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 nerve cells 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

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:

• MLA
• APA
• Chicago

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>.

Latest in Parkinson’s Research Showcased at MJFF Conference

FoxFeed Blog

Posted by  Rachel Dolhun, MD, November 04, 2014

Hundreds of Parkinson’s researchers gathered in October to discuss the latest in drug development and biomarker studies. 

More than 250 of the brightest minds working on Parkinson’s disease (PD) — scientists, clinicians and industry leaders from around the world — convened in New York City on October 29 for the eighth annual Parkinson’s Disease Therapeutics Conference, hosted by The Michael J. Fox Foundation.

The day was filled with updates on the biomarker search and on the status of symptomatic and disease-modifying drugs in development.

Below we summarize a few of the highlights.  

Vaccine Targeting Alpha-Synuclein Deemed Safe 

Alpha-synuclein — the protein that clumps in cells in PD — is a promising target for disease-modifying therapies. Researchers believe that removing this “sticky protein” may slow or even stop Parkinson’s progression. Austrian company AFFiRiS created a vaccine to stimulate the body to make antibodies against alpha-synuclein, hopefully clearing it from the brain.

At the conference Achim Schneeberger, MD, of AFFiRiS shared that their MJFF-funded Phase I clinical trial found the vaccine safe and well tolerated. Each of 24 people with early Parkinson’s received a total of four vaccinations over three months. Side effects were mild; the most common was an injection site reaction of pain or redness.

Phase I trials are not designed to evaluate efficacy of a therapy. Still, investigators saw an antibody response in 15 of the 24 who were vaccinated. They also noted an improvement in motor function in the vaccinated group as compared to a control group that did not receive the vaccine.

MJFF is supporting the next step — the same study participants will receive a fifth vaccination. The goal is to boost the level of antibodies against alpha-synuclein to ensure longer lasting effects.

Expanding the Search for a Tool to Speed Research

The investigation of PD presents many hurdles. The disease process begins long before symptoms appear, no test exists to confirm diagnosis or to track progression, and Parkinson’s shows differently in each individual. 

Biomarkers — objective measures that aid in diagnosis, disease tracking and faster testing of therapies — would address these challenges. Finding accurate biomarkers is the goal of the Parkinson’s Progression Markers Initiative (PPMI).

MJFF and industry partners established PPMI in 2010, and the international, observational study has evolved over time. PPMI has enrolled more than 400 people with newly diagnosed Parkinson’s and 200 control volunteers without PD. They undergo extensive and standardized motor, memory and other testing and submit blood, urine and spinal fluid samples. All of the original study participants have now completed one year of study visits.

At the PD Therapeutics Conference, principal investigator Ken Marek, MD, spoke about the growth of PPMI. Early this year — to increase understanding of the role of genetics and Parkinson’s — PPMI began recruiting people with certain genetic mutations associated with PD. In addition, to find a way to diagnose the disease earlier, people without PD but with symptoms that often predate Parkinson’s (smell loss or REM sleep behavior disorder) are also joining the study.

As its model proves strong, PPMI also has expanded to incorporate additional motor and memory testing, specialized brain imaging and skin biopsies.

Collection of this valuable data over time and collaboration among investigators will lead to biomarkers that will accelerate advancement of disease-modifying therapies.

Continuous Levodopa Lessens Motor Fluctuations 

In an MJFF-supported Phase II clinical trial, the first liquid formulation of the popular PD drug combo levodopa/carbidopa decreased motor fluctuations — “off” time and dyskinesia — in people with moderate Parkinson’s disease.

The “pump-patch” delivery system provides a continuous amount of medication under the skin, avoiding the irregular absorption that occurs when the drug is taken orally.

Sheila Oren, MD, of biotech Neuroderm reported that people with moderate PD who used the pump-patch in place of their regular medication experienced a decrease in “off” time of over two hours and an improvement in time without dyskinesia. Drug levels remained at a consistent steady concentration in the blood.

Dr. Oren’s team is now evaluating the same dose and a higher dose in people with more advanced Parkinson’s disease, and preliminary test results are promising. This may be an alternate option for those considering deep brain stimulation.

Investigators say the drug will reach the pharmacy by 2018.

https://www.michaeljfox.org/foundation/news-detail.php?latest-in-parkinson-research-showcased-at-mjff-conference

Even when you're older, you need chaperones: Protective genes reduce as we age

   

November 3, 2014

Northwestern University

Summary:Aging is the most significant risk factor for developing neurodegenerative diseases, and the risk increases disproportionately with age. Now a team of scientists has uncovered some clues as to why. The researchers are the first to find that the quality of protective genes called molecular chaperones declines dramatically in the brains of older humans, both healthy and not, and that the decline is accelerated even more in humans with neurodegenerative disease.

 Aging is the most significant and universal risk factor for developing neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS) and Alzheimer's, Parkinson's and Huntington's diseases. This risk increases disproportionately with age, but no one really knows why.

Now a team of scientists from Northwestern University, Proteostasis Therapeutics, Inc. and Harvard University has uncovered some clues. The researchers are the first to find that the quality of protective genes called molecular chaperones declines dramatically in the brains of older humans, both healthy and not, and that the decline is accelerated even more in humans with neurodegenerative disease.

Molecular chaperones are a special set of highly conserved genes that watch over cells, keeping them and the entire organism healthy by preventing protein damage.

The researchers specifically found the decline in 100 genes, approximately one-third of all human molecular chaperone genes. Then, with additional studies, they winnowed that number down to 28 human genes specifically involved in age-associated neurodegeneration. These critical genes provide a basis for a biomarker, an early indicator of disease and a target for new therapeutics.

"Imagine if we had biomarkers that tell doctors how you are doing in terms of aging, warning of any problems long before neurological deficits appear," said Northwestern's Richard I. Morimoto, one of the senior scientists on the study. "This would be a remarkable tool, especially considering the increases in life expectancy in many parts of the world.

"Let's say a person is age 50, but we see his molecular chaperones have declined and aren't repairing proteins and cellular damage. The chaperones are acting more like age 85 or 90. That's a sign that medical intervention could help," he said.

Morimoto is the Bill and Gayle Cook Professor of Biology in the Department of Molecular Biosciences and director of the Rice Institute for Biomedical Research in Northwestern's Weinberg College of Arts and Sciences.

"Molecular chaperones really are the barrier we have between disease and no disease," Morimoto said. "If this critical system declines, it leads to misfolded and damaged proteins, and eventually tissues become dysfunctional and die. If we can keep the chaperones healthy, we should be able to keep the person healthy."

The study will be published in the Nov. 6 issue of the journal Cell Reports.

To zero in on the subnetwork of 28 key genes, the scientists combined genomic analysis of human brain tissue, from both healthy individuals and those with neurodegenerative diseases (Alzheimer's, Parkinson's and Huntington's), with functional studies of C. elegans, a transparent roundworm. (The worm has a biochemical environment similar to that of human beings and is a popular research tool for the study of human disease.)

"To our surprise, the results from the studies of humans and C. elegans told us the same thing -- 10 percent of the 332 human genes are really important to cell health," Morimoto said. "Now we are down to 28 genes. This really tells us what to focus on."

After observing the dramatic decline in the health of molecular chaperones in humans both healthy and with neurodegenerative disease, the researchers systematically and individually "knocked down" all 219 chaperone genes in C. elegans (using neurodegenerative disease models) to see what effect the gene's absence had on an animal's function.

They identified a subnetwork of 16 molecular chaperone genes in C. elegans that are critical to preventing protein misfolding and damage to the cell. These genes correspond to 28 human "cousin" genes.

Humans encode approximately 25,000 genes, and getting any process down to a small number of genes will help scientists put their fingers on what's most important.

"It's a lot easier to enhance a handful of genes, such as those we've identified," Morimoto said. "The next step is to understand the basis for the decline of these specific chaperones and to develop treatments that prevent their decline. The goal is not to make people live forever but rather to match health span more closely with life span -- to improve the quality of life being lived."

Story Source:

The above story is based on materials provided by Northwestern University. The original article was written by Megan Fellman. Note: Materials may be edited for content and length.

Journal Reference:

1  Marc Brehme, Cindy Voisine, Thomas Rolland, Shinichiro Wachi, James H. Soper, Yitan Zhu, Kai Orton, Adriana Villella, Dan Garza, Marc Vidal, Hui Ge, Richard I. Morimoto. A Chaperome Subnetwork Safeguards Proteostasis in Aging and Neurodegenerative Disease. Cell Reports, 2014; DOI: 10.1016/j.celrep.2014.09.042

Cite This Page:

•   MLA APA Chicago

Northwestern University. "Even when you're older, you need chaperones: Protective genes reduce as we age." ScienceDaily. ScienceDaily, 3 November 2014. <www.sciencedaily.com/releases/2014/11/141103114238.htm>.