Section: Rotations

Lawrence J. Hayward, M.D., Ph.D.

Academic Role: Associate Professor

Faculty Appointment(s) In:
   Neurology

Joint Faculty In:
   Biochemistry and Molecular Pharmacology
   Physiology

Other Affiliation(s):
   Interdisciplinary Graduate Program
   Program in Neuroscience

Potential Rotation Projects

Project #1.  Transgenic animal models of motor neuron degeneration:

Active projects include the development and characterization of novel in vivo models relevant to amyotrophic lateral sclerosis (ALS, Lou Gehrig's disease) and related motor neuron diseases.  This project will provide the student with familiarity in the design and analysis of models using mouse or zebrafish systems.  Depending on the length of the rotation, opportunities for phenotypic analysis of transgenic animals can be tailored to student interest.  Techniques employed include fluorescence imaging, electrophysiology, biochemistry, and behavioral analysis.

Project #2.  Misfolding of mutant Cu,Zn superoxide dismutase (SOD1) in ALS : 

More than 100 distinct missense mutations have been identified in the gene encoding SOD1 in families with inherited forms of ALS.  A consensus is emerging that these mutant residues increase the propensity of the nascent enzyme to populate folding intermediate conformations that may cause toxicity to motor neurons.  We are interested in defining structural aspects of the misfolded proteins and their potential interactions with other cellular constituents.  Rotation projects are available in which the student will apply biochemical methods, mass spectrometry, and fluorescence imaging to characterize the consequences of SOD1 misfolding in cellular systems.

Project #3.   Physiology of periodic paralysis: 

Hyperkalemic periodic paralysis is a muscle disorder characterized by attacks of weakness or muscle stiffness (myotonia) that can be triggered by exercise or potassium ingestion.   We have developed a knock-in mouse model of this disorder in which the Met-1592-Val mutant Na channel is expressed in muscle.  We are interested to study the physiological triggers of attacks in these animals and the basis for the occurrence of myopathic changes with aging.

Office: S5-717
Phone: 508-856-4147
E-mail: Lawrence.Hayward@umassmed.edu
Keywords: Protein Folding, Animal Models of Disease, Neurodegeneration, Motor Neuron Disease, Ion Channels

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