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Portrait of Julius Axelrod
Photo: Unknown author, http://resource.nlm.nih.gov/101442525 · Public domain via Wikimedia Commons

Nobel Prize in Physiology or Medicine · 1970

Julius Axelrod

He showed how nerve cells recycle their chemical messengers, the key to modern antidepressants, and helped bring paracetamol into medicine.

The Nobel citation: “for their discoveries concerning the humoral transmitters in the nerve terminals and the mechanism for their storage, release and inactivation”
Born
May 30, 1912, New York, NY, USA
Died
December 29, 2004, Rockville, MD, USA
Shared with
Sir Bernard Katz, Ulf von Euler
Affiliation at the time
National Institutes of Health, USA

Medicine prize

1970

Shared with 2 other laureates.

Age that year

58years

Born in 1912.

Headline credited impact

205,000–695,000people benefited

People in 32 OECD countries whose depression responds to reuptake blockers beyond placebo. How it was built

Sources cited

25

Fact-checked September 24, 2026.

  • Every medical school he applied to turned him down. In 1970 he said it had been hard for Jews to get in, and that a name like Bigelow would probably have helped.
  • He spent 11 years testing vitamins in food for New York City, and earned his PhD only at 42, after he had already discovered liver enzymes that break down many drugs.
  • His first paper, written with Bernard Brodie in 1948, pointed to the painkiller now sold as paracetamol and Tylenol. Neither man thought to patent it.
  • When the head of the NIH asked what he would like after winning the Nobel Prize, he reportedly answered: a parking space.
  • He lost the sight of his left eye in a lab accident, which kept him out of the World War II draft.

The breakthrough

Reuptake: how nerve endings switch off and recycle their chemical signals

Nerve cells talk to each other by releasing chemical messengers across tiny gaps called synapses. One of these messengers is noradrenaline, which helps the body respond to stress and danger. Each message has to be switched off within a split second, or signals would blur together. For another messenger, acetylcholine, an enzyme simply chops it up, and most scientists assumed noradrenaline was destroyed the same way. Axelrod did find one such enzyme, COMT, in 1957. But when he and others blocked the known enzymes, the effects of injected adrenaline and noradrenaline still faded quickly. Using radioactively labelled noradrenaline, he and the visiting scientist Georg Hertting showed in 1961 that nerve endings soak most of the released messenger back up and store it for reuse. Picture a garden sprinkler that, after each burst, sucks most of the water back into its own tank. Axelrod also showed that cocaine, amphetamine and the tricyclic antidepressants jam this recycling pump, leaving more noradrenaline in the gap for longer. That explained how these drugs work and pointed the way to new ones. Reuptake later turned out to be the most common way the nervous system ends its signals, including for serotonin and dopamine.[1],[4],[5],[6],[7],[8],[13]

“I wasn't that good a student, but if my name was Bigelow I probably would have gotten in.”
Julius Axelrod, Axelrod to a newspaper reporter in 1970, reflecting on his rejection by medical schools in the 1930s, when, he said, it was hard for Jews to be admitted. As quoted in the National Library of Medicine's guide to his papers.[9]

What it meant for humanity

Axelrod's discoveries reach into millions of medicine cabinets. His finding that nerve endings recycle their messengers, and that tricyclic antidepressants block this recycling, gave psychiatry its first clear account of how those drugs work. Drug companies then set out to build more selective blockers. The best known, fluoxetine (Prozac), was approved in the United States in 1987. Between 2015 and 2018, 13.2% of American adults took an antidepressant in any given month. Related drugs that act on the same family of transporters are used for anxiety, obsessive-compulsive disorder, attention deficit hyperactivity disorder and help with quitting smoking.

His first research, with Bernard Brodie from 1946, showed that two popular painkillers of the day worked by turning into N-acetyl-p-aminophenol in the body, and that this compound relieved pain without the blood damage the older drugs could cause. It was later marketed as Tylenol, and is known in much of the world as paracetamol. Neither man patented it.

In 1953 he found the liver enzymes, now called the cytochrome P450 system, that break down a wide range of drugs. His enzyme COMT became the target of drugs taken with L-dopa for Parkinson's disease, and his map of how adrenaline is broken down helped explain the urine test that became the standard way to diagnose adrenaline-secreting tumours. His pineal gland research helped establish melatonin as a regulator of daily rhythms. He also trained more than 60 postdoctoral scientists, many of whom became leaders in neuroscience.

  • Showed in the early 1960s that tricyclic antidepressants, cocaine and amphetamine block the reuptake of noradrenaline, explaining how antidepressants work and guiding the design of SSRIs such as Prozac.[7],[8],[13],[14]
  • With Bernard Brodie in 1948, identified N-acetyl-p-aminophenol (paracetamol, or acetaminophen) as the active, safer form of older painkillers and suggested using it directly. Neither man patented it.[7],[8],[11]
  • Discovered in 1953 the liver's microsomal drug-metabolizing enzymes, later known as the cytochrome P450 system, which break down a wide range of drugs.[7],[11],[12]
  • Discovered the enzyme COMT in 1957. It later became the target of drugs given with L-dopa for Parkinson's disease, and his map of adrenaline's breakdown helped explain the urine test that became standard for diagnosing adrenaline-secreting tumours.[7],[12]
  • With Richard Wurtman and others, showed that the pineal gland turns information about light and dark into rhythms of the hormone melatonin, opening the modern study of melatonin and sleep.[7],[12]
  • Trained more than 60 postdoctoral fellows, including Solomon Snyder, Leslie Iversen and Jacques Glowinski, who went on to shape neuroscience and psychopharmacology.[7],[8],[10]

Impact in numbers

Axelrod's largest legacy is understanding: he showed how the body switches off many nerve signals and how drugs interfere with that switch. We count two things. First, a small share of the people helped by reuptake-blocking antidepressants. Using only a snapshot of American adults, we estimate 2.0 to 5.7 million people responding to these drugs beyond what placebo would give, and credit Axelrod with 5%, because the drugs themselves were found or designed by others. Second, the harm side of paracetamol, which he and Brodie proposed as a medicine in 1948: overdose deaths in the United States and England and Wales, of which we charge him 5%. We do not count paracetamol's benefits because we found no reliable count of the people it has helped, so his numbers understate the good. Also uncounted are his discovery of the liver's drug-metabolizing enzymes, COMT and the Parkinson's drugs aimed at it, his melatonin research, and the more than 60 scientists he trained.

HealthFundamental science

Each number is the laureate’s credited share of a real-world outcome, cumulative to 2025. The whole outcome, the share of credit, and the reasoning are shown so you can check the arithmetic. Outcomes shared with other laureates are counted once on the impact page.

  • Low confidenceRippleModeledHealth

    People in 32 OECD countries whose depression responds to reuptake blockers beyond placebo

    205,000–695,000

    people benefited, credited share

    That is 5% of 4.1–13.9 million people benefited since 1988.

    How this number was built

    Snapshot of current users, a floor. US: 13.2% of adults took an antidepressant in the past 30 days (CDC, 2015-18) x 258.3M adults = 34.1M. 31 other OECD countries (latest year 2014-21; OECD via OWID) use 48.2M defined daily doses a day in 685M people; at 1.0-1.4 doses per user (one clinic: 1.0-1.6 for sertraline, paroxetine, escitalopram, s25; lower ratios mean more users) = 34.5-48.2M. Total 68.6-82.3M; assume 80-90% take reuptake blockers = 54.9-74.1M. Gain over placebo: placebo response 35-40% (Furukawa 2016); odds ratios 1.37-2.13, least and most effective of 21 drugs (Cipriani 2018) = +7.45 to +18.7 points. 54.9M x 0.0745 = 4.1M; 74.1M x 0.187 = 13.9M. Assumes trial response in depression holds for all users, including those treated for anxiety or pain. Past users excluded. Share 0.05: Axelrod proved reuptake and that tricyclics block it; industry teams designed the selective drugs.[7],[13],[14],[15],[16],[17],[18],[22],[23],[24],[25]

    Sources: US Centers for Disease Control and Prevention, National Center for Health Statistics; US Census Bureau; Our World in Data, from OECD; Our World in Data, from United Nations; Healthcare (MDPI), via PubMed; NHS Business Services Authority; The Lancet; The Lancet Psychiatry; British Journal of Pharmacology; Nature Reviews Drug Discovery; National Academy of Sciences / National Academies Press

  • HarmLow confidenceDirectModeledHealth

    Deaths from paracetamol (acetaminophen) overdose in the US and England and Wales, 1980-2025

    230–1,325

    deaths caused, credited share

    That is 5% of 4,600–26,500 deaths caused since 1980.

    How this number was built

    FDA analysis (Nourjah 2006): about 458 US deaths a year from paracetamol overdose, 100 of them unintentional. England and Wales (Hawton 2013): the 1998 pack-size law cut paracetamol-only suicide and open-verdict deaths by about 17 a quarter, a 43% fall, implying about 40 a quarter (158 a year) before and 90 a year after. Low: US unintentional deaths only, 100 x 46 years (1980-2025) = 4,600. High: all US deaths, 458 x 46 = 21,070, plus England and Wales 158 x 19 (1980-98) = 3,000 and 90 x 27 (1999-2025) = 2,430; total about 26,500. Rates held flat though use changed; other countries excluded, so likely an undercount. Share 0.05: Brodie and Axelrod proposed the compound as a drug in 1948, but it was already known as a breakdown product of acetanilide, companies marketed it, and most deaths are intentional overdoses.[7],[12],[20],[21]

    Sources: Pharmacoepidemiology and Drug Safety; BMJ; National Academy of Sciences / National Academies Press; Encyclopedia.com / Charles Scribner's Sons

The double edge

No weapon or deliberate harm is tied to Axelrod, but two drug families his work helped launch carry real risks. Paracetamol, which he and Brodie proposed as a safer painkiller, can severely damage the liver in overdose. An FDA analysis counted about 56,000 emergency visits, 26,000 hospital stays and 458 deaths a year in the United States from paracetamol overdoses, about 100 of those deaths unintentional. After Britain cut pack sizes in 1998, deaths from paracetamol-only overdoses in England and Wales fell by an estimated 43%. Reuptake-blocking antidepressants help many people, but their edge over placebo is modest: 35% to 40% of trial patients improve on placebo alone. In trials reviewed by the FDA in children and teenagers, the drugs roughly doubled the rate of suicidal thoughts or behaviour, a rise of about 2 percentage points, although no one in those trials died by suicide. The first SSRI to reach the market, zimelidine, was withdrawn for serious side effects. Axelrod also put forward some ideas that did not hold up well, including a contested theory of cell signalling, and had an early authorship dispute with his mentor Brodie.

  • Moderate

    Paracetamol overdoses

    Paracetamol can severely damage the liver in overdose. An FDA analysis estimated about 56,000 US emergency visits, 26,000 hospital stays and 458 deaths a year from overdoses, about 100 of the deaths unintentional. Britain's 1998 limit on pack sizes was followed by an estimated 43% fall in deaths from paracetamol-only overdoses in England and Wales, an estimated 765 fewer deaths over about 11 years.[7],[20],[21]

  • Moderate

    Antidepressants: modest benefit and a warning for the young

    In a review of 522 trials, every antidepressant beat placebo, but 35% to 40% of patients on placebo also improve. FDA reviewers found that in pediatric trials the drugs raised the rate of suicidal thoughts or behaviour by about 2 percentage points, roughly doubling it, though there were no suicides. SSRIs commonly cause sexual side effects, and the first SSRI, zimelidine, was withdrawn for serious side effects.[13],[17],[18],[19]

  • Minor

    A contested theory of cell signalling

    In 1980 Axelrod and Fusao Hirata proposed that receptors pass on their signals by adding methyl groups to fats in the cell membrane. Writing in 1996, he acknowledged that the idea had drawn much criticism and that it was still unsettled whether this process plays any real part in signalling.[8]

  • Minor

    A credit dispute with his mentor

    His work on the breakdown of amphetamine-like drugs led to a dispute with Bernard Brodie over authorship, and Axelrod left Brodie's laboratory. He nonetheless called Brodie his mentor and credited him with launching his research career.[8],[9],[12]

Against the odds

Axelrod faced no pogroms or exile, but the America he grew up in put real barriers in front of poor Jewish children. He was born in 1912 in a tenement on Manhattan's Lower East Side, which he later called a Jewish ghetto, to immigrants from Polish Galicia. His father made and sold baskets, and one biographer notes that neither parent could read English well. After a year at New York University his money ran out, so he moved to the free City College, working after class and studying on the subway. When he graduated in 1933, every medical school he applied to turned him down. Many American medical schools then capped the number of Jewish students they admitted, and in 1970 he said plainly that a different name would probably have got him in. The Great Depression left him grateful for a $25-a-month lab job, followed by eleven years testing vitamin levels in food for New York City. During those years he lost the sight of his left eye when a bottle of ammonia exploded. Without a doctorate he found promotion blocked, even after major discoveries, so in his early 40s he went back to school, earning a PhD at 42. The work that won him the Nobel Prize came after that.

  • 1930

    Poverty

    His money ran out after one year at New York University, so he transferred to the tuition-free City College of New York, where he worked after classes and did most of his studying on the subway.[7],[8]

  • 1933

    Quota

    Every medical school he applied to rejected him, in part, his biographers say, because of the widespread quotas on Jewish students. In 1970 he told a reporter that it had been hard for Jews to get into medical school.[7],[9],[10]

  • 1933

    Poverty

    Graduating in the depths of the Great Depression, he took a laboratory job at New York University paying $25 a month, then spent 1935 to 1946 testing vitamins in food for a New York City health laboratory.[7],[8]

  • —

    Other

    While working at the city laboratory he lost the sight of his left eye when a bottle of ammonia exploded. He wore an eye patch and later a darkened lens for the rest of his life.[8],[9],[12]

  • 1954

    Other

    Despite having discovered how the liver breaks down many drugs, he could not win promotion at the National Heart Institute without a doctorate, so he took a year off to earn a PhD, which he received at 42.[8],[9]

Jewish background

Both parents JewishIdentified as Jewish, secular

His parents, Isadore and Molly (born Leichtling) Axelrod, were Jewish immigrants from Polish Galicia who settled on Manhattan's Lower East Side, then, in his words, a Jewish ghetto. His biographers differ on how observant the home was, but he grew up speaking Yiddish and went to religious school every day after public school. He became an atheist early, yet he identified with Jewish culture. He spoke openly about the quotas that kept Jews out of medical school and campaigned for Soviet refusenik scientists and for Israel's place in international bodies. His funeral was held two days after his death, in keeping with Jewish tradition, but with no rabbi present.[7],[8],[9],[12]

Key dates

  1. May 30, 1912

    Born in New York City to Jewish immigrants from Polish Galicia, in a tenement on the Lower East Side.[1],[7],[8]

  2. 1933

    Graduates from the City College of New York; every medical school he applies to rejects him.[2],[7],[8]

  3. 1935

    Starts 11 years as a chemist at New York City's Laboratory of Industrial Hygiene, testing vitamins added to foods.[2],[8]

  4. 1938

    Marries Sally Taub, a teacher who also grew up on the Lower East Side. They have two sons.[2],[7]

  5. 1946

    Joins Bernard Brodie at Goldwater Memorial Hospital to find out why popular painkillers damage the blood.[7],[8]

  6. 1948

    With Brodie, shows that acetanilide works through N-acetyl-p-aminophenol (paracetamol) and suggests it as a safer painkiller.[7],[8]

  7. 1953

    At the NIH, discovers liver microsomal enzymes that break down drugs, later known as the cytochrome P450 system.[7],[8],[11]

  8. 1955

    Earns a PhD from George Washington University at 42 and becomes chief of pharmacology in a National Institute of Mental Health laboratory.[2],[8]

  9. 1957

    Discovers catechol-O-methyltransferase (COMT), an enzyme that breaks down adrenaline, noradrenaline and dopamine.[4],[7],[8]

  10. 1961

    With Georg Hertting, shows that sympathetic nerves take back up and store the noradrenaline they release.[8],[13]

  11. 1964

    With Jacques Glowinski, shows that antidepressant drugs block the uptake of noradrenaline in the brain.[7],[8],[13]

  12. 1970

    Shares the Nobel Prize in Physiology or Medicine with Bernard Katz and Ulf von Euler.[1],[3]

  13. 1984

    Retires from government service at 72 but keeps doing research as a guest scientist at the National Institute of Mental Health.[8],[9]

  14. December 29, 2004

    Dies at 92 in Rockville, Maryland.[1],[11]

Sources

  1. 1.Julius Axelrod - Facts · NobelPrize.org
  2. 2.Julius Axelrod - Biographical · NobelPrize.org (from Les Prix Nobel 1970), 1970
  3. 3.Press release: The Nobel Prize in Physiology or Medicine 1970 · Karolinska Institutet / NobelPrize.org, 1970
  4. 4.Noradrenaline: fate and control of its biosynthesis (Nobel Lecture, 12 December 1970) · NobelPrize.org, 1970
  5. 5.Award ceremony speech, Nobel Prize in Physiology or Medicine 1970 (Börje Uvnäs) · NobelPrize.org, 1970
  6. 6.Speed read: Passing the message on · NobelPrize.org, 2009
  7. 7.Julius Axelrod, 1912-2004 (Biographical Memoirs, Volume 87), by Solomon H. Snyder · National Academy of Sciences / National Academies Press, 2005
  8. 8.Julius Axelrod (autobiographical chapter), The History of Neuroscience in Autobiography, Volume 1, ed. Larry R. Squire · Society for Neuroscience, 1996
  9. 9.Julius Axelrod Papers 1910-2004: biographical note and chronology · National Library of Medicine
  10. 10.Julius Axelrod (1912-2004), by J. T. Coyle · Molecular Psychiatry, 2005
  11. 11.Dr Julius Axelrod, 1912-2004, by Solomon H. Snyder · Neuropsychopharmacology, 2005
  12. 12.Axelrod, Julius, by Carl F. Craver (Complete Dictionary of Scientific Biography), with other reference entries · Encyclopedia.com / Charles Scribner's Sons, 2008
  13. 13.Neurotransmitter transporters and their impact on the development of psychopharmacology, by Leslie Iversen · British Journal of Pharmacology, 2006
  14. 14.Case history: the discovery of fluoxetine hydrochloride (Prozac), by Wong, Perry and Bymaster · Nature Reviews Drug Discovery, 2005
  15. 15.Antidepressant Use Among Adults: United States, 2015-2018 (NCHS Data Brief No. 377) · US Centers for Disease Control and Prevention, National Center for Health Statistics, 2020
  16. 16.U.S. Adult Population Grew Faster Than Nation's Total Population From 2010 to 2020 · US Census Bureau, 2021
  17. 17.Comparative efficacy and acceptability of 21 antidepressant drugs for the acute treatment of adults with major depressive disorder, by Cipriani et al. · The Lancet, 2018
  18. 18.Placebo response rates in antidepressant trials, by Furukawa et al. · The Lancet Psychiatry, 2016
  19. 19.Suicidality in pediatric patients treated with antidepressant drugs, by Hammad, Laughren and Racoosin · Archives of General Psychiatry, 2006
  20. 20.Estimates of acetaminophen (paracetamol)-associated overdoses in the United States, by Nourjah et al. · Pharmacoepidemiology and Drug Safety, 2006
  21. 21.Long term effect of reduced pack sizes of paracetamol on poisoning deaths and liver transplant activity in England and Wales, by Hawton et al. · BMJ, 2013
  22. 22.Antidepressant drug consumption per 1,000 people (OECD Health Statistics, N06A defined daily doses per 1,000 inhabitants per day) · Our World in Data, from OECD, 2023
  23. 23.Population (UN World Population Prospects, via Our World in Data) · Our World in Data, from United Nations, 2024
  24. 24.Medicines Used in Mental Health - England - 2015/16 to 2022/23 · NHS Business Services Authority, 2023
  25. 25.Analysis of Antidepressants Utilization for Patients Visiting Psychiatric Out-Patient Clinic in a Tertiary Care Hospital (Mehdi S et al., Healthcare 10:2081) · Healthcare (MDPI), via PubMed, 2022

Fact-checked on September 24, 2026 by a separate AI fact-checking pass that re-opened the sources, with 8 corrections made. How we check

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