Vernon Ingram, 82, Found Sickle Cell Cause

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Massachusetts Institute of Technology professor Vernon Ingram, whose landmark discovery on the cause of sickle cell anemia made him a pioneer in the field of molecular biology, died in Boston on Aug. 17 after a fall. He was 82.

In 1957, Ingram discovered that a single amino acid substitution is responsible for the molecular abnormality that leads to sickle cell anemia.

Graham Walker, a professor of biology at MIT, said Wednesday the find was “one of the absolutely seminal discoveries in the history of molecular biology.” In popular sources, he is often referred to as “The father of molecular medicine.”

In recent years, Ingram, of Cambridge, had focused on neuroscience, especially Alzheimer’s disease. In particular, he looked at how the amyloid protein which builds up around diseased neurons destroys their ability to communicate.

“He was a dyed-in-the-wool, inveterate experimentalist,” Walker said. “He was going at full speed right up until the end.”

Born in Breslau, Germany, Ingram studied at Birkbeck College at the University of London, where he earned his bachelor’s degree in chemistry in 1945 and doctorate in organic chemistry in 1949.

In 1952 he returned to England, where he studied protein chemistry in the Cavendish Laboratory of Cambridge University. Along with Francis Crick, co-discoverer of the structure of DNA, he investigated whether genes code for proteins, now scientific orthodoxy but then very much still in question.

A few years later, while studying the genetics of hemoglobin, the molecule that carries oxygen in the blood, he discovered that the misshapen hemoglobin molecules that characterize sickle cell anemia are caused by a single mutation. The difference was minute — approximately one amino acid out of 500. It was the first direct demonstration that mutation could cause disease.

In addition to having clinical implications, it was the first time a mutation had been demonstrated at a single point in the genetic chain.

Ingram joined the MIT faculty in 1958.


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