Martin Picard

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Dr. Martin Picard
BornMartin Picard

18 May 1984 (age 41)

Lasalle, Québec, Canada
CitizenshipCanadian, American
EducationMcGill University (BSc)

McGill University (PhD)

University of Pennsylvania (Postdoc)
Kown ForMitochondrial Psychobiology
Children1
AwardsBaszucki Prize in Science (2024)

Herbert Weiner Early Career Award (2023)

Neal E. Miller Award (2019)
FieldsCell Biology; Biomedicine
ThesisAssessment of mitochondrial function in skeletal muscle during disease, disuse, and normal aging
Doctoral advisorsTanja Taivassalo; Russell T Hepple
X@MitoPsychoBio
Websitewww.picardlab.org

Martin Picard (born May 18, 1984) is a Canadian-American mitochondrial psychobiologist and author. He is a Professor of Behavioral Medicine at Columbia University Irving Medical Center, with appointments in the Department of Psychiatry, Department of Neurology, and the Robert N. Butler Columbia Aging Center.[1] Since 2024, he has held the Endowed Chair in Energy and Health and leads the Mitochondrial Psychobiology Laboratory.[2] Picard's research integrates the science of energy and mitochondria biology with the human stress physiology, aging, brain function, and mental health.[3][4][5] He has also played leadership roles towards developing a first-principles based Science of Health.[6][7]

Picard has published over 155 peer-reviewed articles and book chapters.[8] In the first ten years of his career, he raised over $20M in research funding to support transdisciplinary research initiatives and international collaborations.[9] In 2024, he received the inaugural Baszucki Prize in Science for his work connecting brain energetics and mitochondria to the human experience.[10]

Early life and Education

Picard was born near Montreal, Québec, Canada.[11] He received a B.Sc. with honors in Physiology from McGill University in 2007, where he conducted undergraduate research in neuroimmunology under the supervision of Julie Desbarats.[11] He completed a Ph.D. at McGill in 2012 in Mitochondrial Biology of Aging, under the mentorship of Tanja Taivassalo and Russell Hepple, focusing on mitochondrial biology in skeletal muscle during aging and disease.[11] During this time, he also completed two CIHR-funded fellowships in systems biology (computational biology) and psychosocial oncology.[11]

In 2009, Picard graduated from a three-year program in holistic health at the Montreal Institute of Classical Homeopathy (MICH). He pursued additional training in India, Toronto, and New York and maintained a part-time clinical practice from 2009 to 2012.[11]

From 2012 to 2015, he completed a postdoctoral fellowship at the University of Pennsylvania’s and the Children's Hospital of Philadelphia's Center for Mitochondrial and Epigenomic Medicine, where he worked on mitochondrial genetics, epigenetics, and stress signaling under Douglas C Wallace,[12] while also advised by neuroscientist Bruce S McEwen at The Rockefeller University.[13]

Academic career

Picard joined Columbia University in 2015 as an Assistant Professor of Behavioral Medicine, was promoted to Associate Professor in 2019, and to Professor in 2024.[14] He also holds research appointments at the New York State Psychiatric Institute and the Research Foundation for Mental Hygiene.[15] From 2015 to 2020, he was a visiting scientist at the Wellcome Centre for Mitochondrial Research in Newcastle Upon Tyne, UK where he worked closely with Sir Doug Turnbull.[16]

His laboratory, based at the Vagelos College of Physicians and Surgeons, initially focused on mitochondrial signaling and its role in cellular aging, stress responses, and mental health.[17] He co-directs the Columbia Science of Health Program, an initiative aimed at understanding health across biological, psychological, and functional dimensions.[18] Since 2016, at the Columbia Neurological Institute, he has also followed patients with mitochondrial diseases under the mentorship of neuromuscular neurologist Michio Hirano, MD. [19]

In 2018, his research group was renamed the Mitochondrial Psychobiology Lab, reflecting a shift toward studying the interaction between psychological processes and mitochondrial biology.[20] He has described this emerging field as Mitochondrial Psychobiology, a term introduced in a 2019 publication.[21] In 2024, with behavioral neuroscientist Carmen Sandi, Picard co-organized the inaugural Banbury Meeting on Mitochondrial Psychobiology.[22]

Research Contributions

Picard's research spans cellular imaging, mitochondrial bioenergetics, cellular aging biology, clinical and psychosocial sciences.

Mind-mitochondria connection

Picard contributed to early evidence that physiological stress responses stress in mice may be regulated by mitochondrial biology.[23] He developed the NIH-funded Mitochondrial Stress, Brain Imaging, and Epigenetics (MiSBIE) study to investigate how variations in mitochondria affect stress response and the human mind. [24] Related studies from his laboratory demonstrated that brief mental stress can lead to mitochondrial DNA release into the bloodstream[25] and saliva.[26][27] An initial hypothesis proposed that this mtDNA release served as a pro-inflammatory signal,[28] but later studies challenged this interpretation, suggesting potential links to mitochondrial transfer mechanisms.[29][30][31][32]

In 2018, Picard co-authored a study with psychologist Elissa S Epel examining the Mitochondrial Health Index (MHI) in immune cells, which reported a positive mood-to-mitochondrial energy transformation capacity over time periods of days.[33] Subsequent work by Caroline Trumpff and colleagues reported that brain mitochondrial proteomic profiles and single-cell gene expression patterns (scRNAseq) were associated with psychosocial exposures reported before death.[34][35] The authors proposed that mitochondrial biology and psychological experiences are bidirectionally related or influenced by shared underlying factors, and proposed a conceptual framework called the Hallmarks of Psychobiology.[36][37]

Energetics and reversibility of aging

As part of his doctoral research, Picard investigated skeletal muscle–specific changes in mitochondrial biology with aging, reporting that mitochondrial decline is not a universal feature of aging, that it varies by muscle,[38] and that the experimental methods used to examine this question can alter conclusions.[39][40][41] Subsequently, the Cellular Lifespan Study[42] developed by Gabriel Sturm in his laboratory examined longitudinal molecular and energetic aspects of cellular aging[43], reporting that senescence is associated with an increase in energy demand, or hypermetabolism.[44] Picard’s team also reported the presence of nuclear mitochondrial DNA insertions (NUMTs) in aging cultured human cells and in the human brain, which their research found to be associated with early mortality.[45][46][47]

Using the cellular lifespan system[48], Picard’s group reported that mitochondrial defects were associated with hypermetabolism and cellular aging, as indicated by markers such as telomere shortening, epigenetic clocks, gene expression profiles, and the Hayflick limit.[49] Along with clinical evidence in patients with mitochondrial diseases[49] these findings led to the hypermetabolic theory of mitochondrial diseases, which suggests that mitochondrial OxPhos defects do not decrease but rather increase the overall cellular energy expenditure, forcing energy tradeoffs that drive symptoms.[50]

In 2021, using hair greying as a model to examine heterogeneity and the dynamics of the aging process, Picard’s team published findings suggesting that human hair greying is transiently reversible and linked to life stress.[51][52][53] They developed the Hair Pigmentation Pattern (HPP) method, which was used to examine associations between psychological stress, mitochondrial biology, and changes in hair pigmentation.[54] To bridge molecular and cellular hallmarks of aging with clinical phenotypes, Picard proposed the Brain-body Energy Conservation (BEC) model of aging[44], which frames aging as a process influenced by energy regulation and tradeoffs where the brain coordinates systemic energy allocation.[55]

Holistic view of mitochondria

Drawing from parallels with bacterial behavior[56] and other work, Picard has described mitochondria as signal processing organelles involved in cellular communication processes.[57][58] In 2015, he reported the intermitochondrial structural alignment of cristae in mouse heart tissue[59]. He later described the presence of mitochondrial nanotunnels in human cells.[60] Picard also described social behaviors of mitochondria, including communication, specialization, division of labor, coordination, among others, outlining a picture of mitochondria as organelles with the foreshadowing signs of our own sociality.[61][5] With cell biologist Tim Shutt, he also proposed a conceptual analogy referring to mitochondria as a chief executive organelle (CEO) of the cell.[62][63]

Electron microscopy work from Picard’s laboratory[64][65] and other research groups[66][67][68] has identified profound structural diversity among mitochondria from different organs and cell types, as well as within individual cells, referred to as mitotypes.[69] Picard has argued for more specific language around mitochondrial science.[70] In 2023, he developed the first systematic nomenclature system of cell-dependent mitochondrial properties, mitochondrial features, activities, functions, and behaviors, moving the field beyond binary classifications of function and dysfunction.[71]

Brain bioenergetics

The first-generation Mitochondrial Health Index (MHI)[72] and second-generation Mitochondrial Respiratory Capacity (MRC)[73][74], developed in Picard’s laboratory, were designed to assess mitochondrial energetics in brain tissues. Using these methods, Picard’s laboratory mapped the distribution of brain mitochondria and their associations with anxiety-like behaviors in mice.[75][76][77] They also developed Human MitoBrainMap v1.0, a systematic map of mitochondrial biology across the human brain[73][74] intended to support research on the relationship between mitochondrial biology, brain activity, and behavior.[78][79]

Transdisciplinary science and human health

Picard has proposed a transdisciplinary framework for understanding health[80][81] emphasizing the role of subjective experiences such as self-rated health in assessing well-being.[82] He has suggested that mitochondria may function at the intersection of biological and psychosocial processes.[83][84] He described their topological and functional positioning of mitochondria as a potential transducer of physiological signals related to health and aging.[85][86]

In published work and interviews, Picard has discussed the historical focus of biomedical research on disease over health,[87][88][89][90] and proposed an alternative framework integrating concepts of energy, communication, and structure as a path to create a more accurate, actionable framework in human health.[87][88] In 2025, with Alan Cohen and investigators at the Columbia Science of Health Program, drawing analogies to field physics Picard introduced a theoretical model describing health as a "field-like-state."[91] According to this view, health may not be directly observable, but could be inferred through its effects on various biological and psychological systems.[91][92]

Assay development in mitochondrial science

Picard’s early research included the development of laboratory assays to measure live mitochondrial functions in small human skeletal muscle biopsy samples[93][94]. These methods were applied to study the nature of mitochondrial recalibrations in COPD muscle[95] and to conduct a comparative analysis of two commonly used techniques in mitochondrial science: isolated mitochondria and permeabilized myofibers. The study reported fuctional differences between these preparations[96] and examined their implications for the study of skeletal muscle mitochondrial aging[97]. Picard also implemented quantitative microscopy techniques to profile mitochondrial morphology and network reorganization[98], applying them to muscle[99][100] and brain cells.[101] Using a combination of biochemical and imaging methods, Picard identified the origin of heteroplasmic mitochondrial DNA deletions in aging skeletal muscle.[102][103]

Mitochondrial allostatic load (MAL)

In 2014, Picard proposed the concept of Mitochondrial Allostatic Load (MAL)[104], expanding the framework of allostatic load by Bruce S. McEwen and Elliot Stellar.[105] His research has explained how psychological stress may influence mitochondrial biology in animal models, human studies, and population-level data.[106][107] Picard has also discussed limitations in the interpretation of mitochondrial biomarkers, such as mitochondrial DNA copy number,[108] and explored the metabolic demands associated with the stress response.[109] One study from his group estimated a 60% increase in cellular energy expenditure in response to glucocorticoid stress.[110] This led to the proposed Energetic Model of Allostatic Load (EMAL), which proposes that chronic stress is damaging because it forces the disallocation of energy towards stress response processes, away from growth, maintenance, and repair processes, leading to damage accumulation.[111][112]

In a separate survey-based study, Picard and collaborators also reported on mitochondrial disease patients' beliefs around the link between mood and symptom severity.[113]

These studies contributed to a broader body of work proposing mitochondria as mediators between metabolic and psychological processes.

Awards and honors

Picard has served as Principal Investigator on several; grants funded by the National Institutes on Aging (NIA) and the National Institute of Mental Health (NIMH) and has also received support from philanthropic organizations, including Baszucki Group and the Wharton Fund. He has participated in advisory roles on initiatives related to aging, mental health, and the Coalition for Metabolic Health.[121][122]

Selected publications

  • Mosharov EV, Rosenberg AM, Monzel AS, Osto CA, Stiles L, Rosoklija GB, Dwork AJ, Bindra S, Junker A, Zhang Y, Fujita M, Mariani MB, Bakalian M, Sulzer D, De Jager PL, Menon V, Shirihai OS, Mann JJ, Underwood M, Boldrini M, Thiebaut de Schotten M, Picard M. A human brain map of mitochondrial respiratory capacity and diversity. Nature 2025 PubMed Research Briefing
  • Trumpff C, Monzel AS, Sandi C, Menon V, Klein HU, Fujita M, Lee A, Petyuk V, Hurst C, Duong DM, Seyfried NT, Wingo A, Wingo T, Wang Y, Thambisetty M, Ferrucci L, Bennett DA, De Jager PL, Picard M. Psychosocial experiences are associated with human brain mitochondrial biology. PNAS 2024; 121(27):e2317673121 PubMed
  • Shaulson ED, Cohen AA, Picard M. The brain-body energy conservation model of aging. Nat Aging 2024; 4(10):1354-1371 PubMed
  • Sturm G, Karan KR, Monzel AS, Santhanam BS, Taivassalo T, Bris C, Duplaga SA, Cross M, Towheed A, Higgins-Chen A, McManus MJ, Cardenas A, Lin J, Epel ES, Rahman S, Vissing V, Grassi B, Levine M, HorvathS, Haller RG, Lanaers G, St-Onge MP, Wallace DC, Tavazoie S, Procaccio V, Kaufman BA, Seifert EL, Hirano H, Picard M. OxPhos defects cause hypermetabolism and reduce lifespan in cells and in patients with mitochondrial diseases. Commun Biol 2023; 6(1):22 PubMed
  • Monzel AS, Enriques JA, Picard M. Multifaceted mitochondria: Moving mitochondrial science beyond function and dysfunction. Nat Metab 2023; 5(4):546-562 PubMed
  • Picard M, Shirihai O. Mitochondrial signal transduction. Cell Metab 2022; 34(11):1620-1653 PubMed
  • Picard M. Why do we care more about disease than health? Phenomics 2022; 2:145–155 Link
  • Rosenberg A, Rausser S, Ren J, Mosharov EV, Sturm G, Ogden RT, Patel P, Soni RK, Lacefield C, Tobin DJ, Paus R, Picard M. Quantitative mapping of human hair graying and reversal in relation to life stress. eLife 2021; 10:e67437 PubMed eLife Digest eLife Insight
  • Picard M, Sandi C. The social nature of mitochondria: Implications for human health. Neurosci Biobehav Rev2021; 120(5):595-610 PubMed
  • Picard M, Trumpff C, Burelle Y. Mitochondrial psychobiology: Foundation and applications. Curr Opin Behav Sci 2019; 28:142-151PubMed
  • Picard M, Prather AA, Puterman E, Cuillerier A, Coccia M, Aschbacher K, Burelle Y, Epel ES. A mitochondrial health index sensitive to mood and caregiver stress. Biol Psychiatr 2018; 84(1):9-17 PubMed
  • Picard M, McEwen BS. Psychological stress and mitochondria: A systematic review (Part I). Psychosom Med2018; 80(2):141-153PubMed
  • Picard M, McEwen BS. Psychological stress and mitochondria: A conceptual framework (Part II). Psychosom Med2018; 80(2):126-140 PubMed
  • Picard M, McManus MJ, Csordas G, Varnai P, Dorn GW, Williams D, Hajnoczky G, Wallace DC. Inter-mitochondrial coordination of cristae at regulated membrane junctions. Nat Commun 2015; 6:6259 PubMed
  • Picard M, McManus MJ, Gray J, Nasca C, Moffat C, Kopinsky P, Seifert E, McEwen BS, Wallace DC. Mitochondrial functions modulate neuroendocrine, metabolic, inflammatory and transcriptional responses to psychological stress. PNAS 2015; 112(48):E6614-23 PubMed

Media and outreach

Picard’s work has been featured in major media outlets including The New York Times[123], The New Yorker[124], Quanta Magazine[125], Nature[126], Scientific American[127], The Transmitter[128], The Today Show[129], and TEDx[130].

Picard has presented publicly on the relationship between psychological well-being, states of mind and the biology of energy, mitochondria, and human health and healing.[131][132][133] He is the author of a forthcoming book ENERGY, published by Henry Holt in 2027.[134]

Personal Life

Martin Picard is father to one son (born 2019).[135]

References

  1. ↑ "Martin Picard, PhD – Curriculum Vitae" (PDF). Picard Lab. Retrieved 2025-07-15.
  2. ↑ "Mitochondrial Psychobiology Lab - Home". MITOLAB. Retrieved 2025-07-17.
  3. ↑ "Picard Lab – Mitochondrial Psychobiology". Picard Lab. Retrieved 2025-07-15.
  4. ↑ Coeur des sciences - UQAM (2024-12-09). La vie, c'est les mitochondries - Une conférence de Martin Picard - 19 novembre 2024. Retrieved 2025-09-26 – via YouTube.
  5. ↑ 5.0 5.1 Picard, Martin (2025-06-01). "The Hidden Social Lives of Mitochondria". Scientific American. Retrieved 2025-09-26.
  6. ↑ Picard, Martin (2022-06-01). "Why Do We Care More About Disease than Health?". Phenomics. 2 (3): 145–155. doi:10.1007/s43657-021-00037-8. ISSN 2730-5848.
  7. ↑ "Members". Columbia University Mailman School of Public Health. 2024-05-02. Retrieved 2025-09-26.
  8. ↑ "Martin Picard". scholar.google.com. Retrieved 2025-09-26.
  9. ↑ "RePORT ⟩ RePORTER". reporter.nih.gov. Retrieved 2025-09-26.
  10. ↑ "Baszucki Group Announces Columbia University's Martin Picard, PhD, as Inaugural Recipient of $1.5 Million Baszucki Prize in Science". Metabolic Mind. 2024. Retrieved 2025-07-15.
  11. ↑ 11.0 11.1 11.2 11.3 11.4 "Mitochondrial Psychobiology Lab - Members". MITOLAB. Retrieved 2025-07-17.
  12. ↑ "Martin Picard, PhD". Columbia Neurology. 2020-10-14. Retrieved 2025-07-17.
  13. ↑ Picard, Martin; Juster, Robert-Paul; McEwen, Bruce S. (May 2014). "Mitochondrial allostatic load puts the 'gluc' back in glucocorticoids". Nature Reviews Endocrinology. 10 (5): 303–310. doi:10.1038/nrendo.2014.22. ISSN 1759-5037.
  14. ↑ "Martin Picard, PhD". Columbia University Department of Neurology. 14 October 2020. Retrieved 2025-07-15.
  15. ↑ "Martin Picard, PhD". Columbia University Department of Psychiatry. 2017-02-09. Retrieved 2025-07-17.
  16. ↑ "Mitochondrial Psychobiology Lab - Members". MITOLAB. Retrieved 2025-07-17.
  17. ↑ "Martin Picard, PhD". Columbia University Department of Neurology. 14 October 2020. Retrieved 2025-07-15.
  18. ↑ "Martin Picard, PhD". Columbia University Department of Neurology. 14 October 2020. Retrieved 2025-07-15.
  19. ↑ "Martin Picard: Exploring the Mind-Mitochondria Connection". Columbia University Irving Medical Center. 2023-09-18. Retrieved 2025-07-16.
  20. ↑ "Picard Lab – Mitochondrial Psychobiology". Picard Lab. Retrieved 2025-07-15.
  21. ↑ Picard, Martin; Trumpff, Caroline; Burelle, Yan (2019-08-01). "Mitochondrial psychobiology: foundations and applications". Current Opinion in Behavioral Sciences. Psychoneuroimmunology. 28: 142–151. doi:10.1016/j.cobeha.2019.04.015. ISSN 2352-1546.
  22. ↑ "‪Mitochondrial psychobiology‬". scholar.google.com. Retrieved 2025-09-26.
  23. ↑ Picard, Martin; McManus, Meagan J.; Gray, Jason D.; Nasca, Carla; Moffat, Cynthia; Kopinski, Piotr K.; Seifert, Erin L.; McEwen, Bruce S.; Wallace, Douglas C. (2015-12-01). "Mitochondrial functions modulate neuroendocrine, metabolic, inflammatory, and transcriptional responses to acute psychological stress". Proceedings of the National Academy of Sciences of the United States of America. 112 (48): E6614–6623. Bibcode:2015PNAS..112E6614P. doi:10.1073/pnas.1515733112. ISSN 1091-6490.
  24. ↑ Kelly, Catherine; Trumpff, Caroline; Acosta, Carlos; Assuras, Stephanie; Baker, Jack; Basarrate, Sophia; Behnke, Alexander; Bo, Ke; Bobba-Alves, Natalia; Champagne, Frances A.; Conklin, Quinn; Cross, Marissa; De Jager, Philip; Engelstad, Kris; Epel, Elissa (October 2024). "A platform to map the mind-mitochondria connection and the hallmarks of psychobiology: the MiSBIE study". Trends in Endocrinology and Metabolism: TEM. 35 (10): 884–901. doi:10.1016/j.tem.2024.08.006. ISSN 1879-3061.
  25. ↑ Trumpff, Caroline; Marsland, Anna L.; Basualto-Alarcón, Carla; Martin, James L.; Carroll, Judith E.; Sturm, Gabriel; Vincent, Amy E.; Mosharov, Eugene V.; Gu, Zhenglong; Kaufman, Brett A.; Picard, Martin (August 2019). "Acute psychological stress increases serum circulating cell-free mitochondrial DNA". Psychoneuroendocrinology. 106: 268–276. doi:10.1016/j.psyneuen.2019.03.026. ISSN 1873-3360.
  26. ↑ Trumpff, Caroline; Rausser, Shannon; Haahr, Rachel; Karan, Kalpita R.; Gouspillou, Gilles; Puterman, Eli; Kirschbaum, Clemens; Picard, Martin (September 2022). "Dynamic behavior of cell-free mitochondrial DNA in human saliva". Psychoneuroendocrinology. 143 105852. doi:10.1016/j.psyneuen.2022.105852. ISSN 1873-3360.
  27. ↑ Trumpff, Caroline; Shire, David; Michelson, Jeremy; Bobba-Alves, Natalia; Yu, Temmie; Sloan, Richard P.; Juster, Robert-Paul; Hirano, Michio; Picard, Martin (2025-09-01). "Saliva and blood cell-free mtDNA reactivity to acute psychosocial stress". Psychoneuroendocrinology. 179 107506. doi:10.1016/j.psyneuen.2025.107506. ISSN 0306-4530.
  28. ↑ Trumpff, Caroline; Michelson, Jeremy; Lagranha, Claudia J.; Taleon, Veronica; Karan, Kalpita R.; Sturm, Gabriel; Lindqvist, Daniel; Fernström, Johan; Moser, Dirk; Kaufman, Brett A.; Picard, Martin (July 2021). "Stress and circulating cell-free mitochondrial DNA: A systematic review of human studies, physiological considerations, and technical recommendations". Mitochondrion. 59: 225–245. doi:10.1016/j.mito.2021.04.002. ISSN 1872-8278.
  29. ↑ Trumpff, Caroline; Michelson, Jeremy; Lagranha, Claudia J.; Taleon, Veronica; Karan, Kalpita R.; Sturm, Gabriel; Lindqvist, Daniel; Fernström, Johan; Moser, Dirk; Kaufman, Brett A.; Picard, Martin (2021-07-01). "Stress and circulating cell-free mitochondrial DNA: A systematic review of human studies, physiological considerations, and technical recommendations". Mitochondrion. 59: 225–245. doi:10.1016/j.mito.2021.04.002. ISSN 1567-7249.
  30. ↑ Trumpff, Caroline; Shire, David; Lee, Seonjoo; Stanko, Katie; Wilson, Annette; Kaufman, Brett A.; Picard, Martin; Marsland, Anna L. (2025-04-10), "Effects of acute psychological stress on blood cell-free mitochondrial DNA (cf-mtDNA): A crossover experimental study", medRxiv : The Preprint Server for Health Sciences, medRxiv, doi:10.1101/2025.04.08.25325479, retrieved 2025-06-16
  31. ↑ Liu, Delin; Gao, Youshui; Liu, Jiao; Huang, Yigang; Yin, Junhui; Feng, Yuyao; Shi, Linjing; Meloni, Bruno P.; Zhang, Changqing; Zheng, Minghao; Gao, Junjie (2021-02-16). "Intercellular mitochondrial transfer as a means of tissue revitalization". Signal Transduction and Targeted Therapy. 6 (1): 65. doi:10.1038/s41392-020-00440-z. ISSN 2059-3635.
  32. ↑ Liu, Delin; Gao, Youshui; Liu, Jiao; Huang, Yigang; Yin, Junhui; Feng, Yuyao; Shi, Linjing; Meloni, Bruno P.; Zhang, Changqing; Zheng, Minghao; Gao, Junjie (2021-02-16). "Intercellular mitochondrial transfer as a means of tissue revitalization". Signal Transduction and Targeted Therapy. 6 (1): 65. doi:10.1038/s41392-020-00440-z. ISSN 2059-3635.
  33. ↑ Picard, Martin; Prather, Aric A.; Puterman, Eli; Cuillerier, Alexanne; Coccia, Michael; Aschbacher, Kirstin; Burelle, Yan; Epel, Elissa S. (2018-07-01). "A Mitochondrial Health Index Sensitive to Mood and Caregiving Stress". Biological Psychiatry. 84 (1): 9–17. doi:10.1016/j.biopsych.2018.01.012. ISSN 0006-3223.
  34. ↑ Trumpff, Caroline; Monzel, Anna S.; Sandi, Carmen; Menon, Vilas; Klein, Hans-Ulrich; Fujita, Masashi; Lee, Annie; Petyuk, Vladislav A.; Hurst, Cheyenne; Duong, Duc M.; Seyfried, Nicholas T.; Wingo, Aliza P.; Wingo, Thomas S.; Wang, Yanling; Thambisetty, Madhav (2024-07-02). "Psychosocial experiences are associated with human brain mitochondrial biology". Proceedings of the National Academy of Sciences of the United States of America. 121 (27): e2317673121. Bibcode:2024PNAS..12117673T. doi:10.1073/pnas.2317673121. ISSN 1091-6490.
  35. ↑ Kwon, Diana. "Life Experiences May Shape the Activity of the Brain's Cellular Powerhouses". Scientific American. Retrieved 2025-09-26.
  36. ↑ Kelly, Catherine; Trumpff, Caroline; Acosta, Carlos; Assuras, Stephanie; Baker, Jack; Basarrate, Sophia; Behnke, Alexander; Bo, Ke; Bobba-Alves, Natalia; Champagne, Frances A.; Conklin, Quinn; Cross, Marissa; De Jager, Philip; Engelstad, Kris; Epel, Elissa (October 2024). "A platform to map the mind-mitochondria connection and the hallmarks of psychobiology: the MiSBIE study". Trends in Endocrinology and Metabolism: TEM. 35 (10): 884–901. doi:10.1016/j.tem.2024.08.006. ISSN 1879-3061.
  37. ↑ Picard, Martin (2022-08-01). "Energy transduction and the mind–mitochondria connection". The Biochemist. 44 (4): 14–18. doi:10.1042/bio_2022_118. ISSN 0954-982X.
  38. ↑ Picard, Martin; Ritchie, Darmyn; Thomas, Melissa M.; Wright, Kathryn J.; Hepple, Russell T. (2011). "Alterations in intrinsic mitochondrial function with aging are fiber type-specific and do not explain differential atrophy between muscles". Aging Cell. 10 (6): 1047–1055. doi:10.1111/j.1474-9726.2011.00745.x. ISSN 1474-9726.
  39. ↑ Picard, Martin; Ritchie, Darmyn; Thomas, Melissa M.; Wright, Kathryn J.; Hepple, Russell T. (2011). "Alterations in intrinsic mitochondrial function with aging are fiber type-specific and do not explain differential atrophy between muscles". Aging Cell. 10 (6): 1047–1055. doi:10.1111/j.1474-9726.2011.00745.x. ISSN 1474-9726.
  40. ↑ Picard, Martin; Taivassalo, Tanja; Gouspillou, Gilles; Hepple, Russell T. (2011). "Mitochondria: isolation, structure and function". The Journal of Physiology. 589 (18): 4413–4421. doi:10.1113/jphysiol.2011.212712. ISSN 1469-7793.
  41. ↑ Picard, M (May 2012). "Assessment of mitochondrial function in skeletal muscle during disease, disuse and normal aging". PhD Dissertation, McGill University, Canada.
  42. ↑ Sturm, Gabriel; Monzel, Anna S.; Karan, Kalpita R.; Michelson, Jeremy; Ware, Sarah A.; Cardenas, Andres; Lin, Jue; Bris, Céline; Santhanam, Balaji; Murphy, Michael P.; Levine, Morgan E.; Horvath, Steve; Belsky, Daniel W.; Wang, Shuang; Procaccio, Vincent (2022-12-03). "A multi-omics longitudinal aging dataset in primary human fibroblasts with mitochondrial perturbations". Scientific Data. 9 (1): 751. Bibcode:2022NatSD...9..751S. doi:10.1038/s41597-022-01852-y. ISSN 2052-4463.
  43. ↑ Sturm, Gabriel; Cardenas, Andres; Bind, Marie-Abèle; Horvath, Steve; Wang, Shuang; Wang, Yunzhang; Hägg, Sara; Hirano, Michio; Picard, Martin (2019-04-10). "Human Aging DNA Methylation Signatures are Conserved but Accelerated in Cultured Fibroblasts". Epigenetics. 14 (10): 961–976. doi:10.1101/605295. Retrieved 2025-06-16.
  44. ↑ 44.0 44.1 Shaulson, Evan D.; Cohen, Alan A.; Picard, Martin (October 2024). "The brain-body energy conservation model of aging". Nature Aging. 4 (10): 1354–1371. doi:10.1038/s43587-024-00716-x. ISSN 2662-8465.
  45. ↑ Zhou, Weichen; Karan, Kalpita R.; Gu, Wenjin; Klein, Hans-Ulrich; Sturm, Gabriel; De Jager, Philip L.; Bennett, David A.; Hirano, Michio; Picard, Martin; Mills, Ryan E. (August 2024). "Somatic nuclear mitochondrial DNA insertions are prevalent in the human brain and accumulate over time in fibroblasts". PLOS Biology. 22 (8): e3002723. doi:10.1371/journal.pbio.3002723. ISSN 1545-7885.
  46. ↑ Doss, Rose M.; Breuss, Martin W. (2024-08-23). "A somatic view of the genomic impact of mitochondrial endosymbiosis". PLOS Biology. 22 (8): e3002756. doi:10.1371/journal.pbio.3002756. ISSN 1545-7885.
  47. ↑ Picard, Martin. "Jumping Genes from Mitochondria Can Be Fast and Deadly". Scientific American. Retrieved 2025-09-26.
  48. ↑ Sturm, Gabriel; Monzel, Anna S.; Karan, Kalpita R.; Michelson, Jeremy; Ware, Sarah A.; Cardenas, Andres; Lin, Jue; Bris, Céline; Santhanam, Balaji; Murphy, Michael P.; Levine, Morgan E.; Horvath, Steve; Belsky, Daniel W.; Wang, Shuang; Procaccio, Vincent (2022-12-03). "A multi-omics longitudinal aging dataset in primary human fibroblasts with mitochondrial perturbations". Scientific Data. 9 (1): 751. Bibcode:2022NatSD...9..751S. doi:10.1038/s41597-022-01852-y. ISSN 2052-4463.
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