Department of Pharmacology and Experimental Therapeutics,Boston University School of Medicine
Boston, Massachusetts | United States
Main Specialties: Neurology
Additional Specialties: Toxicology, Neurology, Pharmacology
I earned my bachelors degree in Psychology from Boston University, where I made the Dean's list and was a member of Psi Chi, the International Honor Society in Psychology. I went on to earn my Doctoral degree in Behavioral Neuroscience from the Boston University School of Medicine, where I trained in the Department of Neurology under the supervision of Drs. Robert G. Feldman MD Professor and Chair, Department of Neurology and Raymon Durso MD, Director, Neuropharmacology Laboratory, VA Healthcare System. I subsequently completed a three year National Institutes on Aging funded Post Doctoral Fellowship in the Biochemistry of Aging under the guidance of Dr. David H. Farb in the Department of Pharmacology and Experimental Therapeutics at the Boston University School of Medicine. My extensive training, first at the bedside in the Department of Neurology, and then at the bench in the Department of Pharmacology and Experimental Therapeutics at the BUSM has provided me with genuine translational research experience in clinical and basic neuroscience and neurotoxicology. I am currently using cutting edge in vivo electrophysiological techniques to study chemical-induced changes in neural network activity in an effort to identify novel therapeutics for age-related neurodegenerative diseases.
Primary Affiliation: Department of Pharmacology and Experimental Therapeutics,Boston University School of Medicine - Boston, Massachusetts , United States
PubMed Central Citations
Laboratory of Molecular Neurobiology
Pfizer Global Research and Development
Safety Assessment and Laboratory Animal Resources
Drug Safety R&D
Center for Memory and Brain
Laboratory of Molecular Neurobiology
School of Public Health
Boston University School of Medicine
Boston University School of Medicine
179PubMed Central Citations
J Occup Environ Med 2018 04;60(4):e207-e209
J Ind Med. 2017 Nov 10.
American Journal of Industrial Medicine
Unmasking of latent neurodegenerative disease has been reported following exposure to chemicals that share one or more mechanisms of action in common with those implicated in the specific disease. For example, unmasking of latent Parkinson's disease (PD) has been associated with exposure to anti-dopaminergic agents, while the progression of pre-existing mild cognitive impairment and unmasking of latent Alzheimer's disease has been associated with exposure to general anesthetic agents which promote Aβ protein aggregation. This literature review and clinical case report about a 45-year-old man with no family history of motor neuron disease who developed overt symptoms of a neuromuscular disorder in close temporal association with his unwitting occupational exposure to volatile organic compounds (VOCs) puts forth the hypothesis that exposure to VOCs such as toluene, which disrupt motor function and increase oxidative stress, can unmask latent ALS type neuromuscular disorder in susceptible individuals.
Neurology 2017 Jan 28;88(4):338-339. Epub 2016 Dec 28.
From the Laboratory of Molecular Neurobiology (M.H.R.), Department of Pharmacology & Experimental Therapeutics, Boston University School of Medicine, MA; and Department of Environmental Health Sciences (E.F.), School of Public Health, University at Albany, Rensselaer, NY.
Ratner, M.H., Jabre, J.F. Neurobehavioral Toxicology. In Reference Module in Neuroscience and Biobehavioral Psychology, Elsevier, 2017. ISBN 9780128093245
Reference Module in Neuroscience and Biobehavioral Psychology,.
The field of neurobehavioral toxicology is the branch of toxicology dedicated to understanding the adverse effects of chemical and biological agents on the nervous system. Paracelsus, the Swiss German philosopher, physician credited as the founder of toxicology once said, “Poison is in everything, and there is no thing that is without poison. The dosage makes it either a poison or a remedy.” Unfortunately many chemicals intended to improve the quality of our lives also have the potential to cause acute and permanent changes in our behavior. This article reviews these behavioral manifestations in terms of the acute and persistent chemical induced changes in brain function and how behavioral testing is used in conjunction with clinical neurological, neurophysiological, and neuroimaging studies to make the differential diagnosis of toxic encephalopathy, toxic neuropathy and neurotoxicant-induced parkinsonism.
Current Topics in Toxicology
Marcia H Ratner. “The Future Role of In vivo Electrophysiology in Preclinical Drug Discovery”. EC Pharmacology and Toxicology 2.2 (2016): 108-109.
EC Pharmacology and Toxicology
EC Pharmacol Toxicol 2016 Sept 2(2):108-109.
EC Pharmacology and Toxicology
Although a mainstay of preclinical drug discovery, the translational value of animal behavioral models of neurodegenerative diseases and psychiatric disorders remains controversial. Thus, there is an unmet need for better animal models. In vivo electrophysiology permits the measurement of drug-induced changes in neural network activity while providing the investigator with objective biomarkers of neurological function which can be used to increase the translational value of behavioral observations made with preclinical animal models. This powerful method, which can be used in freely behaving animals, typically employs microelectrode arrays, which in turn allow investigators to simultaneously record single unit activity and local field potentials (LFPs) from multiple cells in multiple brain regions. Recordings can also be made from specific brain regions implicated in disease. For example, drug-induced changes in both single unit activity and LFPs in the CA3 and CA1 subregions of the hippocampus are potential biomarkers of drug effects on spatial learning and memory function implicated in animal models of prodromal Alzheimer’s disease. This translational preclinical method is also well suited for target-based as well as repurposing studies.
Hippocampus 2015 Dec 14;25(12):1541-55. Epub 2015 Jul 14.
Laboratory of Molecular Neurobiology, Department of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, Massachusetts.
Ratner MH, Feldman RG. Parkinson’s Disease. Pfeiffer RF, and Ebadi M, (Eds). Chapter 6., Environmental Toxins and Parkinson’s Disease. CRC Press. Boca Raton. 2004; 51-62.
Clinics in Occupational and Environmental Medicine
Metals are ubiquitous. Exposure to metals has been associated with producing acute and chronic effects on the human nervous system ranging from disabling neuropathies to life-threatening encephalopathies. Many metals produce constellations of symptoms that strongly resemble those of idiopathic neurodegenerative diseases. Metals have been hypothesized as an etiology of Parkinson's disease, Alzheimer's disease, ans amyotrophic lateral sclerosis (ALS). Understanding the mechanisms of action of metals commonly encountered in the workplace and environment is essential for clinicians interested in preventing and treating their neurotoxic effects. This article deals with four frequently encountered metals: arsenic, lead, manganese, and mercury.
Curr Opin Neurol. 1999 Dec;12(6):725-31.
Current Opinion in Neurology.
The role of environmental and occupational exposures to neurotoxicants in the pathogenesis of neurodegenerative disease has not been fully elucidated. Recent published research on whether genetic polymorphisms contribute to individual susceptibility to develop neurodegenerative diseases such as Parkinson's disease have been equivocal at best. This review relates putative mechanisms of neurotoxicant-induced cell damage to polymorphisms in the genes that encode for the enzymes involved in the metabolism of neurotoxicants. The effects that genetically induced alterations in enzyme functioning have on neurotoxicant metabolism and how this relates to the risk of neurotoxic effects among exposed individuals are reviewed. A pragmatic approach to future research in the area of neurodegenerative disease is developed on the basis of the interrelationship between known routes of neurotoxicant metabolism and human genetics.
This article provides the neurologist with simple methods that can be applied to all clinical neurologic evaluations, regardless of the future potential for litigation. This article defines the appropriate application and interpretation of conventional neurologic, neurophysiologic, neuropsychological, and biochemical diagnostic tests that are sensitive to neurotoxic exposures. This article also provides the neurologist with guidance in the preparation of clinical findings and tips on the recognition and use of supportive literature that is often required for admissibility of evidence at a deposition or testimony.
Environ Health Perspect. 1999 May;107(5):417-22.
Environmental Health Perspectives
This paper describes symptoms and findings in a 57-year-old painter who had been exposed to various organic solvents for over 30 years. He began to work as a painter at 16 years of age, frequently working in poorly ventilated areas; he used solvents to remove paint from the skin of his arms and hands at the end of each work shift. The patient and his family noticed impaired short-term memory function and changes in affect in his early forties, which progressed until after he stopped working and was thus no longer exposed to paints and solvents. After the patient's exposures had ended, serial neuropsychological testing revealed persistent cognitive deficits without evidence of further progression, and improvement in some domains. Magnetic resonance imaging revealed global and symmetrical volume loss, involving more white than gray matter. The findings in this patient are consistent with chronic toxic encephalopathy and are differentiated from other dementing processes such as Alzheimer's disease, multi-infarct (vascular) dementia, and alcoholic dementia. Previous descriptions in the literature of persistent neurobehavioral effects associated with chronic exposure to organic solvents corroborate the findings in this case.