Wednesday, November 5, 2014
Tuesday, November 4, 2014
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:
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>.
New technology allows medical professionals to step into their patients' shoes
Date:
November 3, 2014
University of Royal Transports is a piece of technology that uses a low cost Raspberry Pi computer system, and allows users to recreate symptoms including dizziness and speech problems, along with wearable technology which creates a 6Hz tremor in the participant’s right hand.
Credit: Image courtesy of University of Royal Holloway London
A pioneering piece of technology will allow users to experience the world through the eyes of a person with Young-Onset Parkinson's disease- which could revolutionise the way carers and medical staff treat people with the degenerative condition.
Analogue, a theatre company set up by alumni of Royal Holloway, University of London has designed Transports a piece of technology which uses a low cost Raspberry Pi computer system, and allows users to recreate symptoms including dizziness and speech problems, along with wearable technology which creates a 6Hz tremor in the participant's right hand.
Young-Onset Parkinson's is a form of the neurological condition which affects people aged under 50. Symptoms of the disease include tremors, slowed movement and falls, and with no cure currently available, how care and treatment are managed can make a significant difference to a patient's quality of life.
The revolutionary project has been designed in collaboration with neuroscience specialist, Professor Narender Ramnani from the Department of Psychology at Royal Holloway, along with carers, researchers and people with the disease, at Parkinson's UK to ensure it is as effective and realistic as possible.
Liam Jarvis, Co-director of Analogue and Drama PhD Student at Royal Holloway, said: "Our principal interest is to work out how we can improve and facilitate communication and empathy by using simple technologies to immerse participants in the remote embodied experiences of others. Using inexpensive Raspberry Pi technology, we hope to expand the project to place participants inside different virtual subjects as an aid to better understand the experience of others."
The technology will now be tested with BSc psychology students at Royal Holloway and carers at Parkinson's UK to see how it can help medical practitioners better understand their patients and in the long term improve the treatment of the disease.
Anna Farrer, User Involvement Advisor at Parkinson's UK, said:"We know that people with Parkinson's feel that better public awareness about the condition would mean that they face less discrimination and have a better quality of life. Projects such as Transports have an important role educating the public, raising awareness -- and we hope, changing attitudes."
Holloway LondonParkinson’s disease- which could revolutionize the way carers and medical staff treat people with the degenerative condition
Story Source:
The above story is based on materials provided by University of Royal Holloway London. Note: Materials may be edited for content and length.
Monday, November 3, 2014
New therapies to fight a wide range of brain diseases likely as blood/brain barrier breached by new molecule
New research in The FASEB Journal suggests that a very small single domain antibody called FC5 has proven able to cross the blood-brain barrier, which opens the door to new treatments for brain diseases
Delivering life-saving drugs across the blood-brain barrier (BBB) might become a little easier thanks to a new report published in the November 2014 issue of The FASEB Journal. In the report, scientists describe an antibody, called "FC5," is one-tenth the size of a traditional antibody and able to cross the BBB. Moreover, FC5 uses the same pathways as nutrients that the brain needs to survive, allowing it to "smuggle" larger antibodies across the barrier. Like a Lego building block, FC5 connects into many types of antibody designs, helping them reach their disease targets in the brain. This research could lead the way for the development of new therapies to fight a wide range of brain diseases, such as Alzheimer's disease, Parkinson's disease, cancer, epilepsy, genetic brain diseases, neurodegenerative disease, chronic neuropathic pain, and other conditions.
"Neurological diseases are often devastating for both the affected person and their families. Current treatments are unsatisfactory and have many side effects, and the development of precise, new medicines has so far been unsuccessful because it is difficult or impossible to deliver enough medicine into the brain," said Danica B. Stanimirovic, Ph.D., a researcher involved in the work from the Human Health Therapeutics Portfolio at the National Research Council of Canada in Ottawa, Ontario. "With the technology developed in this collaborative work, we hope to open up opportunities for many promising treatments, including antibodies, against neurological diseases to be evaluated in clinical trials and eventually become available to patients."
To make their discovery, Stanimirovic and colleagues attached FC5 to a larger molecule in different configurations and then tested it in cell models and in rats to determine if it was transporting the larger molecules across the BBB. They also incorporated a peptide (a small protein) into the larger molecule being transported by FC5. This peptide was a pain-fighting molecule that cannot enter the brain by itself through the bloodstream. This FC5-peptide combination was injected into the bloodstream and the pain-fighting peptide crossed the BBB to reach the brain.
"The blood-brain barrier is such a robust security system that it should make today's computer programmers and engineers envious," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Unfortunately for us, this security system might be a little too good in the sense that it makes it extremely difficult to deliver drugs to the brain. This report may finally offer the key to unlocking a wide range of therapies that could dramatically improve millions of lives.
http://www.medicalnewstoday.com/releases/284691.php
New progress in treatment of brain cancer and other neurological diseases
Last updated:
A new technology that may assist in the treatment of brain cancer and other neurological diseases is the subject of an article in a recent issue of the journal Technology, published by World Scientific Publishing Company.
According to the authors, the current medical use of chemotherapy to treat brain cancer can be inefficient because of the blood-brain-barrier that impedes the delivery of drugs out of blood vessels and into the tumor.
The researchers from the Virginia Tech - Wake Forest University School of Biomedical Engineering and Sciences described in their article that they have created "a tool for blood-barrier-brain disruption that uses bursts of sub-microsecond bipolar pulses to enhance the transfer of large molecules to the brain."
The members of the biomedical school are: Rafael V. Davalos, associate professor of biomedical engineering; John H. Rossmeisl Jr., of the Virginia-Maryland Regional College of Veterinary Medicine; Christopher Arena, Paulo A. Garcia, and Michael B. Sano of the Bioelectromechanical Systems Laboratory; and John D. Olson of the Center for Biomolecular Imaging . Garcia is also employed by the Laboratory for Energy and Microsystems innovation at the Massachusetts Institute of Technology. Arena holds a second appointment with the Laboratory for Ultrasound Contract Agent Research at the University of North Carolina - North Carolina State University, Joint Department of Biomedical Engineering.
The new tool is called Vascular Enabled Nanosecond pulse or VEIN pulse. It will "reversibly open the blood-brain-barrier to facilitate the treatment of brain cancer," Davalos explained.
"The sub-lethal nature of these electrical bursts indicates that the VEIN pulse may be useful for treating other neurological disorders such as Parkinson's disease, epilepsy, and Alzheimer's disease," Davalos added.
In their testing, the VEIN pulse treatments were administered using minimally invasive electrodes inserted into the skull of each of the 18 anesthetized male rats. They varied the pulse duration within a burst, the total number of bursts (90 to 900), and the applied field. A key element of their success was that the pulses alternated in polarity to help eliminate muscle contractions and the need for a neuromuscular blockade.
http://www.medicalnewstoday.com/releases/284668.php
LCT completes patient enrollment in Phase I/IIa trial for Parkinson's disease
Australasian biotechnology firm Living Cell Technologies (LCT) has completed patient enrollment in a Phase I/IIa clinical trial of the regenerative cell therapy NTCELL for Parkinson’s disease.
NTCELL is an alginate coated capsule containing clusters of neonatal porcine choroid plexus cells.
The open-label trial will evaluate the safety and clinical effects of NTCELL in patients who can no longer respond to the existing therapy.
The capsule is directed by Parkinson's disease clinician and researcher Dr Barry Snow who leads the Auckland Movement Disorders Clinic at the Auckland District Health Board.
LCT chief executive Dr Ken Taylor said: " I congratulate the clinical team at Auckland Hospital for the coordination and interaction with all required regulatory and ethical authorities required to successfully recruit all patients for this innovative clinical study.
"Now we look forward to the clinical study outcome in 2015. We remain excited about the potential for NTCELL to be the first disease modifying treatment for patients who are failing the current conventional treatment for Parkinson's disease."
The company said that NTCELL also has the potential to be used in a number of other central nervous system (CNS) indications such as Huntington's, Alzheimer's and motor neurone diseases.
Ali's doctor plays down suggestions of boxing link to Parkinson's
Read more at: /Sunday, November 02, 2014 - 11:49 AM
Muhammad Ali’s personal doctor has revealed he cannot be sure that boxing contributed to the former heavyweight world champion’s Parkinson’s Disease.
Ali, considered by many to be the greatest boxer of all time, has suffered with the neurological syndrome since the mid-1980s and it has often been presumed that blows to the head during his 21-year professional career were a contributing factor to his condition.
But Dr Abraham Lieberman, who is the Medical Director of the Muhammad Ali Parkinson Centre, admits that it is not possible to be entirely sure what caused Ali to suffer from Parkinson’s.
“It’s only over the last 10 years that he’s had a lot of trouble walking, with falls,” he told BBC Radio Five Live’s Sportsweek programme.
“So his course has been more that of typical Parkinson’s Disease. If you look at the MRI of his brain it looks pretty good but it’s very difficult to factor in what sort of role did boxing play.
“People ask me about this and I tell them: look at George Foreman. He boxed longer than Muhammad did, took many more blows to the head and he’s on television selling his cookware.
“I think that he (Ali) has typical Parkinson’s Disease. Did the boxing contribute? I don’t know. It may have.”
Dr Lieberman gave the impression of a happy retirement for Ali – who was known as Cassius Clay before joining the Nation of Islam and changing his name – and stressed that, despite some reports, there is no reason to fear for his health.
He said: “He’s had Parkinson’s since about 1984, that’s almost 30 years, that’s a long time in Parkinson’s.
“He’s in good spirits, he has some trouble walking but overall for having had Parkinson’s for 30 years, he’s doing okay.”
He added: “Muhammad is now 72 so you can have a heart attack or you can have a stroke.
“I don’t know that he’s more or less at risk than anyone else but anything can happen to you.
“How do people with Parkinson’s Disease die? They don’t die of Parkinson’s Disease, they develop trouble swallowing and they develop pneumonia and he doesn’t have trouble swallowing.
“They fall, they bang their head – his family takes extraordinary care of him.
“I could have a heart attack or a stroke and die but I don’t see anything immediately that leads me to think he’s going to die in six months or die in a year. I can’t say that.”
http://health.einnews.com/article/232442963/09v4_2lHMQ87zfzo?n=2&code=ga_qGBxHZ2aVYO4P
http://health.einnews.com/article/232442963/09v4_2lHMQ87zfzo?n=2&code=ga_qGBxHZ2aVYO4P
http://www.standardmedia.co.ke/sports/article/2000140283/muhammad-ali-s-doctor-queries-parkinson-s-link#
Sunday, November 2, 2014
November is National Sleep Comfort Month
Building a Better
Night’s Sleep
November is National Sleep Comfort Month, but up to 80 percent of people with PD may experience some level of sleep disturbance.
To help make sure you get a better night’s sleep, print out this tip sheet from the National Parkinson Foundation and keep it on your bed-side table!
Do you experience difficulty with sleeping?
-
Establish regular bedtime and morning awakening times that you maintain seven
days per week.
-
Go to bed at night when you notice feeling drowsy; learn to distinguish between
fatigue and sleepiness.
-
Design and maintain a comforting bedtime ritual.
-
Turn off the T.V. Rarely is the late night news soothing or relaxing!
-
If weaning yourself from a T.V. habit is difficult, substitute a relaxation or nature
sounds CD.
-
Customize your sleep environment; invest in a really good mattress and pillows.
-
Keep noise and light levels low; use a bathroom or hallway nightlight to prevent
falls.
-
Maintain a slightly cool room temperature for better REM sleep.
-
Banish animals from your bed!
-
Designate your bedroom for sleep and sex, not an all-purpose space.
-
Limit daytime napping to a 40-minute NASA nap (yes, tested by astronauts).
-
Avoid strenuous exercise, alcohol, nicotine and caffeine within 4 hours of your
bedtime.
-
Eliminate the common but bad habit of “checking the clock” throughout the night.
-
Limit prescription sedatives to a 2-week period; instead, try over-the-counter
alternatives such as Valerian root capsules, or Calms Forte, a homeopathic
formula.
*UCB does not endorse and is not responsible for the following website and its content.
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