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Thursday, November 6, 2014

Transplant of stem-cell-derived dopamine neurons shows promise for Parkinson's disease


Date:
November 6, 2014
Summary:
Parkinson's disease is an incurable movement disorder that affects millions of people around the world, but current treatment options can cause severe side effects and lose effectiveness over time. In a new study, researchers showed that transplantation of neurons derived from human embryonic stem cells, hESCs, can restore motor function in a rat model of Parkinson's disease, paving the way for the use of cell replacement therapy in human clinical trials.Parkinson's disease is an incurable movement disorder that affects millions of people around the world, but current treatment options can cause severe side effects and lose effectiveness over time.
 In a study published by Cell Press November 6th in Cell Stem Cell, researchers showed that transplantation of neurons derived from human embryonic stem cells (hESCs) can restore motor function in a rat model of Parkinson's disease, paving the way for the use of cell replacement therapy in human clinical trials.

"Our study represents an important milestone in the preclinical assessment of hESC-derived dopamine neurons and provides essential support for their usefulness in treating Parkinson's disease," says senior study author Malin Parmar of Lund University.
Parkinson's disease is caused, in part, by the death of neurons that release a brain chemical called dopamine, leading to the progressive loss of control over dexterity and the speed of movement. Currently available drug and surgical treatment options can lose effectiveness over time and cause serious side effects such as involuntary movements and psychiatric problems. Meanwhile, another approach involving the transplantation of human fetal cells has produced long-lasting clinical benefits; however, the positive effects were only seen in some individuals and can also cause involuntary movements driven by the graft itself. Moreover, the use of tissue from aborted human fetuses presents logistical issues such as the limited availability of cells, hampering the effective translation of fetal tissue transplantation as a realistic therapeutic option.
To rigorously assess an alternative hESC-based treatment approach, Parmar and lead study author Shane Grealish of Lund University transplanted hESC-derived dopamine neurons into brain regions that control movement in a rat model of Parkinson's disease. The transplanted cells survived the procedure, restored dopamine levels back to normal within five months, and established the correct pattern of long-distance connections in the brain. As a result, this therapy restored normal motor function in the animals. Importantly, the hESC-derived neurons show efficacy and potency similar to fetal neurons when transplanted in the rat model of Parkinson's disease, suggesting that the hESC-based approach may be a viable alternative to the approaches that have already been established with fetal cells in Parkinson's patients.
In a related Forum article published in the same issue, Roger Barker of Addenbrooke's Hospital and the University of Cambridge laid out the roadmap for taking stem-cell-derived dopamine neurons to the clinic for treating Parkinson's disease. "This involves understanding the history of the whole field of cell-based therapies for Parkinson's disease and some of the mistakes that have happened," he says. "It also requires a knowledge of what the final product should look like and the need to get there in a collaborative way without being tempted to take shortcuts, because a premature clinical trial could impact negatively on the whole field of regenerative medicine."

Story Source:
The above story is based on materials provided by Cell Press. Note: Materials may be edited for content and length.

Journal Reference:
  1. Shane Grealish, Elsa Diguet, Agnete Kirkeby, Bengt Mattsson, Andreas Heuer, Yann Bramoulle, Nadja Van Camp, Anselme L. Perrier, Philippe Hantraye, Anders Björklund, Malin Parmar. Human ESC-Derived Dopamine Neurons Show Similar Preclinical Efficacy and Potency to Fetal Neurons when Grafted in a Rat Model of Parkinson’s Disease. Cell Stem Cell, 2014; 15 (5): 653 DOI: 10.1016/j.stem.2014.09.017

Cite This Page:
Cell Press. "Transplant of stem-cell-derived dopamine neurons shows promise for Parkinson's disease." ScienceDaily. ScienceDaily, 6 November 2014. <www.sciencedaily.com/releases/2014/11/141106131845.htm>.

Scientists create Parkinson's disease in a dish


Date:
November 6, 2014
Source:
New York Stem Cell Foundation
Summary:
A team of scientists created a human stem cell disease model of Parkinson's disease in a dish. Studying a pair of identical twins, one affected and one unaffected with Parkinson's disease, another unrelated Parkinson's patient, and four healthy control subjects, the scientists were able to observe key features of the disease in the laboratory, specifically differences in the patients' neurons' ability to produce dopamine, the molecule that is deficient in Parkinson's disease.


A team of scientists led by The New York Stem Cell Foundation (NYSCF) Research Institute successfully created a human stem cell disease model of Parkinson's disease in a dish. Studying a pair of identical (monozygotic) twins, one affected and one unaffected with Parkinson's disease, another unrelated Parkinson's patient, and four healthy control subjects, the scientists were able to observe key features of the disease in the laboratory, specifically differences in the patients' neurons' ability to produce dopamine, the molecule that is deficient in Parkinson's disease. In addition, the scientists also identified a potential strategy for developing novel therapies for Parkinson's disease.

Attributed to a combination of genetic and nongenetic factors, Parkinson's disease has no completely effective therapy or cure. Parkinson's disease is moderately heritable, but the mechanisms of this inheritance are not well understood. While genetic forms of the disease exist, sporadic forms are far more common.
"The unique scenario of identical twins, one with this disease and one without, allowed our scientists an unprecedented look into the mechanisms of Parkinson's disease," said Susan L. Solomon, NYSCF Chief Executive Officer. "Advanced stem cell research techniques allow us to push the boundaries of science and see what actually goes wrong at the cellular level, step by step during the disease process."

DNA mutations resulting in the production of a specific enzyme called glucocerebrosidase (GBA) have been linked to a five-fold greater risk of developing Parkinson's disease; however, only 30% of individuals with this mutation have been shown to develop Parkinson's disease by the age of 80. This discordance suggests that multiple factors contribute to the development of Parkinson's disease, including both genetic and non-genetic factors. To date, there has been no appropriate model to identify and test multiple triggers leading to the onset of the disease.
In this study, published in Cell Reports, a set of identical twins, both with a GBA mutation, provided a unique opportunity to evaluate and dissect the genetic and non-genetic contributions to the development of Parkinson's disease in one twin, and the lack of disease in the other. The scientists made induced pluripotent stem (iPS) cells from skin samples from both twins to generate a cellular model of Parkinson's in a dish, recapitulating key features of the disease, specifically the accumulation of α-synuclein and dopamine deficiency.
Upon analyzing the cell models, the scientists found that the dopamine-producing neurons from both twins had reduced GBA enzymatic activity, elevated α-synuclein protein levels, and a reduced capacity to synthesize and release dopamine. In comparison to his unaffected brother, the neurons generated from the affected twin produced less dopamine, had higher levels of an enzyme called monoamine oxidase B (MAO-B), and poor ability to connect with each other. Treating the neurons with molecules that lowered the activity of MAO-B together with overexpressed GBA normalized α -synuclein and dopamine levels in the cell models. This suggests that a combination therapy for the affected twin may be possible by simultaneously targeting these two enzymes.
"The subject of Parkinson's disease discordant twins gave us an incredible opportunity to utilize stem cell models of disease in a dish to unlock some of the biological mechanisms of disease," said Dr. Scott Noggle, NYSCF Vice President, Stem Cell Research and The NYSCF -- Charles Evans Senior Research Fellow for Alzheimer's Disease. "Working with these various different groups and scientists added to the depth and value of the research and we hope our findings will be applicable to other Parkinson's disease patients and other neurodegenerative disorders."
In this particular scenario, genetic and stem cell analysis identified an avenue for a potentially useful combination therapy for the twin affected by Parkinson's disease and may be applicable more broadly to other Parkinson's patients. While this case study is unique, this type of research and cellular analysis could yield further clues to all cases of genetic and sporadic Parkinson's disease and other related neurological disorders.

Story Source:
The above story is based on materials provided by New York Stem Cell Foundation. Note: Materials may be edited for content and length.

Journal Reference:
  1. Chris M. Woodard, Brian A. Campos, Sheng-Han Kuo, Melissa J. Nirenberg, Michael W. Nestor, Matthew Zimmer, Eugene V. Mosharov, David Sulzer, Hongyan Zhou, Daniel Paull, Lorraine Clark, Eric E. Schadt, Sergio Pablo Sardi, Lee Rubin, Kevin Eggan, Mathew Brock, Scott Lipnick, Mahendra Rao, Stephen Chang, Aiqun Li, Scott A. Noggle. iPSC-Derived Dopamine Neurons Reveal Differences between Monozygotic Twins Discordant for Parkinson’s Disease. Cell Reports, 2014; DOI: 10.1016/j.celrep.2014.10.023

Cite This Page:
New York Stem Cell Foundation. "Scientists create Parkinson's disease in a dish." ScienceDaily. ScienceDaily, 6 November 2014. <www.sciencedaily.com/releases/2014/11/141106132208.htm>.

Blocking mitochondrial fission: An effective treatment for Parkinson's disease?


A study led by a researcher from Plymouth University in the UK, has discovered that the inhibition of a particular mitochondrial fission protein could hold the key to potential treatment for Parkinson's Disease (PD)
The findings of the research are published today, 5th November 2014, in Nature Communications.
PD is a progressive neurological condition that affects movement. At present there is no cure and little understanding of why some people get the condition. In the UK one on 500 people, around 127,000, have PD.
The debilitating movement symptoms of the disease are primarily caused by the death of a type of brain cell that produces a chemical called dopamine. This brain chemical (also known as a neurotransmitter) helps nerve cells to send signals to other nerve cells. A reduction in dopamine from cell death results in a lack of communication between nerve cells, which in turn leads to difficulty in movement control. Understanding why these nerve cells die or do not work properly could lead to new therapies for PD.
Mitochondria are small structures within nerve cells that help keep the cells healthy and working properly – they are, in effect, the power generators of the cell. Mitochondria undergo frequent changes in shape, size, number and location either through mitochondrial fission (which leads to multiple, smaller mitochondria) or mitochondrial fusion (resulting in larger mitochondria). These processes are controlled mainly by their respective mitochondrial fission and fusion proteins. A balance of mitochondrial fission/fusion is critical to cell function and viability.
The research team found that when a particular mitochondrial fission protein (GTPase dynamin-related protein-1 – Drp1) was blocked using either gene-therapy or a chemical approach in experimental models of PD in mice, it reduced both cell death and the deficits in dopamine release – effectively reversing the PD process. The results suggest that finding a strategy to inhibit Drp1 could be a potential treatment for PD.
The research team is led by Dr. Kim Tieu from the Institute of Translational and Stratified Medicine, Plymouth University Peninsula Schools of Medicine and Dentistry. Dr. Tieu is a respected researcher in the field of PD. He initiated this research when he was a principal investigator at the University of Rochester School of Medicine and continued it on his move to Plymouth University in the UK.
He said: "Our findings show exciting potential for an effective treatment for PD and pave the way for future in-depth studies in this field. It's worth noting that other researchers are also targeting this mitochondrial fission/fusion pathway as potential treatments for other neurological diseases such as Alzheimer's disease, Huntington's disease and Amyotrophic Lateral Sclerosis."
Claire Bale, Research Communications Manager at Parkinson's UK, said: "We've known for decades that problems with mitochondria - the batteries of the cell - play a key role in the death of  in Parkinson's, but the research in this area hasn't yet led to new treatments.
http://world.einnews.com/article/233001143

Plymouth breakthrough in study of Parkinson's disease could lead to cure By Plymouth Herald | Posted: November 05, 2014

Dr Kim Tieu

A BREAKTHROUGH in the study of Parkinson’s disease, led by Plymouth experts, could become the first treatment to cure the condition.
A Plymouth team has made the discovery, dubbed “wonderful” by patients, after five years of research, and will continue the study in the hope of creating a drug ready for clinical trials.
Local Parkinson’s patients, who struggle daily with restricted movement, stiffness and depression, are “delighted” with the news that there could be a treatment which would not only mask their symptoms, but reverse the effects of the disease.
The leading charity Parkinson’s UK said it was “excited and encouraged” by the discovery, which signals the “next generation of treatments”.
Parkinson’s disease is caused by the death of brain cells which produce the chemical dopamine – which is involved in controlling our motor functions and is also known as the ‘happy’ hormone.
The study, led by Dr Kim Tieu, shows blocking a certain protein reduced cell death, and could hold the key as a potential cure.
Dr. Kim Tieu from the Institute of Translational and Stratified Medicine, Plymouth University Peninsula Schools of Medicine and Dentistry, said the team is “extremely excited” about the research, which was studied in mice.
He said: “We’re extremely excited about this because to my knowledge this is the first study of this nature in animal models. It has taken four or five years and is exciting to see the significance of this treatment in animal models. It’s also exciting for the funders to see that the project they support is making progress.
“We would like to test these further and if that shows promising results, we would move up to an animal model that is more closely related to humans before clinical trials.
“In terms of time until a treatment is available, it’s difficult to say. There are so many variables that can change the course of this research – things like technology and funding.
“Our next phase of study will be completed in the next four years and after that we will take it to another model in non-human primates, which will take a few more years, and then clinical trials. Things can change dramatically. It might be a bit longer or a bit shorter.
“It’s worth noting that other researchers are also targeting this mitochondrial fission pathway as potential treatments for other neurological diseases such as Alzheimer’s disease, Huntington’s disease and Amyotrophic Lateral Sclerosis.
Dr Tieu added: “For all of us who work in Parkinson’s disease we would like to see our work result in some kind of effective treatment – we all have a common passion for the patients.”
Charity Parkinson’s UK, which funds research and help for patients, is thrilled at this “promising step”.
Claire Bale, research communications manager, said: “Current treatments only mask the symptoms rather than stopping the progression of Parkinson’s – this is the next generation of treatments.
“We've known for decades that problems with mitochondria - the batteries of the cell - play a key role in the death of nerve cells in Parkinson's, but the research in this area hasn't yet led to new treatments.
“This study, which reveals a potential new drug target to protect mitochondria, is a promising step towards slowing down or stopping the progression of Parkinson's. If it becomes an effective treatment, it would be a phenomenal advance. This study is very, very encouraging.
“There is also research into stem cells and vaccines and we don’t know what is going to reach the patients first, however stem cell treatments involve brain surgery which is highly invasive – this is exciting because there could be a simpler drug to give to patients.”
WHAT DO PARKINSON'S DISEASE SUFFERERS SAY?
FOR Parkinson’s patients, treatment is currently a trial-and-error approach of trying different drugs to find out what works for them. But none last forever, and many only mask the symptoms and eventually become ineffective.
Patients at the Parkinson’s UK exercise group, in Plymstock, were excited to hear about the advances local scientists have made. Research has shown gentle exercise can greatly help the symptoms of Parkinson’s disease, but as yet there is no treatment which can reverse or cure the disease.
Karen Rose, 52, from Callington, was told she had Parkinson’s Disease 18 years ago, aged just 34.
She said: “Something like this would be absolutely wonderful. I have got to the stage where I’m taking so many tablets that they’re running out of ideas, so the next stage is a bit more invasive. The best thing would be if you could reverse the symptoms through a drug.”
The alternative is deep brain stimulation, where a brain pacemaker sends electrical impulses into the brain through electrodes. However it involves invasive surgery and isn’t suitable for some patients.
Karen is eager for a treatment which has a real impact on her symptoms. She said: “I will just suddenly freeze – I’ll be making tea and then will have to stop because I can’t move.
“You just have to slow down but I’m very determined to keep going. I run the onset group for Plymouth and a lot of the members there will be thrilled to hear this news.”
Mary Johnson, 79, from Elburton was diagnosed 10 years ago and volunteers her time to help train the doctors of the future.
She said: “If this research turned into a treatment it would be lovely. They can’t do the brain stimulation operation on me because I have diabetes. I take my tablets but what is really helping is these exercise classes. I couldn’t sit or stand on my own before – it’s marvellous. But a treatment to reverse the progression of the disease would be better, especially for younger people.
“I’m really aware of how important research is and how it helps – I go up to help trainee doctors every year in their exams. They examine me and have to work out what I have – anything to help.”
Mike Webber, 67, from Plymstock was diagnosed six years ago, in 2008, and like many patients he is willing to try anything. He said: “The biggest changes were having to give up work. The main affects are slowness and stiffness - if you’re doing something it takes twice as long – I would try anything to help.
“Even doing simple things, you’re ok for half an hour and then you’re shattered for the rest of the day. A treatment to reverse the disease would be fantastic.”
For help or information, and details about local groups, contact Parkinson's UK on 0808 800 0303 or visit www.parkinsons.org.uk
The father of The Herald's health reporter Sian Davies was diagnosed with Parkinson's disease 12 years ago. Here she reacts to the news.
IT’S not often you get to report on groundbreaking research which could potentially provide a cure to a life-changing and debilitating illness - especially when that illness is one your dad was diagnosed with more than a decade ago.
At the age of 15 when I got told that dad had been diagnosed with Parkinson’s, I didn’t really know what it would mean. He was in his 50s and relatively young, and it develops so gradually that it’s hard to notice when you see someone every day. Twelve years on the change is definitely noticeable.
The main difference has been his lack of mobility – dad has ran a marathon, and got a medal for 25 years’ service with our local Search and Rescue team. Now he struggles to walk 100 metres.
What makes Parkinson’s all the more frustrating is when drugs become ineffective, and the search starts again to give sufferers some quality of life. The stiffness and lack of mobility becomes worse as drugs wear off, leaving patients unable to move until their next lot kick in. Dad can be in the garden cutting the grass, and within minutes he struggles to move.
When I spoke to dad about this research, he said if there was something that could reverse the symptoms he would “grab it with both hands”.
He has already been deemed not suitable for deep brain stimulation, and his latest treatment is working well but is likely to become ineffective in a few years.
Parkinson’s is slow to progress but can’t be stopped. However researchers like Dr Tieu are giving patients hope. Parkinson’s UK say that patients have much to be optimistic about, and this news shows that research is vital. These advancements could go on to help sufferers of Alzheimer’s and Huntington’s. If there’s anything the rest of us can do is raise money to fund this research, with the hope that it leads to a cure.


Read more: http://www.plymouthherald.co.uk/Plymouth-breakthrough-study-Parkinson-s-disease/story-24181860-detail/story.html#ixzz3IIOtmsMN 
Follow us: @heraldnewslive on Twitter | theplymouthherald on Facebook

Wednesday, November 5, 2014

High-fat diet postpones brain aging in mice


Date:
November 5, 2014
Source:
University of Copenhagen – The Faculty of Health and Medical Sciences
Summary:
New research suggests that signs of brain aging can be postponed in mice if placed on a high-fat diet. In the long term, this opens the possibility of treatment of children suffering from premature aging and patients with Alzheimer's and Parkinson's disease

Coconut oil and fresh coconut (stock image). The researchers see a particular positive effect when the mice are given the so-called medium chain fatty acids -- e.g., from coconut oil.
Credit: © Picture Partners / Fotolia
New Danish-led research suggests that signs of brain aging can be postponed in mice if placed on a high-fat diet. In the long term, this opens the possibility of treatment of children suffering from premature aging and patients with Alzheimer's and Parkinson's disease. The research project is headed by the Center for Healthy Aging, University of Copenhagen and the National Institute of Health.

When we get older, defects begin to develop in our nervous system, our brain loses some of its intellectual capacity, and the risk of developing diseases such as Parkinson's and Alzheimer's increases. Alzheimer's disease is currently the fastest-growing age-related disease.
Throughout our lives, it is important that our cells -- to the extent possible -- keep our DNA undamaged, and, therefore, the cells have a system that repairs the damage that occurs all the time. Humans age when the repair system ceases to function. In diseases such as Alzheimer's, the researchers also see damage to the DNA
A new research project headed by the Center for Healthy Aging, University of Copenhagen and the National Institute of Health has studied mice having a defect in their DNA repair system. In humans, this defect causes the disorder Cockayne syndrome, where patients prematurely age as children and die at an age of 10-12 years. The study shows that placing a mouse model of Cockayne syndrome on a high-fat diet will postpone aging processes such as impaired hearing and weight loss.
Fat putting a stop to premature aging
"The study is good news for children with Cockayne syndrome, because we do not currently have an effective treatment. Our study suggests that a high-fat diet can postpone aging processes. A diet high in fat also seems to postpone the aging of the brain. The findings therefore potentially imply that patients with Alzheimer's and Parkinson's disease in the long term may benefit from the new knowledge," says Professor Vilhelm Bohr from the Center for Healthy Aging, University of Copenhagen and the National Institute of Health, who has headed the study.
Our brain has a constant need for fuel in the form of either sugar or so-called ketones. Ketones are the brain's fuel reserve, and, in particular, play an important role in periods of low blood sugar levels, e.g. if you are fasting. This is because the body breaks down fat if it needs sugar, and during this process it produces ketones. The researchers see a particular positive effect when the mice are given the so-called medium chain fatty acids -- e.g. from coconut oil.
Brain cells need extra fuel
"In cells from children with Cockayne syndrome, we have previously demonstrated that aging is a result of the cell repair mechanism being constantly active. It eats into the resources and causes the cell to age very quickly. We therefore hope that a diet with a high content of coconut oil or similar fats will have a beneficial effect, because the brain cells are given extra fuel and thus the strength to repair the damage," says postdoc Morten Scheibye-Knudsen from the National Institute of Health.
The study has just been published in the scientific journal Cell Metabolism.

Story Source:
The above story is based on materials provided by University of Copenhagen – The Faculty of Health and Medical Sciences. Note: Materials may be edited for content and length.

Journal Reference:
  1. Morten Scheibye-Knudsen, Sarah J. Mitchell, Evandro F. Fang, Teruaki Iyama, Theresa Ward, James Wang, Christopher A. Dunn, Nagendra Singh, Sebastian Veith, Md Mahdi Hasan-Olive, Aswin Mangerich, Mark A. Wilson, Mark P. Mattson, Linda H. Bergersen, Victoria C. Cogger, Alessandra Warren, David G. Le Couteur, Ruin Moaddel, David M. Wilson, Deborah L. Croteau, Rafael de Cabo, Vilhelm A. Bohr. A High-Fat Diet and NAD Activate Sirt1 to Rescue Premature Aging in Cockayne Syndrome. Cell Metabolism, 2014; 20 (5): 840 DOI: 10.1016/j.cmet.2014.10.005

Cite This Page:
University of Copenhagen – The Faculty of Health and Medical Sciences. "High-fat diet postpones brain aging in mice." ScienceDaily. ScienceDaily, 5 November 2014. <www.sciencedaily.com/releases/2014/11/141105112614.htm>.

Blocking mitochondrial fission: Effective treatment for Parkinson's disease?


Date:
November 5, 2014


Source:
University of Plymouth

Summary:
The inhibition of a particular mitochondrial fission protein could hold the key to potential treatment for Parkinson's disease (PD), a new study has concluded. PD is a progressive neurological condition that affects movement. At present there is no cure and little understanding of why some people get the condition.
******************************************************************** 

 A study led by a researcher from Plymouth University in the UK, has discovered that the inhibition of a particular mitochondrial fission protein could hold the key to potential treatment for Parkinson's Disease (PD).

The findings of the research are published today, 5th November 2014, in Nature Communications.
PD is a progressive neurological condition that affects movement. At present there is no cure and little understanding of why some people get the condition. In the UK one on 500 people, around 127,000, have PD.
The debilitating movement symptoms of the disease are primarily caused by the death of a type of brain cell that produces a chemical called dopamine. This brain chemical (also known as a neurotransmitter) helps nerve cells to send signals to other nerve cells. A reduction in dopamine from cell death results in a lack of communication between nerve cells, which in turn leads to difficulty in movement control. Understanding why these nerve cells die or do not work properly could lead to new therapies for PD.
Mitochondria are small structures within nerve cells that help keep the cells healthy and working properly -- they are, in effect, the power generators of the cell. Mitochondria undergo frequent changes in shape, size, number and location either through mitochondrial fission (which leads to multiple, smaller mitochondria) or mitochondrial fusion (resulting in larger mitochondria). These processes are controlled mainly by their respective mitochondrial fission and fusion proteins. A balance of mitochondrial fission/fusion is critical to cell function and viability.
The research team found that when a particular mitochondrial fission protein (GTPase dynamin-related protein-1 -- Drp1) was blocked using either gene-therapy or a chemical approach in experimental models of PD in mice, it reduced both cell death and the deficits in dopamine release -- effectively reversing the PD process. The results suggest that finding a strategy to inhibit Drp1 could be a potential treatment for PD.
The research team is led by Dr. Kim Tieu from the Institute of Translational and Stratified Medicine, Plymouth University Peninsula Schools of Medicine and Dentistry. Dr. Tieu is a respected researcher in the field of PD. He initiated this research when he was a principal investigator at the University of Rochester School of Medicine and continued it on his move to Plymouth University in the UK.
He said: "Our findings show exciting potential for an effective treatment for PD and pave the way for future in-depth studies in this field. It's worth noting that other researchers are also targeting this mitochondrial fission/fusion pathway as potential treatments for other neurological diseases such as Alzheimer's disease, Huntington's disease and Amyotrophic Lateral Sclerosis."
Claire Bale, Research Communications Manager at Parkinson's UK, said: "We've known for decades that problems with mitochondria -- the batteries of the cell -- play a key role in the death of nerve cells in Parkinson's, but the research in this area hasn't yet led to new treatments.
"This study, which reveals a potential new drug target to protect mitochondria, is a promising step towards slowing down or stopping the progression of Parkinson's."
end text


Story Source:
The above story is based on materials provided by University of Plymouth. The original article was written by Andrew Gould. Note: Materials may be edited for content and length.
end story_source

Journal Reference:
1  Phillip M. Rappold, Mei Cui, Jonathan C. Grima, Rebecca Z. Fan, Karen L. de Mesy-Bentley, Linan Chen, Xiaoxi Zhuang, William J. Bowers, Kim Tieu. Drp1 inhibition attenuates neurotoxicity and dopamine release deficits in vivo. Nature Communications, 2014; 5: 5244 DOI: 10.1038/ncomms6244

end journal_references
Cite This Page:
•   MLA
APA
Chicago

University of Plymouth. "Blocking mitochondrial fission: Effective treatment for Parkinson's disease?." ScienceDaily. ScienceDaily, 5 November 2014. <www.sciencedaily.com/releases/2014/11/141105093500.htm>.