Thomas T. Perls, MD, MPH, FACP
Professor
Boston University School of Medicine
Dept of Medicine
Geriatrics

MD, University of Rochester
MPH, Harvard School of Public Health




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 Boston University 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 School of Medicine, Graduate Medical Sciences



2017 Gerontological Society of America: Fellow
2016 Gerontological Society of America: Joseph T. Freeman Award
2013 International Gerontology Association World Congress: Ewald Busse Research in Gerontology
2010 Glenn Medical Research Foundation: Glenn Award for Resaerch in Biological Mechanisms of Aging
1993 American College of Physicians: Fellow


The Long Life Family Study
08/15/2019 - 03/31/2022 (Subcontract PI)
The Washington University NIH NIA
5U19AG063893-02

Identifying protective omics profiles in centenarians and translating these into preventive and therapeutic strategies
09/15/2019 - 08/31/2021 (PI)
NIH/National Institute on Aging
5UH2AG064704-02

New England Centenarian Study
07/01/2016 - 06/30/2021 (Multi-PI)
PI: Thomas T. Perls, MD, MPH, FACP
The William M. Wood Foundation


Protein Signatures of APOE2 and Cognitive Aging
09/01/2020 - 05/31/2021 (Subcontract PI)
Tufts - New England Medical Center NIH NIA
7R01AG061844-03

Longevity Consortium
08/15/2019 - 05/31/2021 (Subcontract PI)
Sutter Bay Hospitals dba California Pacific Medical Center NIH NIA
5U19AG023122-13

Candidate protective factors for age-associated diseases (target discovery) or factors indicative of healthy aging
09/15/2016 - 09/15/2019 (Co-Investigator)
PI: Paola Sebastiani, PhD
Novartis Institutes for BioMedical Research


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



Longevity Consortium
09/30/2018 - 05/31/2023 (PI)
California Pacific Med Ctr Res Inst NIH-NIA
2U19AG023122-11A1

Protein signatures of APOE and cognitive aging
09/30/2018 - 05/31/2023 (PI)
Trustees of Boston University NIH-NIA
1R01AG061844-01

Identifying protective omics profiles in centenarians and translating these int…
09/15/2019 - 08/31/2021 (Activity-level PI)
PI: George J. Murphy, PhD
Trustees of Boston University NIH-NIA
1UH2AG064704-01

The Long Life Family Study: Boston Field Center
06/01/2014 - 05/31/2020 (PI)
NIH-NIA
5U01AG023755-13

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
2021 The Long Life Family Study 5U19AG063893-03
2021 Phenotyping Core 5U19AG063893-03-6290
2021 Protein Signatures of APOE2 and Cognitive Aging 5R01AG061844-04 3
2021 Centenarian Consortium Project 5U19AG023122-14-5792 235
2020 Identifying protective omics profiles in centenarians and translating these into preventive and therapeutic strategies 5UH2AG064704-02
2020 The Long Life Family Study 5U19AG063893-02
2020 Protein Signatures of APOE2 and Cognitive Aging 7R01AG061844-03 3
2020 Phenotyping Core 5U19AG063893-02-6290
2020 Phenotyping Core 5U19AG063893-02-6290
2020 Centenarian Consortium Project 5U19AG023122-13-5792 235
Showing 10 of 49 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. Renner SW, Qiao Y, Gmelin T, Santanasto AJ, Boudreau RM, Walston JD, Perls TT, Christensen K, Newman AB, Glynn NW. Association of fatigue, inflammation, and physical activity on gait speed: the Long Life Family Study. Aging Clin Exp Res. 2021 Jul 01. PMID: 34196949
     
  2. Gurinovich A, Song Z, Zhang W, Federico A, Monti S, Andersen SL, Jennings LL, Glass DJ, Barzilai N, Millman S, Perls TT, Sebastiani P. Correction to: Effect of longevity genetic variants on the molecular aging rate. Geroscience. 2021 Jun 18.View Related Profiles. PMID: 34143375
     
  3. Andersen SL, Du M, Cosentino S, Schupf N, Rosso AL, Perls TT, Sebastiani P. Slower Decline in Processing Speed Is Associated with Familial Longevity. Gerontology. 2021 May 04; 1-13.View Related Profiles. PMID: 33946077
     
  4. Gurinovich A, Song Z, Zhang W, Federico A, Monti S, Andersen SL, Jennings LL, Glass DJ, Barzilai N, Millman S, Perls TT, Sebastiani P. Effect of longevity genetic variants on the molecular aging rate. Geroscience. 2021 06; 43(3):1237-1251.View Related Profiles. PMID: 33948810; PMCID: PMC8190315; DOI: 10.1007/s11357-021-00376-4;
     
  5. Deelen J, Evans DS, Arking DE, Tesi N, Nygaard M, Liu X, Wojczynski MK, Biggs ML, van der Spek A, Atzmon G, Ware EB, Sarnowski C, Smith AV, Seppälä I, Cordell HJ, Dose J, Amin N, Arnold AM, Ayers KL, Barzilai N, Becker EJ, Beekman M, Blanché H, Christensen K, Christiansen L, Collerton JC, Cubaynes S, Cummings SR, Davies K, Debrabant B, Deleuze JF, Duncan R, Faul JD, Franceschi C, Galan P, Gudnason V, Harris TB, Huisman M, Hurme MA, Jagger C, Jansen I, Jylhä M, Kähönen M, Karasik D, Kardia SLR, Kingston A, Kirkwood TBL, Launer LJ, Lehtimäki T, Lieb W, Lyytikäinen LP, Martin-Ruiz C, Min J, Nebel A, Newman AB, Nie C, Nohr EA, Orwoll ES, Perls TT, Province MA, Psaty BM, Raitakari OT, Reinders MJT, Robine JM, Rotter JI, Sebastiani P, Smith J, Sørensen TIA, Taylor KD, Uitterlinden AG, van der Flier W, van der Lee SJ, van Duijn CM, van Heemst D, Vaupel JW, Weir D, Ye K, Zeng Y, Zheng W, Holstege H, Kiel DP, Lunetta KL, Slagboom PE, Murabito JM. Publisher Correction: A meta-analysis of genome-wide association studies identifies multiple longevity genes. Nat Commun. 2021 Apr 23; 12(1):2463.View Related Profiles. PMID: 33893282; PMCID: PMC8065049; DOI: 10.1038/s41467-021-22613-2;
     
  6. Feitosa MF, Kuipers AL, Wojczynski MK, Wang L, Barinas-Mitchell E, Kulminski AM, Thyagarajan B, Lee JH, Perls T, Christensen K, Newman AB, Zmuda JM, Province MA. Heterogeneity of the Predictive Polygenic Risk Scores for Coronary Heart Disease Age-at-Onset in Three Different Coronary Heart Disease Family-Based Ascertainments. Circ Genom Precis Med. 2021 Jun; 14(3):e003201. PMID: 33844929; PMCID: PMC8214825; DOI: 10.1161/CIRCGEN.120.003201;
     
  7. Sebastiani P, Federico A, Morris M, Gurinovich A, Tanaka T, Chandler KB, Andersen SL, Denis G, Costello CE, Ferrucci L, Jennings L, Glass DJ, Monti S, Perls TT. Protein signatures of centenarians and their offspring suggest centenarians age slower than other humans. Aging Cell. 2021 02; 20(2):e13290.View Related Profiles. PMID: 33512769; PMCID: PMC7884029; DOI: 10.1111/acel.13290;
     
  8. Xiang Q, Andersen SL, Perls TT, Sebastiani P. Studying the Interplay Between Apolipoprotein E and Education on Cognitive Decline in Centenarians Using Bayesian Beta Regression. Front Genet. 2020; 11:606831.View Related Profiles. PMID: 33488674; PMCID: PMC7820893; DOI: 10.3389/fgene.2020.606831;
     
  9. Perls TT. Cognitive Trajectories and Resilience in Centenarians-Findings From the 100-Plus Study. JAMA Netw Open. 2021 01 04; 4(1):e2032538. PMID: 33449091
     
  10. Du M, Andersen SL, Schupf N, Feitosa MF, Barker MS, Perls TT, Sebastiani P. Association Between APOE Alleles and Change of Neuropsychological Tests in the Long Life Family Study. J Alzheimers Dis. 2021; 79(1):117-125.View Related Profiles. PMID: 33216038; PMCID: PMC7952213; DOI: 10.3233/JAD-201113;
     
Showing 10 of 178 results. Show More

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

Bar chart showing 178 publications over 30 distinct years, with a maximum of 11 publications in 2015 and 2019 and 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
202111


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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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