Thomas T. Perls, MD, MPH, FACP
Professor
Boston University Chobanian & Avedisian School of Medicine
Medicine
Geriatrics

MD, University of Rochester
MPH, Harvard School of Public Health
BA, Pitzer College



Expertise in epidemiology, genetics of aging and exceptional longevity.

Dr. Perls is among the international leaders in the field of human exceptional longevity. He is founder and director of the New England Centenarian Study, the largest study of centenarians and their families in the world. He is also a principal investigator of the NIA-funded Long Life Family Study. Dr. Perls is also a vocal critic of the "anti-aging" industry.

Dr. Perls is readily available for media interviews and inquiries for presentations. Please call him at 617-638-6688 or via email at thperls@bu.edu.

He has been responsible for numerous novel and pivotal findings in the field:

• Intact cognitive function amongst centenarians may be a function of demographic selection in which younger elderly with poor function die off leaving behind a select group of survivors with lower relative risk for common causes of cognitive impairment such as Alzheimer’s disease.

• Twenty percent of female centenarians had children after the age of 40 compared with 5% of women from their birth cohort. The results suggest that women who had children after the age of 40 had a 4 times greater risk of living to 100 or older (Nature).

• Delayed age of menopause and therefore the ability to have more children may be an important genetic selective pressure to evolve genetic variants that slow aging and decrease risk for age related diseases.

• Relative to octogenarians and nonagenarians, Alzheimer’s becomes less common amongst centenarians while rarer causes of neuropathology become more common, suggesting that centenarians have a relative resistance to Alzheimer’s, which also correlates with the decreased frequency of the apolipoprotein E-4 allele amongst Caucasian centenarians.

• The first to report a series of families that demonstrate remarkable clustering for exceptional longevity (J Amer Geriatrics Society).

• Siblings of centenarians have markedly increased risks for survival to 100 relative to their birth cohort (Lancet and PNAS).

• The children of centenarians have approximately 60% reduced rates of heart disease, stroke, diabetes and hypertension and 80% reduced overall mortality in their early seventies compared to their average birth cohort.

• A substantial proportion of centenarians live with age-related diseases usually associated with significant mortality, for more than 20 years (40%, called survivors), another group have such diseases after the age of 80 (45%, called delayers) and then there are about 15% of centenarians who have none of these diseases at the age of 100 (called escapers). Despite this, more than 90% of centenarians are functionally independent in their early nineties.

• At even older ages however, semi-super-centenarians (ages 105-109 years) and even more so, supercentenarians (age 110+), usually delay such age related diseases towards the ends of their lives. The supercentenarians particularly do this, experiencing such diseases on average in the last 5% of their extremely long lives (J Gerontology, 2012). These findings support for the first time Jim Fries’ “compression of morbidity” hypothesis that he proposed in his 1980 New England Journal of Medicine article. The observed homogeneity of this age group in terms of the delay or escape of these diseases is consistent with their being the extreme tail of the population and that they are more likely to have genetic factors in common that confer such an extreme survival advantage.

• Dr. Perls, working with a wide range of disciplines including statisticians, geneticists and computer scientists, has led the production of a landmark article in which a genetic model consisting of 281 genetic markers predicts with 85% accuracy whom in their sample of controls and centenarians is age 105+ years (published this January in PLoS ONE). The accuracy of the model is lower, about 60% for nonagenarians and centenarians at age 100, which supports the hypothesis that the genetic component of survival to older and older age beyond 100 gets progressively stringer. The authors made some additionally important findings: the centenarians have just as many disease-associated genetic variants as people dying at younger ages. Presumably, centenarians are able to survive to much older ages in part because of the presence of longevity associated variants that counter the effects of such disease variants. Particularly for the oldest subjects in the study, most of these 281 markers presumably point to such longevity associated variants, including genes already well known in the biology of aging community such as the Werner’s gene, Lamin A (Hutchison Guildford Syndrome) and super oxide dismutase. It’s very interesting that there are variants for genes known to cause premature aging that may have the opposite effect and contribute to exceptional longevity.

• In part in order to search for functional variants associated with the SNPs noted in the above model, Dr. Perls also led an effort to whole genome sequence, for the first time, not just one centenarian, but two supercentenarians, a man and woman, both over the age of 114 years (Frontiers in Genetics, January 2012).
Expertise in geriatrics, epidemiology and omics of healthy aging, Alzheimer's and exceptional longevity.

Dr. Perls is among the international leaders in the field of human exceptional longevity. He is founder and director of the New England Centenarian Study, the largest study of centenarians and their families in the world. He is also a principal investigator of the NIA-funded Long Life Family Study. Dr. Perls is also a vocal critic of the "anti-aging" industry.

Tom Perls MD, MPH attended Pitzer College in Claremont California and then the University of Rochester School of Medicine for his medical degree and Harvard University School of Public Health for his Masters in Public Health, majoring in Quantitative Methods. He performed his residency in internal medicine at Harbor UCLA Medical Center, a half year registrarship in Geriatrics at Mount Royal Hospital in Melbourne Australia and Clinical-Research Geriatrics Fellowship at Harvard Medical School. He was also an Agency for Health Care Quality Research Fellow at Brown University. After fellowship, Dr. Perls was on the faculty at Beth Israel Deaconess Hospital. Since 2002, he has been based at Chobanian and Avedisian School of Medicine and Boston Medical Center and is Professor of Medicine in the Geriatrics Section of the Department of Medicine.

Dr. Perls is readily available for media interviews and inquiries for presentations. Please call him at 617-638-6688 or via email at thperls@bu.edu.

He has been responsible for numerous novel and pivotal findings in the field:

• Intact cognitive function amongst centenarians may be a function of demographic selection in which younger elderly with poor function die off leaving behind a select group of survivors with lower relative risk for common causes of cognitive impairment such as Alzheimer’s disease.

• Twenty percent of female centenarians had children after the age of 40 compared with 5% of women from their birth cohort. The results suggest that women who had children after the age of 40 had a 4 times greater risk of living to 100 or older (Nature).

• Delayed age of menopause and therefore the ability to have more children may be an important genetic selective pressure to evolve genetic variants that slow aging and decrease risk for age related diseases.

• Relative to octogenarians and nonagenarians, Alzheimer’s becomes less common amongst centenarians while rarer causes of neuropathology become more common, suggesting that centenarians have a relative resistance to Alzheimer’s, which also correlates with the decreased frequency of the apolipoprotein E-4 allele amongst Caucasian centenarians.

• The first to report a series of families that demonstrate remarkable clustering for exceptional longevity (J Amer Geriatrics Society).

• Siblings of centenarians have markedly increased risks for survival to 100 relative to their birth cohort (Lancet and PNAS).

• The children of centenarians have approximately 60% reduced rates of heart disease, stroke, diabetes and hypertension and 80% reduced overall mortality in their early seventies compared to their average birth cohort.

• A substantial proportion of centenarians live with age-related diseases usually associated with significant mortality, for more than 20 years (40%, called survivors), another group have such diseases after the age of 80 (45%, called delayers) and then there are about 15% of centenarians who have none of these diseases at the age of 100 (called escapers). Despite this, more than 90% of centenarians are functionally independent in their early nineties.

• At even older ages however, semi-super-centenarians (ages 105-109 years) and even more so, supercentenarians (age 110+), usually delay such age related diseases towards the ends of their lives. The supercentenarians particularly do this, experiencing such diseases on average in the last 5% of their extremely long lives (J Gerontology, 2012). These findings support for the first time Jim Fries’ “compression of morbidity” hypothesis that he proposed in his 1980 New England Journal of Medicine article. The observed homogeneity of this age group in terms of the delay or escape of these diseases is consistent with their being the extreme tail of the population and that they are more likely to have genetic factors in common that confer such an extreme survival advantage.

• Dr. Perls, working with a wide range of disciplines including statisticians, geneticists and computer scientists, has led the production of a landmark article in which a genetic model consisting of 281 genetic markers predicts with 85% accuracy whom in their sample of controls and centenarians is age 105+ years (published this January in PLoS ONE). The accuracy of the model is lower, about 60% for nonagenarians and centenarians at age 100, which supports the hypothesis that the genetic component of survival to older and older age beyond 100 gets progressively stringer. The authors made some additionally important findings: the centenarians have just as many disease-associated genetic variants as people dying at younger ages. Presumably, centenarians are able to survive to much older ages in part because of the presence of longevity associated variants that counter the effects of such disease variants. Particularly for the oldest subjects in the study, most of these 281 markers presumably point to such longevity associated variants, including genes already well known in the biology of aging community such as the Werner’s gene, Lamin A (Hutchison Guildford Syndrome) and super oxide dismutase. It’s very interesting that there are variants for genes known to cause premature aging that may have the opposite effect and contribute to exceptional longevity.

• In part in order to search for functional variants associated with the SNPs noted in the above model, Dr. Perls also led an effort to whole genome sequence, for the first time, not just one centenarian, but two supercentenarians, a man and woman, both over the age of 114 years (Frontiers in Genetics, January 2012).

Member
Boston University
Evans Center for Interdisciplinary Biomedical Research


Graduate Faculty (Primary Mentor of Grad Students)
Boston University Chobanian & Avedisian School of Medicine, Graduate Medical Sciences




Resilience/Resistance to Alzheimer's Disease in Centenarians and Offspring (RADCO)
09/30/2021 - 08/31/2026 (PI)
NIH/National Institute on Aging
3U19AG073172-03S1

Identifying protective omics profiles in centenarians and translating these into preventive and therapeutic strategies
09/01/2022 - 12/31/2025 (PI)
NIH/National Institute on Aging
5UH3AG064704-04

EXCEL Study
07/01/2022 - 06/30/2025 (PI)
American Federation for Aging Research


The Long Life Family Study
08/15/2019 - 03/31/2025 (Multi-PI)
PI: Thomas T. Perls, MD, MPH, FACP
The Washington University NIH NIA
5U19AG063893-05

Candidate protective factors for age-associated diseases (target discovery) or factors indicative of healthy aging
09/15/2016 - 09/15/2024 (Co-Investigator)
PI: Paola Sebastiani, PhD
Novartis Institutes for BioMedical Research


Protein signatures of APOE and cognitive aging
09/01/2020 - 05/31/2024 (Subcontract PI)
Tufts Medical Center, Inc. NIH NIA
R01AG061844

Longevity Consortium
08/15/2019 - 05/31/2024 (Subcontract PI)
Sutter Bay Hospitals dba California Pacific Medical Center NIH NIA
5U19AG023122-15

Identifying protective omics profiles in centenarians and translating these into preventive and therapeutic strategies
09/15/2019 - 06/30/2022 (PI)
NIH/National Institute on Aging
5UH2AG064704-02

New England Centenarian Study
07/01/2016 - 06/30/2022 (Multi-PI)
PI: Thomas T. Perls, MD, MPH, FACP
The William M. Wood Foundation


The New England Centenarian Study
10/01/2014 - 08/31/2016 (PI)
The William M. Wood Foundation



Identifying protective omics profiles in centenarians and translating these into preventive and therapeutic strategies
09/15/2019 - 06/30/2024 (Multi-PI)
PI: Thomas T. Perls, MD, MPH, FACP
Trustees of Boston University,CRC National Institute o
1UH2AG064704-01

Protein signatures of APOE and cognitive aging
06/01/2019 - 05/31/2020 (PI)
Trustees of Boston University,CRC National Institute o
5R01AG061844-02

The Long Life Family Study: Boston Field Center
06/01/2014 - 05/31/2020 (PI)
National Institute on Aging/NIH/DHHS National Institutes
2U01 AG023755-09

Longevity Consortium
09/30/2018 - 05/31/2019 (PI)
California Pacific Medical Center National Institute o
2U19AG023122-11A1

Centenarian Subjects for the Archon Genomics X Prize Whole Genome
12/08/2011 - 08/31/2016 (PI)
X Prize Foundation

Consortium to Study the Genetics of Longevity
09/30/2011 - 07/31/2016 (PI)
California Pacific Med Ctr Res Inst NIH-NIA

The Long Life Family Study
09/30/2010 - 05/31/2014 (PI)
NIH-NIA
5U01 AG023755-08

The Genetics of Human Exceptional Longevity
07/01/2010 - 06/30/2012 (PI)
Glenn Foundation for Medical Research

Characterizing Human Exceptional Longevity
03/01/2006 - 01/31/2012 (PI)
NIH-NIA
5K24 AG025727-05

Characterizing Human Exceptional Longevity
09/15/2009 - 08/31/2011 (PI)
NIH-NIA
3K24 AG025727-04S1

Showing 10 of 20 results. Show All Results

Title


Yr Title Project-Sub Proj Pubs
2024 Resilience/Resistance to Alzheimer's Disease in Centenarians and Offspring (RADCO) 5U19AG073172-04
2024 Administrative Core 5U19AG073172-04-6351
2023 Resilience/Resistance to Alzheimer's Disease in Centenarians and Offspring (RADCO) 5U19AG073172-03
2023 Resilience/Resistance to Alzheimer's Disease in Centenarians and Offspring (RADCO) 3U19AG073172-03S1
2023 Administrative Core 5U19AG073172-03-6351
2023 Identifying protective omics profiles in centenarians and translating these into preventive and therapeutic strategies 5UH3AG064704-04
2023 Phenotyping Core 5U19AG063893-05-6290
2023 The Long Life Family Study 3U19AG063893-05S1
2023 The Long Life Family Study 5U19AG063893-05
2022 Resilience/Resistance to Alzheimer's Disease in Centenarians and Offspring (RADCO) 3U19AG073172-01S1
Showing 10 of 67 results. Show All Results

Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.

iCite Analysis       Copy PMIDs To Clipboard

  1. Yao S, Boudreau RM, Galvin A, Murabito JM, Honig LS, Perls TT, Christensen K, Newman AB. All-cause mortality and cause-specific death in U.S. long-lived siblings: data from the Long Life Family Study. J Gerontol A Biol Sci Med Sci. 2024 Aug 01.View Related Profiles. PMID: 39086360; PMCID: PMC11439495; DOI: 10.1093/gerona/glae190;
     
  2. Reed ER, Chandler KB, Lopez P, Costello CE, Andersen SL, Perls TT, Li M, Bae H, Soerensen M, Monti S, Sebastiani P. Cross-platform proteomics signatures of extreme old age. Geroscience. 2024 Jul 25.View Related Profiles. PMID: 39048883
     
  3. Wang S, Lenzini P, Thygarajan B, Lee JH, Vardarajan BN, Yashin A, Miljkovic I, Warwick Daw E, Lin SJ, Patti G, Brent M, Zmuda JM, Perls TT, Christensen K, Province MA, An P. A Novel Gene ARHGAP44 for Longitudinal Changes in Glycated Hemoglobin (HbA1c) in Subjects without Type 2 Diabetes: Evidence from the Long Life Family Study (LLFS) and the Framingham Offspring Study (FOS). bioRxiv. 2024 May 21. PMID: 38826208; PMCID: PMC11142083; DOI: 10.1101/2024.05.16.594575;
     
  4. Reed ER, Chandler KB, Lopez P, Costello CE, Andersen SL, Perls TT, Li M, Bae H, Soerensen M, Monti S, Sebastiani P. Cross-platform proteomics signatures of extreme old age. bioRxiv. 2024 Apr 14.View Related Profiles. PMID: 38645061; PMCID: PMC11030369; DOI: 10.1101/2024.04.10.588876;
     
  5. Dowrey TW, Cranston SF, Skvir N, Lok Y, Gould B, Petrowitz B, Villar D, Shan J, James M, Dodge M, Belkina AC, Giadone RM, Sebastiani P, Perls TT, Andersen SL, Murphy GJ. A longevity-specific bank of induced pluripotent stem cells from centenarians and their offspring. bioRxiv. 2024 Mar 14.View Related Profiles. PMID: 38559230; PMCID: PMC10979955; DOI: 10.1101/2024.03.12.584663;
     
  6. Don J, Schork AJ, Glusman G, Rappaport N, Cummings SR, Duggan D, Raju A, Hellberg KG, Gunn S, Monti S, Perls T, Lapidus J, Goetz LH, Sebastiani P, Schork NJ. The relationship between 11 different polygenic longevity scores, parental lifespan, and disease diagnosis in the UK Biobank. Geroscience. 2024 Aug; 46(4):3911-3927.View Related Profiles. PMID: 38451433; PMCID: PMC11226417; DOI: 10.1007/s11357-024-01107-1;
     
  7. Xicota L, Cosentino S, Vardarajan B, Mayeux R, Perls TT, Andersen SL, Zmuda JM, Thyagarajan B, Yashin A, Wojczynski MK, Krinsky-McHale S, Handen BL, Christian BT, Head E, Mapstone ME, Schupf N, Lee JH, Barral S. Whole genome-wide sequence analysis of long-lived families (Long-Life Family Study) identifies MTUS2 gene associated with late-onset Alzheimer's disease. Alzheimers Dement. 2024 Apr; 20(4):2670-2679.View Related Profiles. PMID: 38380866; PMCID: PMC11032545; DOI: 10.1002/alz.13718;
     
  8. de Las Fuentes L, Schwander KL, Brown MR, Bentley AR, Winkler TW, Sung YJ, Munroe PB, Miller CL, Aschard H, Aslibekyan S, Bartz TM, Bielak LF, Chai JF, Cheng CY, Dorajoo R, Feitosa MF, Guo X, Hartwig FP, Horimoto A, Kolcic I, Lim E, Liu Y, Manning AK, Marten J, Musani SK, Noordam R, Padmanabhan S, Rankinen T, Richard MA, Ridker PM, Smith AV, Vojinovic D, Zonderman AB, Alver M, Boissel M, Christensen K, Freedman BI, Gao C, Giulianini F, Harris SE, He M, Hsu FC, Kühnel B, Laguzzi F, Li X, Lyytikäinen LP, Nolte IM, Poveda A, Rauramaa R, Riaz M, Robino A, Sofer T, Takeuchi F, Tayo BO, van der Most PJ, Verweij N, Ware EB, Weiss S, Wen W, Yanek LR, Zhan Y, Amin N, Arking DE, Ballantyne C, Boerwinkle E, Brody JA, Broeckel U, Campbell A, Canouil M, Chai X, Chen YI, Chen X, Chitrala KN, Concas MP, de Faire U, de Mutsert R, de Silva HJ, de Vries PS, Do A, Faul JD, Fisher V, Floyd JS, Forrester T, Friedlander Y, Girotto G, Gu CC, Hallmans G, Heikkinen S, Heng CK, Homuth G, Hunt S, Ikram MA, Jacobs DR, Kavousi M, Khor CC, Kilpeläinen TO, Koh WP, Komulainen P, Langefeld CD, Liang J, Liu K, Liu J, Lohman K, Mägi R, Manichaikul AW, McKenzie CA, Meitinger T, Milaneschi Y, Nauck M, Nelson CP, O'Connell JR, Palmer ND, Pereira AC, Perls T, Peters A, Polašek O, Raitakari OT, Rice K, Rice TK, Rich SS, Sabanayagam C, Schreiner PJ, Shu XO, Sidney S, Sims M, Smith JA, Starr JM, Strauch K, Tai ES, Taylor KD, Tsai MY, Uitterlinden AG, van Heemst D, Waldenberger M, Wang YX, Wei WB, Wilson G, Xuan D, Yao J, Yu C, Yuan JM, Zhao W, Becker DM, Bonnefond A, Bowden DW, Cooper RS, Deary IJ, Divers J, Esko T, Franks PW, Froguel P, Gieger C, Jonas JB, Kato N, Lakka TA, Leander K, Lehtimäki T, Magnusson PKE, North KE, Ntalla I, Penninx B, Samani NJ, Snieder H, Spedicati B, van der Harst P, Völzke H, Wagenknecht LE, Weir DR, Wojczynski MK, Wu T, Zheng W, Zhu X, Bouchard C, Chasman DI, Evans MK, Fox ER, Gudnason V, Hayward C, Horta BL, Kardia SLR, Krieger JE, Mook-Kanamori DO, Peyser PA, Province MM, Psaty BM, Rudan I, Sim X, Smith BH, van Dam RM, van Duijn CM, Wong TY, Arnett DK, Rao DC, Gauderman J, Liu CT, Morrison AC, Rotter JI, Fornage M. Gene-educational attainment interactions in a multi-population genome-wide meta-analysis identify novel lipid loci. Front Genet. 2023; 14:1235337.View Related Profiles. PMID: 38028628; PMCID: PMC10651736; DOI: 10.3389/fgene.2023.1235337;
     
  9. Leshchyk A, Xiang Q, Andersen SL, Gurinovich A, Song Z, Lee JH, Christensen K, Yashin A, Wojczynski M, Schwander K, Perls TT, Monti S, Sebastiani P. Mosaic Chromosomal Alterations and Human Longevity. J Gerontol A Biol Sci Med Sci. 2023 Aug 27; 78(9):1561-1568.View Related Profiles. PMID: 36988570; PMCID: PMC10460554; DOI: 10.1093/gerona/glad095;
     
  10. Milman S, Barzilai N, Wilson KA, Van der Willik O, Lederman S, Perls T, Gao T, Leahy AM, Jain P, Montgomery A, Shuldiner AR. SuperAger Initiative: unlocking the genetic potential of exceptional longevity. Nat Aging. 2023 Jun; 3(6):627-628. PMID: 37202472
     
Showing 10 of 201 results. Show More

This graph shows the total number of publications by year, by first, middle/unknown, or last author.

Bar chart showing 200 publications over 33 distinct years, with a maximum of 12 publications in 2021

YearPublications
19901
19931
19941
19952
19964
19973
19984
19994
20004
20016
200210
20037
200410
20055
20065
20076
20088
20096
20103
20114
20128
20138
20145
201511
201610
20177
20187
201911
20206
202112
20227
20237
20247


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In addition to these self-described keywords below, a list of MeSH based concepts is available here.

aging
centenarian
exceptional longevity

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  • Email (see 'Contact Info')
  • Phone (see 'Contact Info')

72 E. Concord St Robinson (B)
Boston MA 02118
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