TY  - JOUR
AU  - OKAMOTO, MASAHIRO
AU  - SHIMODA, RYO
AU  - AMAYA, YUKI
AU  - SOYA, SHINGO
AU  - SOYA, MARIKO
AU  - KOIZUMI, HIKARU
AU  - NAKAMURA, KENGO
AU  - HIRAGA, TAICHI
AU  - Torma, Ferenc Gergely
AU  - SOYA, HIDEAKI
TI  - Accelerated Fear Extinction by Regular Light-Intensity Exercise: A Possible Role of Hippocampal BDNF-TrkB Signaling
JF  - MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
J2  - MED SCI SPORT EXER
VL  - 56
PY  - 2024
IS  - 2
SP  - 221
EP  - 229
PG  - 9
SN  - 0195-9131
DO  - 10.1249/MSS.0000000000003312
UR  - https://m2.mtmt.hu/api/publication/34776881
ID  - 34776881
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Torma, Ferenc Gergely
AU  - Kerepesi, Csaba
AU  - Jókai, Mátyás
AU  - Bábszky, Gergely
AU  - Koltai, Erika
AU  - Ligeti, Balázs
AU  - Kalcsevszki, Regina
AU  - McGreevy, Kristen M.
AU  - Horvath, Steve
AU  - Radák, Zsolt
TI  - Alterations of the gut microbiome are associated with epigenetic age acceleration and physical fitness
JF  - AGING CELL
J2  - AGING CELL
PY  - 2024
SN  - 1474-9718
DO  - 10.1111/acel.14101
UR  - https://m2.mtmt.hu/api/publication/34693196
ID  - 34693196
AB  - Epigenetic clocks can measure aging and predict the incidence of diseases and mortality. Higher levels of physical fitness are associated with a slower aging process and a healthier lifespan. Microbiome alterations occur in various diseases and during the aging process, yet their relation to epigenetic clocks is not explored. To fill this gap, we collected metagenomic (from stool), epigenetic (from blood), and exercise‐related data from physically active individuals and, by applying epigenetic clocks, we examined the relationship between gut flora, blood‐based epigenetic age acceleration, and physical fitness. We revealed that an increased entropy in the gut microbiome of physically active middle‐aged/old individuals is associated with accelerated epigenetic aging, decreased fitness, or impaired health status. We also observed that a slower epigenetic aging and higher fitness level can be linked to altered abundance of some bacterial species often linked to anti‐inflammatory effects. Overall our data suggest that alterations in the microbiome can be associated with epigenetic age acceleration and physical fitness.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Kawamura, Takuji
AU  - Radák, Zsolt
AU  - Tabata, Hiroki
AU  - Akiyama, Hiroshi
AU  - Nakamura, Nobuhiro
AU  - Kawakami, Ryoko
AU  - Ito, Tomoko
AU  - Usui, Chiyoko
AU  - Jókai, Mátyás
AU  - Torma, Ferenc Gergely
AU  - Kim, Hyeon‐Ki
AU  - Miyachi, Motohiko
AU  - Torii, Suguru
AU  - Suzuki, Katsuhiko
AU  - Ishii, Kaori
AU  - Sakamoto, Shizuo
AU  - Oka, Koichiro
AU  - Higuchi, Mitsuru
AU  - Muraoka, Isao
AU  - McGreevy, Kristen M.
AU  - Horvath, Steve
AU  - Tanisawa, Kumpei
TI  - Associations between cardiorespiratory fitness and lifestyle‐related factors with DNA methylation‐based ageing clocks in older men: WASEDA 'S Health Study
JF  - AGING CELL
J2  - AGING CELL
VL  - 23
PY  - 2024
IS  - 1
SN  - 1474-9718
DO  - 10.1111/acel.13960
UR  - https://m2.mtmt.hu/api/publication/34110008
ID  - 34110008
AB  - DNA methylation‐based age estimators (DNAm ageing clocks) are currently one of the most promising biomarkers for predicting biological age. However, the relationships between cardiorespiratory fitness (CRF), measured directly by expiratory gas analysis, and DNAm ageing clocks are largely unknown. We investigated the relationships between CRF and the age‐adjusted value from the residuals of the regression of DNAm ageing clock to chronological age (DNAmAgeAcceleration: DNAmAgeAccel) and attempted to determine the relative contribution of CRF to DNAmAgeAccel in the presence of other lifestyle factors. DNA samples from 144 Japanese men aged 65–72 years were used to appraise first‐ (i.e., DNAmHorvath and DNAmHannum) and second‐ (i.e., DNAmPhenoAge, DNAmGrimAge, and DNAmFitAge) generation DNAm ageing clocks. Various surveys and measurements were conducted, including physical fitness, body composition, blood biochemical parameters, nutrient intake, smoking, alcohol consumption, disease status, sleep status, and chronotype. Both oxygen uptake at ventilatory threshold (VO 2 /kg at VT) and peak oxygen uptake (VO 2 /kg at Peak) showed a significant negative correlation with GrimAgeAccel, even after adjustments for chronological age and smoking and drinking status. Notably, VO 2 /kg at VT and VO 2 /kg at Peak above the reference value were also associated with delayed GrimAgeAccel. Multiple regression analysis showed that calf circumference, serum triglyceride, carbohydrate intake, and smoking status, rather than CRF, contributed more to GrimAgeAccel and FitAgeAccel. In conclusion, although the contribution of CRF to GrimAgeAccel and FitAgeAccel is relatively low compared to lifestyle‐related factors such as smoking, the results suggest that the maintenance of CRF is associated with delayed biological ageing in older men.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Yamazaki, Yudai
AU  - Suwabe, Kazuya
AU  - Nagano-Saito, Atsuko
AU  - Saotome, Kousaku
AU  - Kuwamizu, Ryuta
AU  - Hiraga, Taichi
AU  - Torma, Ferenc Gergely
AU  - Suzuki, Kenji
AU  - Sankai, Yoshiyuki
AU  - Yassa, Michael A
AU  - Soya, Hideaki
TI  - A possible contribution of the locus coeruleus to arousal enhancement with mild exercise: evidence from pupillometry and neuromelanin imaging
JF  - CEREBRAL CORTEX COMMUNICATIONS
J2  - CEREB CORTEX COMMUN
VL  - 4
PY  - 2023
IS  - 2
SN  - 2632-7376
DO  - 10.1093/texcom/tgad010
UR  - https://m2.mtmt.hu/api/publication/34776890
ID  - 34776890
AB  - Acute mild exercise has been observed to facilitate executive function and memory. A possible underlying mechanism of this is the upregulation of the ascending arousal system, including the catecholaminergic system originating from the locus coeruleus (LC). Prior work indicates that pupil diameter, as an indirect marker of the ascending arousal system, including the LC, increases even with very light-intensity exercise. However, it remains unclear whether the LC directly contributes to exercise-induced pupil-linked arousal. Here, we examined the involvement of the LC in the change in pupil dilation induced by very light-intensity exercise using pupillometry and neuromelanin imaging to assess the LC integrity. A sample of 21 young males performed 10 min of very light-intensity exercise, and we measured changes in the pupil diameters and psychological arousal levels induced by the exercise. Neuromelanin-weighted magnetic resonance imaging scans were also obtained. We observed that pupil diameter and psychological arousal levels increased during very light-intensity exercise, which is consistent with previous findings. Notably, the LC contrast, a marker of LC integrity, predicted the magnitude of pupil dilation and psychological arousal enhancement with exercise. These relationships suggest that the LC-catecholaminergic system is a potential a mechanism for pupil-linked arousal induced by very light-intensity exercise.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Kolonics, Attila
AU  - Bori, Zoltán
AU  - Torma, Ferenc Gergely
AU  - Ábrahám, Dóra
AU  - Fehér, János
AU  - Radák, Zsolt
TI  - Exercise combined with postbiotics treatment results in synergistic improvement of mitochondrial function in the brain of male transgenic mice for Alzheimer’s disease
JF  - BMC NEUROSCIENCE
J2  - BMC NEUROSCI
VL  - 24
PY  - 2023
IS  - 1
SN  - 1471-2202
DO  - 10.1186/s12868-023-00836-x
UR  - https://m2.mtmt.hu/api/publication/34477681
ID  - 34477681
N1  - Összes idézések száma a WoS-ban: 0
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Jókai, Mátyás
AU  - Torma, Ferenc Gergely
AU  - McGreevy, Kristen M.
AU  - Koltai, Erika
AU  - Bori, Zoltán
AU  - Bábszky, Gergely
AU  - Bakonyi, Péter
AU  - Gombos, Zoltán
AU  - György, Bernadett
AU  - Aczél, Dóra Tímea
AU  - Tóth, László
AU  - Osváth, Péter
AU  - Fridvalszki, Marcell Norbert
AU  - Téglás, Tímea
AU  - Pósa, Anikó
AU  - Kujach, Sylwester
AU  - Olek, Robert
AU  - Kawamura, Takuji
AU  - Seki, Yasuhiro
AU  - Suzuki, Katsuhiko
AU  - Tanisawa, Kumpei
AU  - Goto, Sataro
AU  - Kerepesi, Csaba
AU  - Boldogh, Istvan
AU  - Ba, Xueqing
AU  - Davies, Kelvin J. A.
AU  - Horvath, Steve
AU  - Radák, Zsolt
TI  - DNA methylation clock DNAmFitAge shows regular exercise is associated with slower aging and systemic adaptation
JF  - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)
J2  - GEROSCIENCE
VL  - 45
PY  - 2023
IS  - 5
SP  - 2805
EP  - 2817
PG  - 13
SN  - 2509-2715
DO  - 10.1007/s11357-023-00826-1
UR  - https://m2.mtmt.hu/api/publication/33866054
ID  - 33866054
AB  - DNAmPhenoAge, DNAmGrimAge, and the newly developed DNAmFitAge are DNA methylation (DNAm)-based biomarkers that reflect the individual aging process. Here, we examine the relationship between physical fitness and DNAm-based biomarkers in adults aged 33–88 with a wide range of physical fitness (including athletes with long-term training history). Higher levels of VO 2 max ( ρ  = 0.2, p  = 6.4E − 4, r  = 0.19, p  = 1.2E − 3), Jumpmax ( p  = 0.11, p  = 5.5E − 2, r  = 0.13, p  = 2.8E − 2), Gripmax ( ρ  = 0.17, p  = 3.5E − 3, r  = 0.16, p  = 5.6E − 3), and HDL levels ( ρ  = 0.18, p  = 1.95E − 3, r  = 0.19, p  = 1.1E − 3) are associated with better verbal short-term memory. In addition, verbal short-term memory is associated with decelerated aging assessed with the new DNAm biomarker FitAgeAcceleration ( ρ : − 0.18, p  = 0.0017). DNAmFitAge can distinguish high-fitness individuals from low/medium-fitness individuals better than existing DNAm biomarkers and estimates a younger biological age in the high-fit males and females (1.5 and 2.0 years younger, respectively). Our research shows that regular physical exercise contributes to observable physiological and methylation differences which are beneficial to the aging process. DNAmFitAge has now emerged as a new biological marker of quality of life.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Cikes, Domagoj
AU  - Elsayad, Kareem
AU  - Sezgin, Erdinc
AU  - Koltai, Erika
AU  - Torma, Ferenc Gergely
AU  - Orthofer, Michael
AU  - Yarwood, Rebecca
AU  - Heinz, Leonhard X.
AU  - Sedlyarov, Vitaly
AU  - Miranda, Nasser Darwish
AU  - Taylor, Adrian
AU  - Grapentine, Sophie
AU  - al-Murshedi, Fathiya
AU  - Abot, Anne
AU  - Weidinger, Adelheid
AU  - Kutchukian, Candice
AU  - Sanchez, Colline
AU  - Cronin, Shane J. F.
AU  - Novatchkova, Maria
AU  - Kavirayani, Anoop
AU  - Schuetz, Thomas
AU  - Haubner, Bernhard
AU  - Haas, Lisa
AU  - Hagelkruys, Astrid
AU  - Jackowski, Suzanne
AU  - Kozlov, Andrey V.
AU  - Jacquemond, Vincent
AU  - Knauf, Claude
AU  - Superti-Furga, Giulio
AU  - Rullman, Eric
AU  - Gustafsson, Thomas
AU  - McDermot, John
AU  - Lowe, Martin
AU  - Radák, Zsolt
AU  - Chamberlain, Jeffrey S.
AU  - Bakovic, Marica
AU  - Banka, Siddharth
AU  - Penninger, Josef M.
TI  - Author Correction: PCYT2-regulated lipid biosynthesis is critical to muscle health and ageing
JF  - NATURE METABOLISM
J2  - NAT METAB
VL  - 2023
PY  - 2023
IS  - 5
SP  - 495
SN  - 2522-5812
DO  - 10.1038/s42255-023-00791-1
UR  - https://m2.mtmt.hu/api/publication/33745909
ID  - 33745909
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Cikes, Domagoj
AU  - Elsayad, Kareem
AU  - Sezgin, Erdinc
AU  - Koltai, Erika
AU  - Torma, Ferenc Gergely
AU  - Orthofer, Michael
AU  - Yarwood, Rebecca
AU  - Heinz, Leonhard X.
AU  - Sedlyarov, Vitaly
AU  - Miranda, Nasser Darwish
AU  - Taylor, Adrian
AU  - Grapentine, Sophie
AU  - al-Murshedi, Fathiya
AU  - Abot, Anne
AU  - Weidinger, Adelheid
AU  - Kutchukian, Candice
AU  - Sanchez, Colline
AU  - Cronin, Shane J. F.
AU  - Novatchkova, Maria
AU  - Kavirayani, Anoop
AU  - Schuetz, Thomas
AU  - Haubner, Bernhard
AU  - Haas, Lisa
AU  - Hagelkruys, Astrid
AU  - Jackowski, Suzanne
AU  - Kozlov, Andrey
AU  - Jacquemond, Vincent
AU  - Knauf, Claude
AU  - Superti-Furga, Giulio
AU  - Rullman, Eric
AU  - Gustafsson, Thomas
AU  - McDermot, John
AU  - Lowe, Martin
AU  - Radák, Zsolt
AU  - Chamberlain, Jeffrey S.
AU  - Bakovic, Marica
AU  - Banka, Siddharth
AU  - Penninger, Josef M.
TI  - PCYT2-regulated lipid biosynthesis is critical to muscle health and ageing
JF  - NATURE METABOLISM
J2  - NAT METAB
VL  - 5
PY  - 2023
IS  - 3
SP  - 495
EP  - 515
PG  - 20
SN  - 2522-5812
DO  - 10.1038/s42255-023-00766-2
UR  - https://m2.mtmt.hu/api/publication/33712726
ID  - 33712726
N1  - Received 08 February 2021, Accepted 10 February 2023, Published 20 March 2023
AB  - Muscle degeneration is the most prevalent cause for frailty and dependency in inherited diseases and ageing. Elucidation of pathophysiological mechanisms, as well as effective treatments for muscle diseases, represents an important goal in improving human health. Here, we show that the lipid synthesis enzyme phosphatidylethanolamine cytidyltransferase (PCYT2/ECT) is critical to muscle health. Human deficiency in PCYT2 causes a severe disease with failure to thrive and progressive weakness. pcyt2-mutant zebrafish and muscle-specific Pcyt2-knockout mice recapitulate the participant phenotypes, with failure to thrive, progressive muscle weakness and accelerated ageing. Mechanistically, muscle Pcyt2 deficiency affects cellular bioenergetics and membrane lipid bilayer structure and stability. PCYT2 activity declines in ageing muscles of mice and humans, and adeno-associated virus-based delivery of PCYT2 ameliorates muscle weakness in Pcyt2-knockout and old mice, offering a therapy for individuals with a rare disease and muscle ageing. Thus, PCYT2 plays a fundamental and conserved role in vertebrate muscle health, linking PCYT2 and PCYT2-synthesized lipids to severe muscle dystrophy and ageing.
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - McGreevy, Kristen M.
AU  - Radák, Zsolt
AU  - Torma, Ferenc Gergely
AU  - Jókai, Mátyás
AU  - Lu, Ake T.
AU  - Belsky, Daniel W.
AU  - Binder, Alexandra
AU  - Marioni, Riccardo E.
AU  - Ferrucci, Luigi
AU  - Pośpiech, Ewelina
AU  - Branicki, Wojciech
AU  - Ossowski, Andrzej
AU  - Sitek, Aneta
AU  - Spólnicka, Magdalena
AU  - Raffield, Laura M.
AU  - Reiner, Alex P.
AU  - Cox, Simon
AU  - Kobor, Michael
AU  - Corcoran, David L.
AU  - Horvath, Steve
TI  - DNAmFitAge: biological age indicator incorporating physical fitness
JF  - AGING-US
J2  - AGING-US
VL  - 15
PY  - 2023
SN  - 1945-4589
DO  - 10.18632/aging.204538
UR  - https://m2.mtmt.hu/api/publication/33668410
ID  - 33668410
N1  - Funding Agency and Grant Number: National Excellence Program; Scientific Excellence Program; Alzheimer's Society; Wellcome Trust; Royal Society; National Institute of Health (NIH); Center for Information Technology, NIH; National Heart, Lung, and Blood Institute (NHLBI); National Institute on Minority Health and Health Disparities (NIMHD); NHLBI; U.S. Department of Health and Human Services; UK's Biotechnology and Biological Sciences Research Council; Age UK; Medical Research Council; University of Edinburgh; Centre for Cognitive Ageing and Cognitive Epidemiology (Pilot Fund award) [1U01AG060908]; Wellcome Trust Institutional Strategic Support Fund [126823]; University of Queensland [TKP2020-NKA-17]; National Institute on Aging [AS-PG-19b-010]; National Centre for Research and Development (NCBR) in Poland;  [221890/Z/20/Z];  [N01-HC-25195];  [HHSN268201500001I];  [HHSN268201800013I];  [HHSN268201800014I];  [HHSN268201800015I];  [HHSN268201800010I];  [HHSN268201800011I];  [HHSN268201800012I];  [HHSN268201600018C];  [HHSN268201600001C];  [HHSN268201600002C];  [HHSN268201600003C];  [HHSN268201600004C];  [G0701120];  [G1001245];  [MR/M013111/1];  [MR/R024065/1];  [R01AG061378];  [R33AG070455];  [DOB-BIO10/06/2019]
            Funding text: SH, KMM, REM, and ATL supported from 1U01AG060908. ZR, FT, and MJ supported from the National Excellence Program (126823) , Scientific Excellence Program, TKP2020-NKA-17. REM: Alzheimer's Society AS-PG-19b-010. SRC: Sir Henry Dale Fellowship by Wellcome Trust and Royal Society grant 221890/Z/20/Z.FHS is funded by National Institute of Health (NIH) contract N01-HC-25195 and HHSN268201500001I. The laboratory and analytical work: the Division of Intramural Research, National Heart, Lung, and Blood Institute (NHLBI) , NIH. The analytical component was also funded by the Center for Information Technology, NIH.The Jackson Heart Study (JHS) is supported and conducted in collaboration with Jackson State University (HHSN268201800013I) , Tougaloo College (HHSN268201800014I) , the Mississippi State Department of Health (HHSN268201800015I) and the University of Mississippi Medical Center (HHSN268201800010I, HHSN268201800011I and HHSN268201800012I) contracts from the National Heart, Lung, and Blood Institute (NHLBI) and the National Institute on Minority Health and Health Disparities (NIMHD) . The authors also wish to thank the staffs and participants of the JHS.WHI program is funded by the NHLBI, and the U.S. Department of Health and Human Services through contracts HHSN268201600018C, HHSN268201600001C, HHSN268201600002C, HHSN268201600003C, and HHSN268201600004C.The LBC1921 was supported by the UK's Biotechnology and Biological Sciences Research Council. The LBC1936 is supported by Age UK, the Medical Research Council (G0701120, G1001245, MR/M013111/1, MR/R024065/1) , and the University of Edinburgh. Methylation typing was supported by Centre for Cognitive Ageing and Cognitive Epidemiology (Pilot Fund award) , Age UK, The Wellcome Trust Institutional Strategic Support Fund, The University of Edinburgh, and The University of Queensland.CALERIE was conducted in collaboration with Columbia University Mailman School of Public Health with support from National Institute on Aging grants R01AG061378 and R33AG070455.Research on the Polish Study is financed by the National Centre for Research and Development (NCBR) in Poland within the framework of call 10/2019 related to scientific research and studies for national defense and security [project no. DOB-BIO10/06/2019] .
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Aczél, Dóra Tímea
AU  - Torma, Ferenc Gergely
AU  - Jókai, Mátyás
AU  - Kristen, McGreevy
AU  - Boros, Anita
AU  - Yasuhiro, Seki
AU  - Istvan, Boldogh
AU  - Steve, Horvath
AU  - Radák, Zsolt
TI  - The Circulating Level of Klotho Is Not Dependent upon Physical Fitness and Age-Associated Methylation Increases at the Promoter Region of the Klotho Gene
JF  - GENES
J2  - GENES-BASEL
VL  - 14
PY  - 2023
IS  - 2
PG  - 12
SN  - 2073-4425
DO  - 10.3390/genes14020525
UR  - https://m2.mtmt.hu/api/publication/33648648
ID  - 33648648
N1  - Received: 22 December 2022 / Revised: 6 February 2023 / Accepted: 15 February 2023 / Published: 19 February 2023
LA  - English
DB  - MTMT
ER  -