Mignot, Yanagisawa Win Lasker Award for Narcolepsy Discovery

Type 1 narcolepsy results from the autoimmune destruction of the brain’s orexin-producing neurons. The disorder affects an estimated one in 3,000 people and is marked by rapid transitions into REM sleep and cataplexy, or sudden muscle weakness triggered by strong emotions.
Yanagisawa was not initially studying sleep: his team was searching for molecules that activate previously unidentified “orphan” receptors in the brain. The researchers first suspected orexin regulated appetite, but mice lacking the peptide showed narcolepsy-like behavior rather than major changes in feeding or body weight.
Mignot’s work identified mutations in the gene encoding orexin receptor 2 while he was investigating inherited narcolepsy in Doberman pinschers, Labrador retrievers and Dachshunds.
Mignot recalled that colleagues considered his effort to explain narcolepsy through dog genetics “crazy,” but said, “I really believed in it.” At the time he entered the field, many patients went decades without a diagnosis and had their symptoms attributed to laziness or a lack of willpower.
The researchers will share a $250,000 honorarium, and the 2026 Lasker Awards will be formally presented at a ceremony in New York City on September 17. The Lasker Foundation awards are widely regarded as among the leading U.S. biomedical prizes.
Two sleep researchers have won the 2026 Albert Lasker Basic Medical Research Award for discovering that a missing brain chemical causes Type 1 narcolepsy. Life Science Nordic reports that Emmanuel Mignot of Stanford University and Masashi Yanagisawa of the University of Tsukuba independently found that lacking orexin, a peptide that keeps people awake, leads to the disorder. Their work in the late 1990s transformed how doctors understand and treat the condition, which affects about one in 3,000 people.
The pair will share a $250,000 prize and see their achievements formally recognized at a September 17 ceremony in New York City. Stanford News notes that Mignot studied inherited narcolepsy in dogs, while Yanagisawa discovered orexin while researching brain molecules in mice. Their findings led to new medicines, including a recently approved drug that treats the disorder by restoring orexin function.
Mignot focused on narcolepsy that ran in families of Doberman pinschers, Labrador retrievers, and Dachshunds. He discovered mutations in the gene for orexin receptor 2, a protein that cells use to respond to orexin. Medical Xpress reports that colleagues initially thought his approach was "crazy" and questioned the value of studying dog sleep disorders.
Mignot persisted because he believed the genetic path held answers. At that time, many patients went decades without diagnosis, with doctors attributing their symptoms to laziness or weak willpower rather than a real neurological disorder. His dog research would prove the doubters wrong.
Yanagisawa was not originally studying sleep. Newswise explains that his team searched for molecules that activate unknown "orphan" brain receptors. The researchers initially suspected orexin controlled appetite, since it seemed logical for an undiscovered peptide.
But mice without orexin showed narcolepsy-like symptoms instead of eating changes. The animals suddenly fell asleep during the day and lost muscle tone when excited. This unexpected finding redirected Yanagisawa toward sleep science and led him to the same conclusion Mignot had reached: orexin was the missing link in narcolepsy.
Type 1 narcolepsy stems from autoimmune destruction of brain cells that produce orexin. Le Monde notes the disorder affects roughly one person per 2,000 people and causes rapid, uncontrolled transitions into REM sleep. People with narcolepsy also experience cataplexy—sudden muscle weakness triggered by strong emotions like laughter or surprise.
Before Mignot and Yanagisawa's breakthrough, the biological basis remained a mystery. Doctors could only manage symptoms, not address the root cause. The discovery opened the door to targeted medicines that restore orexin signaling, fundamentally changing how the disorder is treated and diagnosed.
Publishers
13
Articles
13
Reach
26