemia Tied to Dementia Risk - NYTimes.com | Neurology | Scoop.it
A large study finds further evidence that anemia — a common condition in the elderly — increases the risk for dementia. Read more…
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