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Researchers sought to identify patients at risk for freezing of gait.
Anxiety and positive responses to the Freezing of Gait-Questionnaire (FOG-Q3) are key predictors clinicians can use to assess risk for freezing of gait (FOG) in patients with Parkinson disease(PD), according to findings published in Movement Disorders.
Investigators evaluated longitudinal data from patients with PD (n=221) from the Parkinson's Disease Research Clinic at the University of Sydney in Australia between 2008 and 2016. All patients were interviewed at least twice and were divided into 3 groups based upon responses to item 3 of the Freezing of Gait-Questionnaire (FOG-Q3) at both baseline and follow-up. These 3 groups included nonfreezers (n=88), transitional freezers (n=41), and continuing freezers (n=92).
The researchers found overall group effects for dopamine dose equivalence ([DDE] P =.001), Unified Parkinson's Disease Rating Scale motor subsection ([UPDRS-III] P <.001), tremor dominant (TD)/non-TD ratio (P <.001), Mini-Mental State Examination ([MMSE] P <.001), Digit Span (DS)-Backwards (P =.002), Trail Making Test part A and B ([TMT-B-A] P =.003), and Hospital Anxiety and Depression Scale ([HADS-A] P <.001).
A risk prediction model consisting of nonfreezers (n=52) and transitional freezers (n=23) found that FOG-Q total (P =.01), HADS-A (P =.001), and HADS-D (P =.067) represented good predictors for FOG, with a predictive success of 84%. For the HADS-A and HADS-D, anxiety was found to be the strongest predictor for FOG in patients with PD.
A lack of DDE data caused the study to exclude DDE from the logistic regression analysis, potentially limiting the study findings.
The investigators note that anxiety “should be targeted as part of preventive efforts for potential freezers” and indicates further research is needed to determine how this targeted therapy could delay onset of FOG.
Retired English rugby star, Mike Tindall, appeared on British television to talk about his father’s battle with Parkinson’s disease. Talking to Good Morning Britain, Tindall explained that his father Philip had been experiencing symptoms of the disease for about 18 months before finally seeing a doctor.
According to an article in the Daily Mail, 71-year-old Philip Tindall was diagnosed with the disease 14 years ago and is now cared for by his wife, Linda. Like Mike, Philip played rugby before becoming a banker, and the two would often spend days in the garden throwing a ball around. Mike shares how frustrated his father is that he’s not able to play with his granddaughters.
Mike, who’s married to the Queen’s granddaughter Zara Philips, has organized an annual celebrity golf day with proceeds going towards Parkinson’s disease charities in the U.K.
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Parkinsons’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or another qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.
DECEMBER 20, 2017 BY WENDY HENDERSON IN SOCIAL CLIPS.
While living with a chronic illness can be challenging, there are ways that you can make life easier and live a happy and fulfilling life. Establishing good habits and routines takes time, but as Gunnar Esiason points out in his blog Own It, there are some “common sense approaches” to living life with a chronic illness that everyone can find useful.
Follow Directions
It’s tempting to cut corners sometimes, especially if you’re running late or tired, but taking medications and therapies as prescribed and for the required amount of time will prevent you from becoming sick. Skipping meds or only partially doing therapies, not cleaning or maintaining equipment may save you a little bit of time in the short run, but may result in you becoming sick.
Designate a First Responder
Designate a person (or persons) who you can rely on to know what to do if you have a medical emergency. This can be a member of your family, a colleague, or a friend. Make sure they know how to respond to any exacerbations you may experience.
Be Organized
Keep any medications, equipment or paperwork that has to do with your health condition in good order. If you need to take medications at different times of the day, set reminders on your cellphone. Keep all paperwork in an organized folder so everything you need is easily found. Use weekly pill boxes to keep a week’s supply of meds ready. Ensure all equipment is cleaned after use so it’s ready for the next time.
Use Trusted Sources for Information
Dr. Google is notoriously wrong, as are most of your well-meaning colleagues and friends. Use trusted sources for information regarding your chronic illness. Non-profit organizations are great places to find accurate and up-to-date information. Your health care team is also a phone call away if you have any questions that need to be answered.
Get the Most Out of Your Appointments
Often, particularly when you’re first diagnosed, there is a lot of information to process. Taking notes when you meet your health care team will help you to remember all that you’ve been told. Also, preparing a list of questions before you go to your appointments will ensure that you don’t forget anything important while you’re there. Take a friend or family member along for support — they’ll often think of things you may miss.
Have Faith in Yourself
You may think that the journey you’re about to embark on will be too difficult or that you won’t be able to keep up with the treatments. Have faith in yourself — you are stronger than you realize. In the beginning, there will be many changes, but life will soon settle into a new normal and you’ll be surprised at how well you’re handling things.
Ask for Help
Don’t be too afraid or too proud to ask for help. Family and friends will want to help you out in any way they can, just as you would if the roles were reversed. Focus on your health and staying well, and allow others to do things for you. If you require financial aid or help to procure necessary equipment, non-profit organizations are a great place to start. Local volunteer groups can offer caregiving help as well as help around the house and garden.
Don’t Let Negative Feelings Get You Down
Feeling angry, frustrated, sad, or disappointed are all extremely normal reactions to a chronic illness, but you’ll need to work through these feelings and push them to one side. Focus your energy on getting well and try to be positive about your treatment.
Be Adaptable
It’s likely that you won’t be able to live your life exactly as you did before. Depending on the severity and type of chronic illness you have, you may find that you simply can’t do as much as you used to. Be more selective with your calendar so you have more energy and enthusiasm to enjoy each activity and event. Ditch bad lifestyle habits that could make your chronic illness worse, and try to embrace new healthy ones instead. Learn that it’s OK to say no to people — your health comes first and they should be able to accept that.
Laugh
Laughter is great medicine. It won’t cure your chronic illness, but it will make living life with it more fun. Take time to do the things you enjoy and that give you pleasure, spend time with people who make you happy and take joy wherever you can find it.
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Parkinson’s News Today is strictly a news and information website about the disease. It does not provide medical advice, diagnosis or treatment. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website.
Researchers at the University of California found that tau and beta-amyloid protein deposits in the brains of Parkinson’s patients does not influence their cognitive function. They found, interestingly, that those with greater tau accumulation had higher levels of β-amyloid in the brain.
Every nerve cell needs a certain amount of tau protein to stay healthy. In Parkinson’s disease, excess tau gets tangled up inside brain cells and damages neurons.
As changes in the brain caused by the disease gradually spread, they often begin to affect cognitive functions, including memory and the ability to make sound judgments.
Dementia is increasingly being recognized in cases of Parkinson’s disease. Almost half of Parkinson’s dementia patients have toxic levels of tau and β-amyloid (Aβ) in their nerve cells, or neurons.
But a direct correlation between tau aggregation and cognitive function in Parkinson’s patients without dementia has not yet been found.
With that in mind, scientists designed a cross-sectional study to compare tau accumulation in 15 cognitively normal Parkinson’s patients, 14 patients with mild cognitive impairment, and 49 healthy individuals (controls). They also assessed whether Aβ, tau, and cognition were related in Parkinson’s patients without dementia.
The participants underwent cognitive evaluation and neuro-imaging studies, including structural magnetic resonance imaging (MRI) and positron emission tomography (PET) to measure Aβ and tau.
In the PET scan, participants are injected with a special dye with radioactive tracers. These tracers bind to either tau or β-amyloid and when highlighted by the PET scanner, a signal is detected. The brighter the signal, the higher the amount of protein aggregation.
Of the 29 Parkinson’s disease patients, six (21%) were Aβ-positive, of whom one was mildly cognitively impaired, and 23 (79%) were found to be negative for β-amyloid, according to the researchers. Of the 49 healthy controls, 25 were negative for β-amyloid and 24 were Aβ-positive.
Findings suggest there’s no difference in the patterns of Aβ and tau in Parkinson’s patients or healthy individuals, and that the molecular mechanism behind dementia is not increased in cognitively normal Parkinson’s patients.
Additionally, no significant association between Parkinson’s patients’ cognitive status (normal vs. mild impairment), age, β-amyloid and tau levels was found.
However, tau deposits were significantly increased in Aβ-positive patients within brain regions related to dementia, compared to Parkinson’s patients who were found without deposits of β-amyloid.
“Results of the present study suggest that deposits of tau in patients with [Parkinson’s disease] without dementia are related to age and Aβ-status,” researchers concluded.
A team from NUI Galway has built a device that helps those with Parkinson’s to manage one of the disease’s most debilitating symptoms.
Some major strides towards the treatment and possible cure for Parkinson’s have been made in recent years, such as a collagen implant that helps to support transplanted healthy cells in the brain.
But, in the short-term, those living with the central nervous system disorder may receive a helpful solution with a new device developed by a team of researchers at NUI Galway’s Cúram medical device research centre.
The device, called ‘cueStim’, is designed to help those living with the disease to overcome ‘freezing of gait’ (FOG), a feeling whereby their feet are stuck or glued to the floor, preventing them from moving forward.
FOG can often be triggered by cognitive factors such as distraction or anxiety, or while passing through doorways or tight spaces.
Worn across the waist, the device electrically stimulates a change in the body capable of triggering an exit from FOG or to prevent an event occurring.
The cueStim is controllable through Bluetooth via a smartphone and will allow a person to get moving again.
The project’s co-principal investigator, Dr Leo Quinlan, said of the breakthrough: “The severity of FOG depends on the stage of the disease, and it can have a very severe impact on quality of life, affecting people with Parkinson’s’ ability to walk for extended periods of time, and is a common cause of falls in Parkinson’s disease.”
Part of EU research project
This first-generation device resulted from NUI Galway’s involvement in the €4.7m European FP7 project Rempark and through Cúram’s Human Movement Laboratory.
The latter is currently working to further enhance the technology, particularly in the area of usability and human factors through the EscapeFOG project by working with Parkinson’s patients at the Clare Parkinson’s Support Group.
The group’s public relations officer, TJ Waters, said of the undertaking: “The opportunity to view first-hand the research being undertaken to improve the quality of life for people with Parkinson’s was an experience not to be missed.
“Clare Parkinson’s Support Group members are delighted to have an active role in this exciting project, which will be of benefit ultimately to people with Parkinson’s throughout the world.”
The Cúram group has called on anyone looking to participate in future studies to contact the system’s lead designer, Dean Sweeney, via email.
Colm Gorey is a journalist with Siliconrepublic.com
December 21, 2017 by Tristan Horrom, Veterans Affairs Research
Richard Hutton, a patient at the Parkinson's Disease Research, Education, and Clinical Center at the Corporal Michael J. Crescenz VA Medical Center in Philadelphia, underwent deep brain stimulation back in 2009. Here, he gets checked by Dr. Meredith Spindler. Credit: Tommy Leonardi
A treatment called deep brain stimulation (DBS) could extend the life of people with Parkinson's disease. Researchers at the Edward Hines, Jr. VA Hospital in Illinois found that patients who received stimulation via an implanted device had a modest survival advantage compared with those treated with medication only.
The results appeared in the Nov. 18, 2017, issue of Movement Disorders.
Previous studies have shown that DBS can improve motor function in people with Parkinson's disease. The treatment involves electrodes surgically inserted into specific areas of the brain. An impulse generator battery—similar to what is used in pacemakers—is also implanted, under the collarbone or in the abdomen. The battery creates electrical impulses that the electrodes deliver to the brain tissue.
Dr. Frances Weaver, lead author on the study, explained the benefit of DBS: "Overall, DBS surgery has been viewed quite positively by both patients and providers. There is an immediate effect on patients who have DBS on their motor function—the dyskinesia [involuntary muscle movements] is either gone or greatly reduced. The patient can move around and do things they hadn't been able to."
While deep brain stimulation may improve function compared with those who do not receive it, little evidence exists on whether the treatment has any benefits to life expectancy. To answer that question, the researchers looked at data for 611 Veterans with Parkinson's disease who had a deep brain stimulation device implanted. They compared this with data on 611 Veterans with Parkinson's but without the device. The data came from VA and Medicare administrative files from between 2007 and 2013.
The researchers found that patients treated with deep brain stimulation survived an average of 6.3 years after the surgery, versus 5.7 years for the non-DBS patients after the date they might have gotten surgery based on their match to a surgery patient—a difference of eight months. The researchers had paired each DBS patient with a clinically and demographically similar non-DBS patient—for example, in terms of age and symptom severity—and tracked survival from the date when surgery either took place, for the DBS group; or might have theoretically taken place, for the non-DBS group.
The average age of veterans in the study was 69, reflecting the higher prevalence of Parkinson's among older people. The older age of the study group could have led to more deaths from age-related conditions, but the researchers point out that a majority of the causes of death for those who died during the study period were related to Parkinson's disease.
While the survival edge in the DBS group is modest, the researchers point out that quality of life is also improved following DBS, mostly because the treatment can help control symptoms such as tremors and rigidity.
While the results suggest that deep brain stimulation could improve survival rates for patients with Parkinson's disease, the researchers note a few limitations to the study. They explain that it is possible that deep brain stimulation patients were healthier than their counterparts in the medication-only group. Patients with the implanted surgical device were more likely to have been monitored closely, so other chronic conditions may have been diagnosed and treated earlier. The study group was also mostly male—because the veteran population is majority male—meaning that the results cannot necessarily be generalized to women with Parkinson's disease.
Parkinson's disease is a neurodegenerative disorder. It affects neurons in the brain that produce dopamine. Its cause is currently unknown, and so far there is no cure. Parkinson's itself is not fatal, but complications related to the disease often lead to death. Common symptoms of Parkinson's disease include tremor, slowness of movement, limb rigidity, and walking and balance problems. People with Parkinson's disease have a shorter life expectancy than those without the disease.
While medication can manage symptoms of the disease, it has not been shown to improve survival for those with Parkinson's. As Weaver explains, patients usually undergo DBS surgery when the medication is no longer effective. "The surgery may get patients back to where they were when the medication was effective. That is, DBS is typically as effective as the medication—if the medication was still working," she says.
The researchers believe that more research is warranted into whether DBS can extend life expectancy in Parkinson's disease. It remains unclear whether the treatment modifies the actual disease, or just helps control the related conditions that may shorten life. According to Weaver, the improved quality of life after DBS may improve survival. It is also possible that the ongoing monitoring required with DBS means that patients are getting more medical attention in general, leading to better care. More research is needed to see what direct effect DBS has on neuroplasticity or brain function.
Freezing of gait, an absence of forward progression of the feet despite the intention to walk, is a debilitating symptom of Parkinson's disease. Laser shoes that project a line on the floor to the rhythm of the footsteps help trigger the person to walk. The shoes benefit the wearer significantly, according to research by the University of Twente and Radboud university medical center, which will be published on December 20 in Neurology, the scientific journal of the American Academy of Neurology.
Walking problems are common and very disabling in Parkinson's disease. In particular, freezing of gait is a severe symptom which generally develops in more advanced stages. It can last seconds to minutes and is generally triggered by the stress of an unfamiliar environment or when medication wears off. Because the foot remains glued to the floor but the upper body continues moving forward, it can cause the person to lose her balance and fall.
Lines on the floor
Parkinson patient experience a unique phenomenon. By consciously looking at objects on the floor, such as the lines from a zebra crossing ('visual cues'), and stepping over them, they are able to overcome their blockages during walking. This activates other circuits in the brain, hereby releasing the blockages and allowing the person to continue walking. This is why patients often make use of floor tiles at home. With the lasershoes, these useful cues can be continuously applied in everyday life, to walk better and safer. The principle behind the laser shoes is simple: upon foot contact, the left shoe projects a line on the floor in front of the right foot. The patient steps over or towards the line, which activates the laser on the right shoe, and so on (see videos below the text).
Video 1: Patient walking with laser shoes switched off.
Beneficial effect
The present research study shows a beneficial effect in a large group of patients. The number of 'freezing' episodes was reduced by 46% with the use of the shoes. The duration of these episodes was also divided by two. Both effects were strongest in patients while they had not taken their medication yet. This is typically when patients experience the most problems with walking. But an improvement was also seen after the patients had been taking their medication.
"Our tests were administered in a controlled lab setting with and without medication," says researcher Murielle Ferraye. " Further research in their everyday environment is necessary. We plan on testing this using laser shoes that in the meantime came on the market."
Video 2: Patient walking again, but now with laser shoes turned on. Credit: Radboud University
Activating the laser
Of the nineteen patients who tested the shoes, the majority would be happy to use them. The patients did not seem to mind that the laser was activated for each single step. "Ideally, the laser should only be activated once the blockage is detected, but we're not quite there yet," says Ferraye. "Freezing is a very complex phenomenon."
Murielle Ferraye, who developed the laser shoes, conducted her study at the Donders Institute at Radboud university medical center and the MIRA Institute for Biomedical Technology and Technological Medicine at the University of Twente.
December 21, 2017 by Kylie Gionet, The Conversation
The experimental technique of ‘deep brain stimulation’ has improved the lives of patients with treatment-resistant depression, despite the ‘failure’ of a large clinical trial. Credit: Shutterstock
It was a gloomy, rainy October day in 2007 when Kathryn began to see in colour again. This day marked the moment she started to recover —from a 19-year battle with a profoundly disabling treatment-resistant depression.
Kathryn had gone shopping early that morning. When she left the mall and walked outside, all she saw were the colours of the leaves on the trees.
"Seeing these blazing reds, intense yellows and oranges in a way that I hadn't seen in years," said Kathryn. "I started to sob right in that parking lot."
Severe depression is insidious. Kathryn describes it not as an intense sadness, but as a numbness —the inability to feel anything at all. According to the World Health Organization, depression is the leading cause of disability worldwide. And research on treatment-resistant depression shows that one third of people don't respond to trials of multiple medications and treatment, such as psychotherapy and electroconvulsive therapy.
The day Kathryn's senses came "back online" was two years, two months and five days after undergoing an experimental brain surgery —known as deep brain stimulation (DBS).
But before the Food and Drug Administration can approve DBS, clinical trials must show that it is safe and can effectively fight chronic cases of treatment-resistant depression.
Turning down the sadness
Physicians started experimenting with DBS for chronic, treatment-resistant depression in 2003. In this procedure, a surgeon drills a small hole into the skull and directs an electrode down into a region called Brodmann area 25 (BA25) —what Dr. Andres Lozano, a neurosurgeon at Toronto Western Hospital and leader in the field of DBS, has referred to as the "sadness centre of the brain."
The other end of the electrode is tunnelled down under the skin to a battery, or pacemaker-like device, in the chest. Doctors then use a remote control to turn up or down —like the volume on a speaker —the amount of electricity delivered to that area of the brain.
While DBS refers to "stimulation," it is actually an inhibitory effect that is at work. The current from the electrodes are turning down sadness, pumping the brakes. In people with treatment-resistant depression this area of the brain is very active and medication or psychotherapy can't quieten it down.
Like most surgeries, DBS still carries risks, but it is now an approved treatment for Parkinson's disease and essential tremor.
Failed trial, successful treatment?
DBS is not a cure. If stimulation stops, the depression will return. It's also not a quick-fix. DBS puts the brakes on sadness and, over time, sets other areas of the brain in drive, but the real work happens afterwards.
The summary of the study confirmed the safety of the procedure but did not show significant success in reducing depression at the six- and 12-month period. A closer look at the research's long-term data tells a different story.
St. Jude Medical, the company that sponsored the trial estimated that the study had a low likelihood (17 per cent chance) of success if it continued, and so it stopped recruiting new participants. (St. Jude Medical was acquired by Abbott earlier this year.) "It wasn't going as they expected. It's very expensive. And they made a business decision to stop the trial," said neurologist Dr. Helen Mayberg of Emory University in Atlanta.
Ninety participants initially took part in the study and were randomly assigned to two groups —60 of them receiving active stimulation, the other 30 receiving no stimulation. Patients did not know which group they belonged to.
Initially the BROADEN trial found no significant difference in efficacy between the group receiving stimulation and the group in which the device was implanted but not turned on. But, as Dr. Mayberg said, "a failed trial is not a failed treatment."
There was a second phase of the research, where 77 of the initial 90 patients entered into a four-year follow-up. In this part of the study all patients received treatment. After two years, nearly half of all patients had responded to the therapy —48 per cent (25 patients) achieved an antidepressant response and 25 per cent (13 patients) achieved remission.
This seems to suggest that "it may take longer to get better the more chronically ill you are," said Dr. Mayberg. In her own research, Dr. Mayberg said that unless the DBS system breaks, or has to be removed because of infection, "we actually don't have people ever going back to their pre-surgical state."
Deep brain stimulation for Parkinson’s disease. Credit: Shutterstock
That being said, more compelling evidence is needed to make any real case for DBS. That will require additional studies —which means more patients.
'This is not a pill'
In the BROADEN trial, 28 patients experienced 40 serious adverse events during the first year of the study; eight of these (in seven patients) were related to the device or surgery. Complications included infection, skin erosion and one postoperative seizure. Other serious adverse events were related to the treatment-resistant depression itself. There were two deaths by suicide.
Patients in the BROADEN trial had the most severe cases of treatment-resistant depression, being already 12 years into their depressive episode when they joined. This may explain the slowed response shown in the trial. The placement of the electrodes in DBS is also important to the surgery's success. Thirteen surgical centres participated in the trial, so there were differences in how the surgery was performed from centre to centre.
"This is not a pill, it's a surgical procedure," said Dr. Lozano, "so there's much more variability in the surgical procedure than there is in taking a simple medicine." Following this study, more targeted approaches to the placement of DBS electrodes have since been developed.
Of those patients enrolled in the BROADEN trial, 44 are still being treated today and getting their DBS batteries changed, on average, every three to five years.
When I reached out to Abbott (the sponsors of the trial) they informed me that they continue to provide device support to the trial patients that kept their DBS implants in, and have agreed to supply them with rechargeable batteries. If a patient wants the system removed, Abbott has said it will pay.
Rebuilding a life
Kathryn, one of Dr. Mayberg's first patients (and not part of the BROADEN trial), is one of those for whom DBS has worked. Her road to recovery hasn't been easy. Prior to her DBS surgery, she had tried over 40 different medications, electroconvulsive therapy and psychotherapy. Kathryn had very real plans of suicide throughout the years before her surgery.
"Recovery is actually a very long process. It's not like you just wake up one morning and your depression is gone and your life is wonderful," said Kathryn. It's been 10 years now since that momentous October morning when the grey lifted. Today, Kathryn doesn't take medication and has no residual symptoms of depression. She so far has had no adverse effects to DBS.
Her case is unusual. Most patients need some form of medication. Kathryn wants others considering this road to have realistic expectations.
Just as after any surgery, there is rehabilitation after DBS. When someone has their hip replaced they must learn to walk again, said Dr. Peter Giacobbe, a Toronto psychiatrist at the University Health Network who works with DBS patients and worked closely with Kathryn.
It's the same with surgery for depression, "these people need to learn how to rebuild their lives and undo past ways of connecting with others," he said. "The people who successfully do that, you can see that they're able to go back to work. Their remission rates creep up over one to three years."
As for Kathryn, today she lives a very full life. She works, volunteers, sits on a number of committees and is involved with patient-engagement work related to mental health. It's quite a change for someone who once struggled to leave her bed.
'Til device or death do you part'
"DBS is a long-term prospect," said Dr. Giacobbe. "We work with these people for 15 years [or more]. You get married to them in some ways … it's 'til device or death do you part."
DBS, because it's a surgery, also has the opportunity to further destigmatize mental illness, said Dr. Giacobbe, "by showing people that a physical intervention can help an emotional disorder."
In the meantime, while we wait, we have hope. And for those struggling, hope remains a most powerful medicine.
December 21, 2017 by Deborah Wormser, UT Southwestern Medical Center
C. elegans (roundworms). Credit: UT Southwestern Medical Center
UT Southwestern Medical Center researchers find that an FDA-approved drug to treat high blood pressure seems to extend life span in worms via a cell signaling pathway that may mimic caloric restriction.
The drug, hydralazine, extended life span about 25 percent in two strains of C. elegans (roundworms), one a wild type and the other bred to generate high levels of a neurotoxic protein called tau that in humans is associated with Alzheimer's disease.
"This is the first report of hydralazine treatment activating the NRF2/SKN-1 signaling pathway. We found the drug extends the life span of worms as well as or better than other potential anti-aging compounds such as curcumin and metformin. The treatment also appeared to maintain their health as measured by tests of flexibility and wiggling speed," said Dr. Hamid Mirzaei, Assistant Professor of Biochemistry at UT Southwestern and senior author of the study, published today in Nature Communications.
The NRF2 pathway protects human cells from oxidative stress. The body's ability to protect itself against damaging oxygen free radicals diminishes with age, he said.
One of the hallmarks of aging and neurodegenerative diseases such as Alzheimer's and Parkinson's is oxidative stress, which is believed to result cumulatively from inflammatory and infectious illnesses throughout life, Dr. Mirzaei explained. SKN-1, a C. elegans transcription factor, corresponds to NRF2 in humans. Both play a pivotal role in their respective species' responses to oxidative stress and life span, he said.
The UT Southwestern researchers were searching for a chemical probe they could use in experiments to identify proteins that get oxidized and become toxic during aging. Their screen for a substance that would cross the blood-brain barrier and be nontoxic led them to hydralazine.
"Age-related neurodegenerative diseases are devastating, and those conditions are on the rise due to the increase in the life span of humans. For that reason, it is important to develop treatments to maintain human health as long as possible," said Dr. Mirzaei, who is also an investigator in the Center for Alzheimer's and Neurodegenerative Diseases, part of the Peter O'Donnell Jr. Brain Institute at UT Southwestern.
The researchers did in vivo (in a living creature) and in vitro (in a lab dish) studies on the worms and also studied human cells from a pediatric cancer called neuroblastoma. Compared with untreated controls, roundworms treated with the drug showed about a 25 percent increase in life span (from 15-18 days to about 20-23 days), the team reported.
The results of a series of biochemical experiments indicated that the hydralazine-linked life span extension was dependent on the worms' SKN-1 pathway via a mechanism that appeared to mimic caloric restriction, he said.
To test the potency of hydralazine in the context of neurodegenerative disease, the scientists used a high dose of a chemical stressor called rotenone that is associated with increased risk of Parkinson's disease in humans exposed to high doses. They found that hydralazine provided a significant amount of neuroprotection, Dr. Mirzaei said. The drug also showed a significant decrease in tau toxicity in the C. elegans model of Alzheimer's disease, he added.
"Based on these results, we suggest that hydralazine may be a good candidate for clinical trials for the treatment of age-related disorders in humans as it may also offer general health benefits to the aging population," he said.He stressed that this study is a promising first step, but further studies are needed to corroborate it.
Lewy body dementia (LBD) is a disease associated with abnormal deposits of a protein called α-synuclein in the brain. These deposits, called Lewy bodies, affect neurons in the brain and lead to problems with thinking, movement, behavior, and mood. LBD is one of the most common causes of dementia, after Alzheimer’s disease and vascular disease. Now, a team of investigators led by researchers at University of College London (UCL) has just released data from a comprehensive genome-wide association study showing that LBD has a unique genetic profile, distinct from those of Alzheimer's disease or Parkinson's disease.
"Dementia with Lewy bodies accounts for 10% to 15% of dementia cases, yet our understanding of it lags beyond the more well-known Alzheimer's disease, partly because it's commonly misdiagnosed,” explained senior study investigator Jose Bras, Ph.D., a UCL Institute of Neurology and Alzheimer's Society senior research fellow. “Our findings clarify the disease's distinctive genetic signature, which should, in the future, help improve clinical trials and lead to more targeted treatments.”
The research team genotyped 1743 patients with LBD—including both clinical samples and 1324 pathological samples assessed postmortem—and 4454 controls. Interestingly, two of the genetic loci that were found to be significantly associated with DLB—APOE and GBA—bore the same associations to DLB as they do to Alzheimer's and Parkinson's, respectively. Another one of the loci identified—SNCA—is also associated with Parkinson's, but differently; the researchers found that a different part of the gene is linked to DLB. They also found preliminary evidence for a gene locus that had not been previously associated with DLB, but the results did not reach significance.
Remarkably, the investigators noticed that a few loci typically associated with Alzheimer's and Parkinson's do not appear to be associated with LBD. However, the researchers were able to identify a heritability estimate of LBD for the first time at 36%, which is similar to that of Parkinson's. The heritability was particularly high for four specific chromosomes, suggesting that further research could focus on those chromosomes to identify novel loci.
"As the gene loci that had previously been associated with LBD were also implicated in Alzheimer's and Parkinson's, it was unclear if LBD’s genetic roots were simply a combination of the other two diseases,” noted lead study investigator Rita Guerreiro, Ph.D., a UCL Institute of Neurology and Alzheimer's Society senior research fellow. “We've confirmed that instead it has its own unique genetic profile. The selection of study participants has been a substantial challenge in dementia trials. Our findings can be used to identify more clearly which type of dementia each person has, so that they can take part in the right clinical trial, which could lead to better treatments and diagnostic tools.”
The researchers also hope that by advancing the understanding of which genes play a role in LBD, their results will aid in the development of targeted therapies.
"LBD and Parkinson's have many similarities, as people with LBD often develop Parkinson's symptoms, and Parkinson's often leads to dementia,” Dr. Bras remarked. “By understanding the genetic underpinnings, we can more effectively target treatments to the different groups."
Doug Brown, Ph.D., director of research at Alzheimer's Society, which funded the study, added that "dementia with Lewy bodies is often misunderstood as being a mixture of Alzheimer's and Parkinson's, but this confirms it's actually a unique condition. Despite LBD being one of the most common forms of dementia in older people, until now there simply hasn't been enough information on its causes, so the finding that up to 36% of cases might be genetically inherited is a real revelation.”
"As the largest and most detailed study of its kind, these results will be invaluable in future research, and it's a great milestone on the road towards our goal of understanding and treating all forms of dementia," Dr. Brown concluded.
