Bradlee Heckmann

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Bradlee L. Heckmann
Heckmann ADPD.png
Other namesBrad Heckmann
Alma mater
Known forDiscovery of LC3-associated endocytosis
Scientific career
Alzheimer's disease
InstitutionsUniversity of South Florida

St. Jude Children's Research Hospital
ThesisThe function and regulation of the G0/G1 Switch Gene 2
Doctoral advisorJun Liu
Other academic advisorsDouglas R. Green
Edmund B. Rucker, III

Bradlee L. Heckmann is an American biologist and neuroimmunologist at the Byrd Alzheimer's Center and USF Health Neuroscience Institute and assistant professor in molecular medicine at the USF Health Morsani College of Medicine. Prior to his faculty appointment, Heckmann held the John H. Sununu Endowed Fellowship[1] in immunology at St. Jude Children's Research Hospital. Heckmann's research is focused on understanding the regulation of inflammatory processes in the central nervous system, with particular emphasis on neurodegenerative diseases including Alzheimer's Disease[2] and the role of the autophagy machinery in this setting.


Heckmann graduated from Lexington Catholic High School in Lexington, Kentucky prior to attending the University of Kentucky, where he graduated with a Bachelor of Science in biology. Heckmann went on to complete his doctoral training in Biochemistry & Molecular Biology at the Mayo Clinic College of Medicine.[3] After completing his formal training he joined the laboratory of Douglas R. Green at St. Jude as a postdoctoral fellow.[4]


After studying lipid metabolism and components that regulate lipid turnover while at Mayo Clinic, Heckmann switched his research focus to evaluating the role and regulation of non-canonical autophagy in the brain.[5][6] These studies ultimately led to Heckmann & Green's discovery of a novel form of the endocytic trafficking pathway.[7] Heckmann and Green showed that a protein known as LC3 which helps facilitate vesicle trafficking and fusion, most well known for its role in autophagy, was attached to endosomes that contained β-amyloid,[7] a known contributor to Alzheimer's Disease establishment and pathology in humans. As such they named the discovery LC3-associated endocytosis (LANDO).[8][9][10] They further found that inhibition of LC3-associated endocytosis in microglial immune cells of the brain resulted in impaired recycling of cell receptors that recognize β-amyloid, leading to dramatic increases in inflammatory activation.[7]

Heckmann and Green were the first to show that loss of the LC3-associated endocytosis pathway in microglia greatly exacerbated the disease pathology of Alzheimer's Disease and that the LANDO pathway is protective against β-amyloid induced neuroinflammation and neurodegeneration, work recently published in Cell[7] and featured in mainstream media.[11][12][13][9][10][8]

The potential for therapeutically targeting LC3-associated endocytosis for the treatment of devastating conditions including Alzheimer's Disease and cancer is of significant promise.[8] Additional evidence supporting a significant role for LANDO and other non-canonical uses of the autophagy machinery in neurodegeneration and neuroinflammation were recently published by Drs. Heckmann and Green along with other colleagues including Thomas Wileman demonstrating an important role for LANDO and targeting of neuroinflammation as a therapeutic approach to relieving neuronal and behavioral impairment in a novel, age-associated spontaneous model of Alzheimer's Disease in mice, work that has been published in Science Advances.[14]

Recognition and awards[edit]

Heckmann has received multiple awards and honors stemming from his work primarily on LC3-associated endocytosis as well as mainstream media coverage.[15][16][17] He has been the recipient of honors including a Ruth L. Kirschstein National Research Service Award, an Aegean Young Investigator Award, an LRP award from the National Cancer Institute, and an Excellence in Science Award and nomination for Prize in Neurobiology from the American Association for the Advancement of Science.[18][19] Dr. Heckmann was recently[when?] featured by AZO Network and News Medical as a "thought leader in medicine".[20]

He also has been elected as a member of the Sigma Xi Research Honor Society and is an overseas Fellow of the Royal Society of Medicine.

External links[edit]


  1. ^ ORCID. "Bradlee L. Heckmann (0000-0002-3271-7183)". Retrieved 2020-04-01.
  2. ^ Heckmann, Bradlee L.; Tummers, Bart; Green, Douglas R. (January 2019). "Crashing the computer: apoptosis vs. necroptosis in neuroinflammation". Cell Death & Differentiation. 26 (1): 41–52. doi:10.1038/s41418-018-0195-3. ISSN 1476-5403. PMC 6294765. PMID 30341422.
  3. ^ "The function and regulation of the G0/G1 Switch Gene 2 (G0S2) - ProQuest". Retrieved 2020-04-01.
  4. ^ "Postdoctoral Fellows". Retrieved 2020-04-01.
  5. ^ Heckmann, Bradlee L.; Green, Douglas R. (2019-03-01). "LC3-associated phagocytosis at a glance". Journal of Cell Science. 132 (5): jcs222984. doi:10.1242/jcs.222984. ISSN 0021-9533. PMC 6432721. PMID 30787029.
  6. ^ Heckmann, Bradlee L.; Boada-Romero, Emilio; Cunha, Larissa D.; Magne, Joelle; Green, Douglas R. (2017-11-24). "LC3-Associated Phagocytosis and Inflammation". Journal of Molecular Biology. 429 (23): 3561–3576. doi:10.1016/j.jmb.2017.08.012. ISSN 0022-2836. PMC 5743439. PMID 28847720.
  7. ^ a b c d Heckmann, Bradlee L.; Teubner, Brett J. W.; Tummers, Bart; Boada-Romero, Emilio; Harris, Lacie; Yang, Mao; Guy, Clifford S.; Zakharenko, Stanislav S.; Green, Douglas R. (2019-07-25). "LC3-Associated Endocytosis Facilitates β-Amyloid Clearance and Mitigates Neurodegeneration in Murine Alzheimer's Disease". Cell. 178 (3): 536–551.e14. doi:10.1016/j.cell.2019.05.056. ISSN 0092-8674. PMC 6689199. PMID 31257024.
  8. ^ a b c Jefferson, Robin Seaton. "Newly Discovered Cellular Pathway May Mean New Approach For How We Treat Alzheimer's And Cancer". Forbes. Retrieved 2020-04-01.
  9. ^ a b Hospital, About The Author Mary Powers Mary Powers is a member of the Communications Department at St Jude Children’s Research (2019-07-25). "Lando: Star Wars smuggler or possible ally against Alzheimer's disease?". St. Jude Progress Blog - St. Jude Children’s Research Hospital. Retrieved 2020-04-01. {{cite web}}: |first= has generic name (help)
  10. ^ a b "Gently Used: Can Recycled Microglia Receptors Prevent Plaque? | ALZFORUM". Retrieved 2020-04-01.
  11. ^ "New Research Discovery - Alzheimer's and Toxicity Pathways". BioSpace. Retrieved 2020-04-01.
  12. ^ "LANDO Found to be Key to Microglial Clearance of Amyloid-β and Neuroinflammation". Fight Aging!. 2019-07-05. Retrieved 2020-04-01.
  13. ^ "Pathway discovered that prevents buildup of Alzheimer's protein". Retrieved 2020-04-01.
  14. ^ Heckmann, Bradlee L.; Teubner, Brett J. W.; Boada-Romero, Emilio; Tummers, Bart; Guy, Clifford; Fitzgerald, Patrick; Mayer, Ulrike; Carding, Simon; Zakharenko, Stanislav S.; Wileman, Thomas; Green, Douglas R. (2020-08-01). "Noncanonical function of an autophagy protein prevents spontaneous Alzheimer's disease". Science Advances. 6 (33): eabb9036. Bibcode:2020SciA....6B9036H. doi:10.1126/sciadv.abb9036. ISSN 2375-2548. PMC 7428329. PMID 32851186.
  15. ^ "July 24, 2019". UsAgainstAlzheimer's. Retrieved 2020-05-01.
  16. ^ "Bradlee L. Heckmann | Cell Journalist | Muck Rack". Retrieved 2020-05-01.
  17. ^ "LC3-associated endocytosis: guarding against neuroinflammation & neurodegeneration". LabRoots. Retrieved 2020-05-01.
  18. ^ "Aegean Conferences". Retrieved 2020-05-01.
  19. ^ Heckmann, Bradlee. "Regulation of microglial induced inflammation by non-canonical autophagy". {{cite journal}}: Cite journal requires |journal= (help)
  20. ^ "A potential new way of treating Alzheimer's Disease". 2020-09-07. Retrieved 2020-09-27.