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​​Dystonia Tips and Research Blog

DYT-1, DYT-6 and XDP dystonias: A conversation with an expert

6/21/2020

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Who is Cristopher Bragg?
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DR. CRISTOPHER BRAGG
Dr. Cristopher Bragg is an Assistant Professor of Neurology at Massachusetts General Hospital and Harvard Medical School.  His lab studies cellular mechanisms underlying hereditary dystonias, with a current focus on three forms in particular:  DYT1 dystonia, DYT6 dystonia, and X-Linked Dystonia-Parkinsonism (XDP).  He also serves as the Director of the MGH Collaborative Center for X-Linked Dystonia-Parkinsonism (CCXDP), an international consortium focused exclusively on a rare syndrome that is endemic to the Philippines.
What are DYT1, DYT6, and XDP?
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THAP1 DYT-6 MOLECULAR STRUCTURE
DYT1 and DYT6 are both generalized dystonias that typically develop in childhood or adolescence.  They are often designated as “isolated” or “pure” dystonias, because in most patients, dystonia is the sole or primary symptom.
XDP, in contrast, usually arises in adulthood, most often during the third or fourth decade of life.  Unlike DYT1 and DYT6, XDP combines features of both dystonia and parkinsonism often in a temporal progression.  The pattern that has been documented most frequently consists of an initial focal dystonia that spreads to other body regions— as parkinsonian symptoms also emerge over time.  Some patients, however, may exhibit parkinsonian signs as the first symptom and experience a milder course of disease progression,— and the reasons for this heterogeneity are not yet understood.
What causes these disorders?
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XANDRA BREAKEFIELD PHD
The genetic cause of DYT1 was discovered in 1997 by Drs. Xandra Breakefield and Laurie Ozelius at Massachusetts General Hospital.  It was the culmination of many years of painstaking work that took place long before the human genome was sequenced, when the methods for finding disease-related genes were still in their infancy.   They found that DYT1 patients had a specific deletion in a small stretch of the TOR1A gene, which encodes a protein termed torsinA.  Since that first report, a small number of additional mutations in TOR1A have been found, but the vast majority of DYT1 patients all appear to share the same original gene variant.
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LAURIE OZELIUS PHD
DYT6 dystonia is associated with mutations in the THAP1 gene.  Unlike DYT1, which is caused by the same gene deletion in nearly all cases, DYT6 has been linked to a large number of different mutations in THAP1.  It is not yet known if these different mutations  account for differences in symptoms, as so far there are no clear relationships between variants in THAP1 and patterns of clinical disease.
While cases of DYT1 and DYT6 have been found in multiple patient populations around the world, XDP has arisen uniquely among individuals with ancestry to the island of Panay in the Philippines.  It is caused by the insertion of a long stretch of DNA called a “retrotransposon.”  Retrotransposons come in several varieties, many of which have been derived from ancient viruses that deposited their genetic content into our genomes millions of years ago.  They are considered “mobile DNA” because of their ability to move from one chromosome to another by reinserting copies of themselves into other genomic locations  - a discovery first made by Dr. Barbara McClintock for which she was awarded the Nobel Prize in Medicine in 1983.  All living organisms contain various forms of mobile DNA.  In humans, these elements are scattered throughout our genomes; most are completely benign and have lost their ability to move over the course of evolution.  However, a few types of retrotransposons are still active, and within the Panay population, one such example has become inserted into a gene called TAF1, thereby disrupting its function and causing XDP.
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BREAKEFIELD LABORATORY
Why study these syndromes together?
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XDP DYSTONIA WHICH IS VERY COMMON ON THE ISLAND OF PANAY
Despite the differences between DYT1, DYT6, and XDP, the proteins that are affected in these syndromes play inter-related roles within cells. The DYT6 protein, THAP1, and XDP protein, TAF1, both reside within the cell’s nucleus and regulate how genes are turned on or off, a process known as transcription.  The DYT1 protein, torsinA, acts within the adjacent envelope that surrounds the nucleus and is important for its shape and organization.   Numerous research studies over many years have characterized how torsinA functions within the nuclear envelope and how the mutation that causes DYT1 dystonia may compromise this cellular compartment.  Less is known about THAP1 and TAF1, but recent studies are now revealing how transcription in DYT6 and XDP cells is affected by the dystonia-related variants in these genes. 
The Bragg lab studies these and other dystonic syndromes together by analyzing patient cells and characterizing their patterns of gene transcription, which can reveal cellular pathways that are affected in these cells.  The overall goal of this work is to look for any defects that may be common to multiple forms of dystonia.  If such deficits exist, then they may represent potential targets for designing new therapies that would be of broad benefit to patients with dystonia.
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Dr. Edgar Rodriguez weighs in onĀ Gene Therapy for Brain Diseases: A Path for DYT-1 Dystonia

6/3/2020

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SCIWORTHY.COM (PICTURE) WHICH HAS GREAT IMAGES AND A GREAT SUMMARY WEBSITE OF THIS TOPIC!
Gene Therapy for DYT-1 Dystonia and other diseases?

We sat down with one the experts on gene therapy for DYT-1 dystonia and other central nervous system diseases and we picked his brain on this topic. The interview was fascinating!


​Who is Edgar Rodriguez?
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Dr. Edgardo (Edgar) Rodríguez-Lebrón has 20 years of experience in the gene therapy space with a focus on diseases of the nervous system. He has engineered and developed gene-based therapies to prevent or reverse neurodegenerative processes caused by the accumulation of toxic mutant proteins. He is currently Scientific Advisor to Tyler's Hope, Chief Science Officer of Andante Biologics and a co-founder of early-stage biotech companies developing molecular therapies for CNS diseases. He holds an Adjunct Faculty appointment at the University of Florida where he trained as a graduate student. Go Gators!

Often, diseases that affect the brain are caused by genetic mutations that prevent the normal function of a gene. In other cases, genetic mutations can cause a gene to ‘gain’ a new function that is toxic to the brain. 


​Gene therapies are a class of medicines designed to specifically (i) replace a missing genetic function, (ii) block a ‘gained’ toxic genetic function, or (iii) limit or enhance cellular pathways to support overall brain function. 
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What is a viral-based gene therapy? 
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  • It is a type of gene therapy that uses a virus as a vector, think a ‘shuttle’ or ‘delivery truck’, to introduce genetic cargo into cells. The genetic cargo is designed to replace a missing gene, or suppress the function of a toxic gene, or modify cellular pathways to support normal tissue function.
  • Viruses are fully optimized genetic machines capable of penetrating into cells and delivering genetic material with high efficiency. One virus capable of delivering genetic material to neurons and other cells in the brain in a safe and effective fashion is the adeno-associated virus (AAV).
  • AAV is a naturally occurring virus that has not been connected to any known human disease or pathology. When used as a gene therapy vector, 95% of the AAV’s natural genetic sequence is removed and replaced with the therapeutic genetic cargo.
  • AAV vectors used in gene therapy can enter the cell and deliver therapeutic DNA but are incapable of replicating and cannot sustain a normal virus infection cycle.

What makes AAV a desirable vector for CNS-targeted gene therapies?
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  • AAV is desirable because:
  • AAV has evolved a natural ability to enter human neurons and effectively deliver genetic material to their nucleus.
  • The genetic material delivered by AAV vectors does not become incorporated into human DNA, i.e. the human genome, and instead remains as a stable, independent molecule within the nuclear compartment of the cell. This drastically lowers the risks associated with randomly inserting pieces of genetic material into the human genome.
  • There are many variants or ‘flavors’ of AAV that differ in their protein capsid shell (i.e. the outer covering that shields and encapsulates the genetic material). This diversity allows scientists to select particular AAV vector variants to achieve effective delivery of genetic material into different cells in our bodies, including neurons.
  • For example, some AAV vector variants can be infused into the circulatory system, cross into the brain, and deliver genetic material to neurons in the central nervous system.

What are some recent major developments in AAV CNS gene therapy?
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Recent developments include:
  • The most important recent development was the approval of 2 different AAV-based gene therapy drug products by the FDA. One of these, Zolgensma made by Novartis, is an AAV gene therapy for the treatment of Spinal Muscular Atrophy.
  • More than 40 clinical studies have investigated or are investigating the therapeutic potential of AAV-based gene therapies in human CNS diseases.
  • Artificial intelligence and machine learning algorithms are now being employed to redesign and engineer the AAV protein capsid shells to generate novel variants with more effective, targeted gene delivery properties.
  • Large-scale manufacturing of clinical-grade AAV vectors is becoming streamlined.
What are some of the major hurdles still being faced by AAV-based gene therapies?
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Hurdles include:
  • AAV vectors are live viruses that can be recognized by the immune system as ‘foreign’ agents.
  • More than half of us have already developed some level of ‘immunity’ to naturally occurring variants of AAV that exist in the population.
  • This ‘pre-existing’ immunity to AAV needs to be overcome for AAV gene therapy vectors to effectively reach their target cells and deliver the therapeutic genetic material before being neutralized by the immune system.
  • To address this challenge, clinicians are testing immunosuppressive drug cocktails that could temporarily put the immune surveillance system ‘to sleep’ while the AAV gene therapy delivers the genetic cargo.
  • At the same time, scientists continue to re-engineer the AAV vector capsid shell to make it be like a stealth genetic delivery shuttle system.

How can an AAV-based gene therapy be used in DYT1 dystonia?
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Applications to DYT-1:
  • DYT1 dystonia is primarily caused by the inheritance of mutations in the TOR1A gene.
  • It remains unclear exactly how mutations in TOR1A lead to dystonia. However, multiple studies suggest that the primary TOR1A mutation, p.302/p.303delE, destabilizes the protein, causing a partial loss of gene function. 
  • The matter is further complicated by the fact that the TOR1A protein likes to self-associate. It appears that in DYT1, when the mutant form of TOR1A associates with the normal form of TOR1A, it impairs the function of the normal TOR1A protein.
  • Based on this important knowledge, researchers are designing and testing AAV-based therapies to (1) enhance the function of the normal TOR1A protein, (2) selectively block expression of the mutant TOR1A protein or (3) enhancethe function of the normal TOR1A protein and simultaneously block expression of the mutant form of TOR1A.

What is on the horizon for AAV-based gene therapies as it applies to DYT1?
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On the horizon:
  • Identification of the neurons and brain regions that are primarily affected in DYT1. This will help guide AAV-based gene therapies by providing ‘the right zip code’.
  • Engineering and discovery of new AAV capsid variants that can more broadly target affected brain regions in the DYT1 brain.
  • Deployment of genetic cargo that can facilitate direct and precise ‘editing’ of the TOR1A genomic sequence to replace disease-causing mutated sequences in the TOR1A gene with non-disease causing sequences.
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Dr. Aparna Wagle Shukla weighs in on the "Top 5" things you need to know about COVID-19 and dystonia care

4/14/2020

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COVID-19 and Dystonia Care: What do you need to know?
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While we patiently wait for the COVID-19 crisis to resolve, we approached leading dystonia experts for tips and advice on caring for patients. We were fortunate to sit down with one of the leading clinical and research experts, neurologist Dr. Aparna Wagle Shukla. She shared with us her “top 5” tips for dystonia care during the COVID crisis.

Who is Dr. Aparna Wagle Shukla?
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  • Aparna Wagle Shukla MD is a physician-scientist who provides clinical care for patients with dystonia and she has focused her laboratory on identifying new treatments for focal and generalized forms of dystonia. Dr. Wagle Shukla is the clinical director for Tyler’s Hope Foundation for Dystonia Cure.
  • Dr. Wagle Shukla is an expert on dystonia treatments including pharmacological therapies (pills), botulinum toxin injections, surgical management (DBS), and also on rehabilitation based therapies.
  • Her lab develops novel treatment approaches including exercise. She has performed many studies involving the use of repetitive transcranial magnetic stimulation (TMS); a brain stimulation treatment currently approved by the FDA for treating medication refractory depression.
  • She has been funded by various dystonia organizations and also by the National Institutes of Health. She has published over 75 research articles in prestigious journals such as Brain, Neurology, Journal of Neurology Neurosurgery and Psychiatry (JNNP), Parkinsonism and Related Disorders and Movement Disorders.
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What should every dystonia patient know about the Corona virus?
  • COVID-19 is a viral infection caused by a Coronavirus. The infection first emerged in December 2019 in Wuhan, China.
  • The World Health Organization named the infection COVID-19 (Coronavirus disease of 2019) and declared it a pandemic in March 2020.  The infection has been spreading rapidly across the world….and some have compared it to a raging wildfire.
  • COVID-19 presents with symptoms of fever, common cold symptoms, cough, headaches, muscle aches, difficulty breathing, and in< 20% of patients pneumonia. The pneumonia may requiring hospital support.
  • Signs and symptoms of COVID-19 commonly appear two to 14 days after exposure to the Coronavirus.
  • There is currently no cure and there is no vaccine.
  • Those who believe they may have the illness should seek medical treatment immediately. We can help others and also help ourselves by taking many precautions.
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THERE IS NO VACCINE FOR COVID AT THE CURRENT TIME WHICH MEANS PREVENTION IS THE KEY.
  • We can “flatten the curve” of rising infection numbers.
  • The curve refers to how many patients will present with the Coronavirus and how fast they will seek medical attention. If the curve is steep and goes straight up quickly, all of the infections will come at once and this will quickly overcome the healthcare system since we don’t have enough beds, ventilators, protective gear, etc. By socially distancing and isolating we can prevent a rapid peak, save lives and not overcome the capacity of hospitals.
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What are important precautions every dystonia patient should take at home?
  • Wash your hands. Wash them often with soap and water for at least “20 seconds.” Be sure to wash your hands with soap, scrubbing all the surfaces between and around your fingers for at least 20 seconds and dry them thoroughly. When you cannot wash your hands, use a hand sanitizer that contains at least 60% alcohol.
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  • Carry a small bottle of hand sanitizer. When in public spaces, use a hand sanitizer that contains at least 60% alcohol.
  • Clean the surfaces around you that you may contact. Stay as healthy as possible and use disinfectant wipes especially in public areas.
  • Avoid touching your eyes, nose, and mouth with unwashed hands.
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How important is social distancing for dystonia patients? What is the risk of COVID-19 in dystonia?
  • If there is a COVID-19 outbreak in your community, stay home as much as possible as this will reduce your risk of being exposed.
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  • There is not an increased risk of getting COVID-19 if you have dystonia.
  • There is however an increased risk for complications and you may have a more difficult recovery.
  • Social distancing means avoiding gatherings of people and trying to limit public interactions to only the absolute essentials such as groceries and gasoline purchases.  Though note that even groceries can in many zip codes be delivered.
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  • While in public settings such as grocery stores or when visiting a hospital, one should keep at least 6 feet distance between other people. This will help to avoid droplets containing the virus to be spread .
  • Avoid cruises and all non-essential air travel.
  • The CDC recommends that if in public wear a mask or something to cover your nose and mouth.
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What should a dystonia patients know about medication management during the COVID-19 crisis? What about the need to see a doctor during the COVID crisis?
  • Write down or print a list of all your medications. Include the medication name, strength, times taken and dosages.
  • Stock up on supplies. When you have the option, you may consider switching prescriptions to 90-day supplies. This can reduces trips to the pharmacy.
  • Check all your medications. Take inventory of your list and re-order any that are running low.
  • Make sure you have made a list of your doctors with recent contact information and take it with you in the event of a hospitalization.
  • Call your doctor when you have your very first symptom.
  • Your doctor will likely want to monitor you including your dystonia symptoms and COVID symptoms and your doctor will make the decision as to whether you will need COVID testing.
  • If you have to attend the clinic, emergency room or hospital environment call before you go so arrangements can be made to keep you in a non-crowded waiting room.
  • Many doctors can manage you by telephone or telemedicine for your routine dystonia care as well as for possible COVID symptoms.
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What do you tell dystonia patients with deep brain stimulation (DBS) devices during the COVID-19 outbreak?
  • We advise checking with your DBS provider on options for optimal care of the DBS system while in your home. Some health care providers or DBS centers provide dystonia patients with multiple possible “groups or programs.” This is useful as the patient can cycle through the settings without actually having to come in person to the clinic.
  • Some clinicians offer patients the option to change other settings at home (voltage, how wide are pulses, how many pulses)
  • During the early stages of programming following surgery, some patients will have worsening of their dystonia symptoms after a setting change.  The worsening can in some cases be a consequence of “a part of the brain fighting the “positive changes.” In other words, the DBS can flare the dystonia in some cases, but if you wait, it could get better. Calling your doctor for advice if you worsen is a good idea.
  • One unique aspect to dystonia DBS is that clinical benefits may not manifest for weeks to months.
  • We recommend that dystonia patients do not turn off the DBS device especially at night. This could worsen symptoms in many cases. Additionally, re-activation of the device may result in an uncomfortable side effect. 
  • If your DBS has been in place a long time it may be possible to be managed at home through the COVID crisis.
  • In some dystonia patients running out of battery can result in a serious flare in symptoms. You and your doctor should monitor battery life and plan for replacement to prevent rebound of symptoms. If your hospital deems the DBS battery an elective procedure you and your doctor may need to manage with medications until a replacement surgery is available.
  • Many centers consider DBS battery replacement as an urgent procedure.
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Dr. Vaillancourt's "Top 5" updates in imaging and drug/device development in dystonia

4/5/2020

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​There are so many exciting projects going on in dystonia research that it has become hard to keep up with all of the advances. We sat down with one of the worlds top dystonia and Parkinson imaging researchers (Dr. David Vaillancourt) to talk about the “top 5” updates in therapies and in dystonia imaging research.
​Who is David Vaillancourt?
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  • David Vaillancourt is Chair and Professor in the Department of Applied Physiology and Kinesiology at the University of Florida.
  • He is funded by Tyler’s Hope for a Dystonia Cure to do cutting edge imaging research and he collaborates with UF researchers Yuquing Li and Marcelo Febo.
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Yuquing LI, PHD.,
University of Florida
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Marcelo Febo, PHD.,
​University of Florida
  • Vaillancourt’s research focuses on how the brain regulates voluntary and involuntary movement with a specific focus on motor disorders.
  • He uses advanced neuroimaging techniques to study the functional and structural changes in the brain of humans and animal models.
  • He has used rehabilitative, surgical, and pharmacological interventions, and published his work in journals including Brain, Journal of Neuroscience, JAMA Neurology, Neurology, Human Brain Mapping, Neuroimage, Cerebral Cortex, and Neurobiology of Aging.
  • He has been continuously funded by NIH since 1999, and now directs several grants from NIH.
  • In dystonia he studies the pharmacological and neuroimaging in mouse and human models.
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1) What is imaging and how is it used in dystonia?
  • Neuroimaging is a broad term.  It encompasses imaging using positron emission tomography, magnetic resonance imaging, and other techniques.  In positron emission tomography, the approach is to inject a drug or tracer into the blood stream. This drug or tracer can cross into the brain.  The tracer is then imaged in an effort to measure how the neural receptors respond.  This procedure can be useful in many ways because the tracer can be designed to be specific to the neural receptors in the brain. 
  • In dystonia, the types of tracers that are mostly used are dopamine related tracers and cholinergic related tracers. 
  • Other forms of imaging include functional magnetic resonance imaging and structural magnetic resonance imaging.  These techniques examine how protons in water are affected by blood flow and tissue specific changes.  These methods can help to pinpoint where in the brain dystonia can manifest and where in the brain specific new therapies should be targeted 
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2) What is a specific example in humans for how imaging is being used         in dystonia?
  • In a recent study published in the journal Brain (Corp et al. 2019; PMID: 31099831) the authors used a clever approach.  They studied people with cervical dystonia who had lesions in the brain (e.g. strokes, tumors) causing the dystonia.  Whereas most types of dystonia do not have a visual lesion on the MRI, these authors focused on rare patients with visible lesions on their brain scan.  Next, they used a technique called resting state functional MRI to map a “connectome” type network that presumably links all of these brain regions together. 
  • The authors observed that two regions of the brain were connected to all of the brain lesions across all of the patients with cervical dystonia. Thus there were common nodes of dysfunction possibly underpinning the cause(s) of the dystonia.  The two regions— somatosensory cortex and the cerebellum— were found to link to all of the lesioned regions across all of the cervical dystonia patients.  This new finding tells us two things:
  • 1) It tells us that these two regions may be critical for therapies targeting dystonia; and
  • 2) It tells us that studies in dystonia may consider targeting therapies directly to these parts of the brain or to their connections.
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3) What is a specific example in animals for how imaging is being used         in dystonia?
  • The Calakos Laboratory at Duke University is working on new therapies to potentially help people with dystonia through a large alignment grant funded by Tyler’s Hope for a Dystonia Cure.  Their work is focused on therapies that can target specific cellular pathways.  They are focused on the eIF2alpha signaling pathway in DYT1 dystonia.  In a recent paper (Rittiner et al. 2016; PMID: 27939583) the authors found that patient-derived cells and a mouse model both supported a pathogenic role for this pathway (e.g. it was likely involved in dystonia). The authors also found that this pathway had therapeutic potential and may help to develop a “drug-able” target. 
  • Dr. Calakos is now working with Dr. Vaillancourt to test if a medication can be safely delivered to the brains of mice which are genetically similar to human DYT1 dystonia.  We are using a high-field MRI that goes up to 17 Tesla (a typical MRI is 1.5-3 Tesla).  The high-field MRI will provide enhanced signal for the tiny mouse brain so we can see the brain and the drug of interest. 
  • The experiments will determine if the medication is affecting the brain tissue of the mouse. This type of experiment will help move us closer to a therapeutic for dystonia.
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4) How can imaging be used in humans to assess a new therapeutic               (e.g. drug, device)?
  • If a therapeutic (e.g. drug, device) is deemed safe for humans, it can be further studied 
  • The safety is typically assessed in a Phase 1 study, which will examine different dose levels of a medication and will determine which levels are safe.  If a Phase 1 study is successful, the drug can move to a Phase 2 study where safety and other data readouts will be assessed (e.g. how well it works, what pathways does it affect).  In the Phase 2 study, imaging methods can be used to determine where in the brain a medication is influencing the system. 
  • In moving from a Phase 2 to a Phase 3 study, the investment for a device or pharmaceutical company can be significant, and thus the company will typically want to see several “readouts” that show the medication could will have the potential to work on the disease (e.g. dystonia).
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5) What does this all mean for people with dystonia?
  • I believe that these issues means several things and here is my interpretation:
  • 1) People care about you and care about dystonia.  There are labs across the world working on dystonia.  They are conducting studies in cells, live animals, and in human clinical trials. 
  • 2) Treatments take time to develop.  The studies that I have mentioned, took years to complete.  There are many other studies in the field of dystonia and even though this is a big effort, it takes time--it is 100% worth it. 
  • 3) Stay the course.  In research, sometimes research does not have a positive outcome.  It can take several years to find out you are “going down the wrong path.”  However, sometimes research yields a breakthrough that can change how we treat a patient and improve their quality of life.  This is what we hope for and strive for…so stay the course! We are optimistic we are making progress in imaging and dystonia drug/device research!
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    Dr. Michael Okun

    Executive Director of the Fixel Institute for Neurological Diseases which is part of the Center for Translational Research in Neurodegenerative Diseases, the McKnight Brain Institute, and the University of Florida College of Medicine. To read more books and articles by Michael S. Okun MD check Twitter @MichaelOkun or visit http://parkinsonsecrets.com/

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Tyler's Hope Foundation was established to advance research for a cure, discover effective treatments and to promote awareness and education of DYT1 Dystonia. 

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