Lawrence Hayward, M.D., Ph.D. received his doctorate degrees from Baylor College of Medicine in Houston and completed a neurology residency in 1993 at Massachusetts General Hospital. He then started working in Dr. Robert Brown’s laboratory as a Neuromuscular research and clinical fellow. After following ALS patients in the clinic for several years, Dr. Hayward initiated biochemical studies to identify toxic properties of mutant SOD1 enzymes that cause a familial form of ALS.

Along the way, he also encountered a more personal connection to ALS, when it became clear that a few members of his own extended family had been diagnosed with the disease.

“Although the total number of individuals living with ALS may not be as high as those with more common neurodegenerative conditions, ALS nevertheless impacts families or friends with surprising frequency,” Dr. Hayward explained.

In 2000, he started his own ALS research laboratory at the University of Massachusetts Medical School, where he follows patients in the neuromuscular clinic and teaches medical and graduate students.

Dr. Hayward, an original member of the ATA Board of Directors, became interested first to define the consequences of SOD1 mutations upon the folding of the protein and its interactions in cells and mouse model tissues. Since 2008, his lab has focused on establishing new in vivo ALS models using both mouse and zebrafish systems.

“Genetically engineered mice are highly informative to ALS research because these mammals can mimic the conditions found in ALS patients on an accelerated time scale,” Dr. Hayward said.

He is currently studying newly identified ALS genes that may perturb RNA metabolism, which is normally critical for the health of the motor neurons. Initial studies suggest that mutant variants of an ALS gene called FUS, discovered by Dr. Brown’s group, may alter the ability of motor neurons to deal with environmental stresses. Early support from the ATA to establish mutant FUS transgenic mouse models in the Hayward lab led to an ongoing NIH-sponsored study to characterize the FUS mouse phenotypes.

In a promising new ATA-funded study, Dr. Hayward is examining the earliest consequences of mutant FUS in the motor neurons of zebrafish embryos.

“Because zebrafish eggs can be manipulated more easily than mouse embryos and develop very rapidly to form a functioning spinal cord within 2-3 days, these animals can be used to explore many hypotheses quickly, and the most promising results can further be validated in mouse models," Dr. Hayward explained. “Zebrafish embryos remain transparent as they develop, so scientists can express florescent proteins that allow visualization of the structure and physiological state of specific spinal cord cells in living animals.”

The hope is that zebrafish embryos will allow the characterization of early perturbations caused by the mutant ALS genes that may be driving the subsequent neuronal loss. Scientists can turn on or off genes of interest in hundreds of zebrafish eggs and – a few days later – have many animals ready for analysis or even for screening of drugs that might counteract the effect of the mutants. Findings from the zebrafish can be transferred to the mouse models for further study and the possible discovery of new therapeutic targets in ALS.

For more information about Dr. Hayward, visit or Directors & Staff page.