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LES TURNER ALS FOUNDATION/HERBERT C. WENSKE PROFESSOR IN THE FEINBERG SCHOOL OF MEDICINE DAVEE DEPARTMENT OF NEUROLOGY AND CLINICAL NEUROSCIENCES.
Division director
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Teepu Siddique MD, the Les Turner ALS Foundation/Herbert C. Wenske Foundation Professor at the Feinberg School of Medicine, is an internationally recognized clinician-researcher in neuromuscular medicine. A gold medalist in botany from Islamia College, Lahore, Pakistan and a graduate of Dow Medical College, Karachi, Pakistan, Dr. Siddique completed a flexible internship in Perth-Amboy, NJ, followed by a residency in Neurology at the University of Medicine and Dentistry, New Jersey. He was a fellow in electrophysiology at Cornell and a Fogarty International Scholar at the National Institute for Neurologic Diseases and Stroke. He has held faculty appointments as physician-investigator at University of Southern California, Duke University and, since 1991, here at Northwestern University, where he was appointed the first Abbott Laboratories Susan and Duane Burnham Research Professor. Currently he directs the Division of Neuromuscular Medicine. His research interest include disorders of the motor system and frontal lobe dementias. He led the team that identified the first causative gene in Lou Gehrig disease (amyotrophic lateral sclerosis, ALS) and developed the first genetic model of neurodegenerative disease, which is still the most widely used model for study of ALS. He continues to lead an active research team that has identified additional genes that cause inherited ALS, hereditary spastic paraplegia, mitochondrial myopathy and inherited neuropathy. His current research focuses on the role of environmentally responsive genes in motor neuron degeneration and the use of induced pluripotent stem cells derived from patient skin cells to develop rational therapy for ALS and related disorders. His research has been continuously funded by the National Institutes of Health for his entire 24 year career. He was the first recipient of the Sheila Essey Award awarded by the American Academy of Neurology, given for his seminal work in ALS genetics. Additional honors have included the Hope Through Caring Award from the Les Turner ALS Foundation, the Forbes Norris Award given by the International Alliance for Motor Neuron Disease, as well as numerous community awards. He is the author of more than 200 peer reviewed publications. He serves on the editorial board of several specialty journals and NIH grant reviewing panels. |  |
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Faisal completed his medical training from Aga Khan University in 2005, where he was also junior faculty till 2006. He has worked as visiting research scholar at Yale, Harvard and Oxford, and completed his sub-internships in neurosurgery at UCLA and Henry Ford Hospital. He was awarded the STAR Award for medicine in 2003 and 2004. He has also served on the student editorial boards of Journal of Pakistan Medical Association and studentBMJ, and as reviewer for Archives of Neurology. Faisal joined the inter-departmental neuroscience program at Northwestern in 2006 on a University fellowship and is currently supported through a Mechanism of Aging and Dementia pre-doctoral NIH training fellowship. Faisal's research focus is in basic neural functions and wants to study these by exploring the molecular mechanisms that contribute to human neurodegenerative diseases. Among other disorders, Faisal is studying ALS as a prototype model of motor neuron dysfunction. He is interested in human genetics and the role of protein aggregation in the pathology of ALS and related disorders. Faisal is also interested in TRPV4-mediated human peripheral neuropathies and mitochondrial myopathy. |  |
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In 2000, Hasan completed his medical school from Damascus University. After Medical school Dr. Arrat has done a pathology residency in Damascus University for which he got a master degree. He joined our team in 2007. He is interested in discovering therapeutic drugs for ALS. Currently, he is working on high throuput drug screening on cell and animal model of ALS. |  |
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In 2007, Dr. Ajroud obtained her PhD from the Faculty of Mathematics, Physics and Natural Sciences, Tunis, Tunisia in collaboration with Biotechnology Group, Pasteur Institut of Tunis and the Leukocyte Biology and Inflammation Program of the Renal Unit of Massachusetts General Hospital, Harvard Medical School, Boston MA. Shortly after, she joined Dr. Teepu Siddique`s lab as a post doctoral fellow to work on protein misfolding mechanisms in amyotrophic lateral sclerosis (ALS). She is studying protein characteristics and function in order to identify different mechanisms of protein dysfunction in the biology of ALS. Since May 2008, her work has been continuously funded by the Blazeman Foundation for ALS Post-Doctoral Fellowship. |  |
Bioinformatician
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Kreshnik has joined our group in October of 2008. He obtained undergadute degree with honors from the University of Texas at Arlington and Masters of Science in Biomedical Engineering from a joint program of the University of Texas at Arlington and University of Texas Southwestern Medical Center at Dallas. His research focus is scientific and statistical programming, project management and algorithm development. To learn more about his work please visit Bioinformatics section of our research site. |  |
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Research Professor
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Dr. Lukas has been working with the Lab since 2003. His research interests are in the systems biology of neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and primary open angle glaucoma (POAG). Dr Lukas published our gene and protein expression data from tissues from the G93A-SOD1 mouse model of ALS (Mol. Cell. Proteomics 2006, 7:1233). The results provided differential signatures (protein or gene) that characterize the active disease state. From these signatures new drug targets for slowing or arresting disease progression are being investigated. Dr. Lukas also performs pharmacokinetic studies of new and existing drugs in mice and humans. For example, the metabolism of Riluzole (the only FDA approved drug for ALS) was investigated (Amyotroph. Lateral Scler. 2007, 8:305). In this work, the patient-to-patient variability in drug metabolism was not associated with genetic variants of CYP1A1/2, the enzymes that metabolize Riluzole. Dr. Lukas is currently working on new drug discovery for ALS and the relationship of genetic variants of environmentally sensitive enzymes with their biochemical properties in patient and normal populations. |  |
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Research Coordinator
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Emily is a Certified Clinical Research Professional (CCRP) and Certified Health Education Specialist (CHES) who was hired in August of 2009 to coordinate industry as well as federally funded clinical research studies in the peripheral neuropathy clinic. Her educational background is in health promotion and epidemiology, and she is currently enrolled in the Master of Science in Clinical Research and Regulatory Administration program here at Northwestern. Prior to being here at Northwestern, she worked for a Contract Research Organization (CRO) in Research Triangle Park, North Carolina, coordinating phase II/III multi-center sickle cell anemia research sponsored by the National Heart, Lung, and Blood Institute. |  |
Symptoms are weakness of the neck and limb muscles, muscle pain, and skin rashes affecting the cheeks, eyelids, neck, chest, and limbs. Onset ranges from childhood to late adulthood with progression and severity varying as well. This disease can respond to drug therapy. (Read more about Dermatomyositis)
Symptoms are weakness of the neck and limb muscles, muscle pain, and skin rashes affecting the cheeks, eyelids, neck, chest, and limbs. Onset ranges from childhood to late adulthood with progression and severity varying as well. This disease can respond to drug therapy. (Read more about Dermatomyositis)
Symptoms are weakness of the neck and limb muscles, muscle pain, and skin rashes affecting the cheeks, eyelids, neck, chest, and limbs. Onset ranges from childhood to late adulthood with progression and severity varying as well. This disease can respond to drug therapy. (Read more about Dermatomyositis)
Symptoms are weakness of the neck and limb muscles, muscle pain, and skin rashes affecting the cheeks, eyelids, neck, chest, and limbs. Onset ranges from childhood to late adulthood with progression and severity varying as well. This disease can respond to drug therapy. (Read more about Dermatomyositis)
Symptoms are weakness of the neck and limb muscles, muscle pain, and skin rashes affecting the cheeks, eyelids, neck, chest, and limbs. Onset ranges from childhood to late adulthood with progression and severity varying as well. This disease can respond to drug therapy. (Read more about Dermatomyositis)
Symptoms are weakness of the neck and limb muscles, muscle pain, and skin rashes affecting the cheeks, eyelids, neck, chest, and limbs. Onset ranges from childhood to late adulthood with progression and severity varying as well. This disease can respond to drug therapy. (Read more about Dermatomyositis)
Symptoms are weakness of arms, legs, hands, especially the thighs, wrists, and fingers. Onset is typically after 50 years with progression being slow. ( Read more about IBM)
Symptoms are generalized weakness and muscle wasting with muscle twitches. Onset is in adulthood and progression is rapid, with the average survival being 3-5 years. ALS is usually sporadic, with some cases having autosomal dominant or autosomal recessive inheritance. (Read more about ALS)
Symptoms are generalized muscle weakness, weak cry, difficulty swallowing and sucking, and respiratory problems. Onset is between birth and 3 months with rapid progression leading to early childhood death. Inheritance is autosomal recessive. (Read more about SMA)
Symptoms are weakness in arms, legs, and upper and lower torso. Onset is between 6-12 months with progression varying according to the extent of respiratory involvement. Inheritance is autosomal recessive. (Read more about SMA)
Symptoms are weakness in leg, hip, shoulder, arm, and sometimes respiratory muscles. Onset is between 13 months and adolescence with slow progression and no effect on lifespan. Inheritance is autosomal recessive. (Read more about SMA)
Symptoms are generalized weakness and muscle wasting with muscle twitching. Onset is over 18 years into adulthood with variable progression and normal life expectancy. Inheritance is autosomal recessive. (Read more about SMA)>
Symptoms are weakness and muscle wasting of the bulbar muscles (throat and mouth) and skeletal muscles. Facial and muscle jumping is common; breast development, infertility and testicular wasting can occur. It usually affects only men. Females are carriers who are usually asymptomatic or have a mild form. Onset is adulthood with progression being slow and variable with normal lifespan. Inheritance is X-linked recessive. (Read more about SBMA)
Symptoms are muscle stiffness and cramps usually occurring after periods of rest; however muscle function returns to normal with activity. Onset ranges from infancy to childhood with the disease causing discomfort but normal life-expectancy. Inheritance is autosomal dominant and autosomal recessive. (Read more about Mytonia Congenita)
Symptoms are poor or difficult relaxation of muscles which may worsen after repeated use or exercise and is often associated with hyperkalemic periodic paralysis. Onset is childhood to early adulthood with the disease causing discomfort but normal life-expectancy. Inheritance is autosomal dominant. (Read more about Paramyotonia Congenita)
Symptoms are delayed motor development with possible hip dislocation at birth. Onset is early infancy to childhood with progression varying such that it may be disabling. Inheritance is autosomal dominant. (Read more about Central Core Disease)
Symptoms are delayed motor development with weakness of arms, legs, trunk, face, and throat muscles. Onset is in early childhood with progression varying and may be life-threatening. Inheritance is autosomal dominant or autosomal recessive. (Read more about Nemaline Myopathy)
Symptoms are drooping of upper eyelids, facial weakness, blackout spells, weakness of the limbs and trunk muscles, and absent reflexes. Onset is infancy with slow progression. Inheritance is X-linked recessive, autosomal recessive, or autosomal dominant. (Read more about Myotubular Myopathy)
Symptoms are episodes of generalized muscle weakness with periods of paralysis affecting arms, legs, and neck. Onset ranges from childhood to adulthood with varying frequency of the attacks. These diseases may respond to drug therapy. Inheritance is autosomal dominant. (Read more about Periodic Paralysis)
Symptoms are weakness and fatigability of the muscles of the eyes, fact, neck, throat, limbs, and/or trunk. Onset ranges from childhood to adulthood with progression varying. This disease can respond to drug therapy or removal of the thymus gland as an effective treatment. ( Read more about MG)
Symptoms include weakness and fatigue of the hip muscles with aching back and thigh muscles common; sometimes associated with lung tumors. Onset is typically during adulthood with progression varying based on the success of drug therapy and treatment of malignancy. (Read more about Lambert-Eaton Syndrome)
Symptoms are generalized weakness and fatigability of voluntary muscles including those that control mobility, eye movement, swallowing, and breathing. Onset is infancy or childhood, however can be later, with progression varying in severity. ( Read more about CMS)
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