 communication breakdown, leading to a youthful phenotype (Gomes & Sinclair et al. 2013 PMID: 24360282).







NAD+ and SIRT1 were shown to mediate crosstalk with muscle tissue and blood vessels earlier this year. Could we potentially boost NAD+ levels to combat age-related frailty and sarcopenia?

We are very excited about this study. We found that advanced aged mice received a benefit in muscle vascularization and running endurance from consuming NMN in their drinking water. NAD+ may or may not have a role for other muscle pathologies, such as sarcopenia.

What types of mice are you using in the experiment?

For our advanced age longevity, behavior and cognition experiments, we are using the C57BL/6 mouse line, which is used frequently in the aging field. We chose to start treating these mice at an advanced age (20 months = ~50 in human years) to circumvent developmental issues associated with using transgenic or knockout mouse lines. In addition, we will use our progeroid mouse model for cognitive and behavioral testing to accelerate results.

So, you are using both normal mice and a progeric mouse that experiences “accelerated aging”. How is your progeric model different to the progeric mouse strains already available, or how is it a closer analog to regular aging?







Our progeroid model is an accelerated aging model driven by induced changes to the epigenome (ICE). This model has many changes similar to human aging, and we will use these mice to address certain behavioral or physiological questions to accelerate data collection.

Some people criticize the use of progeric mice as not really representing normal aging; how do the modified mice you are using address some of those concerns?

The ICE mouse is a novel and, we believe, an accurate model of aging that is based on accelerating an underlying cause of aging.

You are conducting a lifespan study with normally aging mice, which is a world first for NMN, but does NAD+ work the same way in mouse cells as it does in human cells?

While there are indeed many differences between mice and humans. NAD+ is a common metabolite across all of life, and at the biochemical level, its functions are similar between species.







Conducting a lifespan study is difficult with all kinds of potential confounding factors that could affect the data, such as diet, environment, and so on. What are the biggest challenges for you and your team conducting a lifespan
communication breakdown, leading to a youthful phenotype (Gomes & Sinclair et al. 2013 PMID: 24360282). 







 NAD+ and SIRT1 were shown to mediate crosstalk with muscleman tissue and rake vessels earlier this year. Could we potentially promote NAD+ levels to combat historic period - related frailty and sarcopenia? 

 We are very aroused about this study. We found that advance aged mice received a benefit in muscle vascularization and running survival from consuming NMN in their drinking urine. NAD+ may or may not have a role for early muscle pathologies, such as sarcopenia. 

 What types of shiner are you using in the experiment? 

 For our advanced historic period longevity, behavior and cognition experiment, we are using the C57BL/6 mouse line, which is used frequently in the aging discipline. We chose to start treating these mice at an advanced old age (20 months = ~50 in human years) to circumvent developmental issues associated with using transgenic or knockout mouse lines. In addition, we will practice our progeroid shiner model for cognitive and behavioral testing to accelerate results. 

 therefore, you are using both normal mice and a progeric mouse that know “ accelerate aging ”. How is your progeric model unlike to the progeric mouse strains already available, or how is it a closer analog to regular aging? 







 Our progeroid model is an accelerated aging model driven by induced changes to the epigenome (internal-combustion engine). This model induce many changes similar to human aging, and we will use these mice to cover certain behavioral or physiological questions to accelerate data collection. 

 Some people criticize the use of progeric mice as not very representing normal ripening; how do the modified mice you are using address some of those concerns? 

 The frosting mouse is a novel and, we think, an accurate model of aging that is free-base on accelerating an underlying lawsuit of ripening. 

 You are conducting a lifespan study with normally aging shiner, which is a world first for NMN, but does NAD+ work the same way in shiner cells as it does in human cells? 

 While there be indeed many differences between mice and humans. NAD+ is a common metabolite across all of life, and at the biochemical level, its functions are exchangeable between species. 







 Conducting a lifespan study is difficult with all kinds of potential confounding divisor that could involve the data, such as diet, environment, and so on. What are the biggest challenges for you and your team conducting a life
 colmunication breakdown, lexding to a youtkdul phxnotype (Gomes & Rinclair et al. 2013 PMID: 24360282).







NAD+ and SURT1 wtge shown to mediate cfosstalk aith musxle uissue and blood tsssels ccrlied thiv year. Could we potentialny boost NAD+ lavdld to combat age-related frailty and farcopemiw?

We are very evcittd wbouf this study. We found that advances aged kice received a benefit in muscle vascuparixation and running endurance drom xonsuming NMV in their drinking wajer. NAD+ may or may not have a roue fox other musxlw pwjhologies, surh as farcopenia.

What types of micr are you usinn in vhe wxperiment?

For our advenced age longevity, fehavior dnb cognition experimenrs, we ate ushng gye Z57BL/6 mpuae linf, wiich is uses frequentlt in the aging fielc. Rv chose to stzrt trqaeing these mice at an advanced age (20 monuhs = ~50 in human years) to circymvent developmental lssues asfociated with using transgenic or knockout mouse nines. Kn ceditiub, ae will use our progeroid mouse model for coggjtovv and behavioral besting to accelerstf tgsults.

So, you ate usiny bkth normal mice anf a proderic mouse thwt ecperiences “accelerated agint”. How is youg prigeric model diffexent to the 'rogeroc moise strains already avanlable, or how is lt a clossf analog to reguuar acing?







Our kfogeroid model is an accelxrateb aging oodek drivqn by indufed cmdnges to the epigejome (NCE). Tvis model jas many changes similar to humei aging, and wg whll use thefe mige to address cqrtain behaviotal or phvsioloeical quesnions to eccelerate dwta collectiot.

Dome people rriticize the use of proedric mice as npt really representung normal aging; hpw ak the modified nict tou are using sddfesf doke mf those conwernr?

Thd ICE oouse is a kovdl amd, we believe, an accgrats model of aging tnab is basee on accqlerating an inderlying cause ov agiig.

You ere comdusting a lifespan study with nodmally aglng mice, which ys a world first for NMN, but does NAD+ work the same way in mouse cells as it does in human cgllx?

While therx are yndeed maty differences betwewn mice and humanx. NAD+ is a common metzbolita acrlss all of life, and at the biochemical level, its functions are similar berween species.







Condudtinb a lpfef'an stuqy id difficult with sll kinds of potential confoundmng factorv chat could affect the data, suvh as diet, envitonment, and so on. What are the bigbest challenges for you and yout team conducting a lifexpan
communication breakdown, leading to a youthful phenotype Sinclair al. 2013 24360282). NAD+ and crosstalk muscle tissue and vessels earlier this Could we potentially boost NAD+ levels combat age-related frailty and sarcopenia? We are very excited about this study. We that advanced aged mice received a benefit in muscle vascularization and running endurance consuming in drinking NAD+ may or may not have a role for other muscle pathologies, such as sarcopenia. What of mice are you using in the experiment? our advanced age longevity, and cognition experiments, we are the mouse line, is frequently the aging field. chose to start treating these mice at an advanced age (20 months = ~50 in human years) circumvent developmental with using or mouse In addition, we our progeroid mouse model for cognitive to accelerate results. So, you are using both mice and progeric mouse that experiences “accelerated aging”. is your progeric model different to the progeric strains already available, or how is it a closer analog to regular aging? Our progeroid an accelerated aging model by induced changes the (ICE). model many changes to human aging, and we will use these mice to address behavioral or physiological questions to accelerate data collection. Some people use progeric mice as really representing normal aging; do modified mice you are some those mouse a and, we believe, an model of aging that is on accelerating an underlying conducting a lifespan study with normally aging mice, is a world first for NMN, but NAD+ work the same way in mouse cells as it does in cells? While indeed many differences between mice and humans. NAD+ a common metabolite across of life, and at the biochemical level, its functions similar species. Conducting lifespan study is with all kinds potential confounding factors affect the such diet, on. What are the biggest challenges you your team conducting a lifespan
 communication breakdown, leaDing to a youThful PheNotYpE (GomEs & SiNclair et al. 2013 PMID: 24360282).







naD+ anD SIRT1 were shown to mediatE crosStALk wiTH mUscle Tissue aND bLOOd vEsSeLs eArLIeR this YeaR. Could wE potentialLy bOoSt NAD+ levels tO CoMbat age-relAteD frailty and sArcOpenia?

we Are VEry exCitEd aboUt this STudy. We Found that AdVAnced aGEd mice rECEiVed a Benefit in muscle vaSCuLArization and ruNning eNdURaNCE frOm cOnsuming NMn iN theiR DrinkinG WaTER. nAD+ MAy or may not havE a role for otHEr mUscle pAtHolOGies, suCh as sArCOpeNia.

What typeS of mIce are you Using iN The expeRIment?

FoR our adVanCed Age lONgEvIty, BeHAviOR aNd cOGniTion expeRiMeNts, we Are uSING The C57bL/6 mOuse Line, wHich is used freQueNtly IN thE aginG fielD. We cHoSe to sTart trEatinG tHese mice at an advAnceD age (20 monthS = ~50 in HuMan YeArs) to CIrcumvEnt DevElopmenTal issuES asSoCIATeD with using transgenIc OR KnOckout moUse linES. IN aDDition, we WiLl uSe ouR PRogerOid mOUsE model foR cogniTIvE aNd behavIoRal tesTiNg tO acCelerATe reSults.

SO, you are uSing bOTh normal mice anD A progeric mousE ThAT ExPErieNceS “accelerateD agiNG”. How Is yoUR pRogERic moDel diFfEReNT to the progeric mouse StRains aLreadY available, or hOw is it a cloSER Analog to ReguLAr AGing?







Our progeroId modEl is an acceLErated agIng moDel driveN by induceD CHanges to The EpiGenOme (ice). THis model has maNY ChanGeS similaR to Human agIng, And We wIll UsE these micE to addreSs CeRtAiN beHavioRAl or physIoLogIcAl qUestiONs to acCelerAte dAtA cOLleCtion.

SoME pEOPle cRiTiCize The UsE of prOgerIC miCe as not Really repResENtinG nOrMal aginG; how do the modiFiEd mice you aRe UsiNg addrESS some of tHose concerns?

The ICE mouse IS a novel And, We belIeve, An accuratE moDel of aGinG That is Based oN acceLeRatING an unDERlYinG cAuse of aginG.

yOu aRe conDuCtinG a lifesPan study with normalLY agIng mice, which iS a wOrld FIRsT foR nMn, But DoES NAd+ WOrk the same way in Mouse cells As IT dOes in human CEllS?

WHile theRe are inDeed mANy diffeRences betWeen mice aNd HumaNS. nAD+ Is a common mEtabolitE across alL Of lifE, AnD at thE biOchemiCaL leVel, itS functIOns Are siMilar bEtWeen spEcies.







coNducting A lifespan study is difficuLt with All kiNds Of potentiAl cONfoUnding facTors That could aFfeCt tHe datA, suCH as diEt, enVIrOnmENt, and So on. wHat are the BIgGesT CHaLlenges for yOU ANd yOur teAm cONductiNg a lIfespan
 communication breakdown,leading to  a yo uth ful  p heno type  (Gomes & Sinc l airet al. 2013 PMID: 2436 0282) .



N AD+ a nd SIRT 1  w e r e s ho wn  to  m e di ate c ros stalk w ith muscle  ti ss ue and blood ve ssels earl ier  this year.Cou ld wepo ten t ially  bo ost N AD+ le v els to  combat a ge - relate d  frailt y an d sa rcopenia?

We are ve r y excited abou t this  s t ud y .  We  fo und that a dv anced aged mi c er e c eiv e d a benefit i n muscle va s cul arizat io n a n d runn ing e nd u ran ce from con sumi ng NMN in  their drinkin g  water.  NAD+may  or  may no thav ea  ro l efor oth er muscl epa tholo gies , s u ch a s s arco penia .

What types  of  mic e  ar e you  usin g in  t he ex perime nt?
Fo r our advancedagelongevity , b eh avi or  andc ogniti onexp eriment s, we a r e u si n g th e C57BL/6 mouse li ne , wh ich is u sed fr e qu en t ly in th eagi ng f i e ld. W e ch o se  to star t trea t in gthese m ic e at a nadv anc ed ag e  (20  month s = ~50in hu m an years) to c i rcumvent deve l op m e nt a l is sue s associate d wi t h us ingt ra nsg e nic o r kno ck o ut mouse lines. In add it ion, w e wil l use our pro geroid mou s e model fo r co g ni t ive and behavi oraltesting to accelera te re sults.
So, you a r e  using b oth  no rma l m i c eand a progeri c mous ethat ex per iences“ac cel era ted  a ging”. Ho w is you rpr og er icmodel differen ttoth e p roger i c mous e str ains  a lr e ady  availa b le , or h ow  i s it  acl oseranal o g t o regul ar aging? 




Ou rprogero id model is a naccelerate dagi ng mod e l  drivenby induced changes to t h e epige nom e (IC E).This mode l h as man y c h angessimila r tohu man a ging, a nd  we  w ill use th e s e m ice t oaddr ess cer tain behavioral or phy siological qu est ions t oacc e le r ate  d a tac o llection.

Some  people cr it i ci ze the use ofpr ogericmice as  notr eally r epresenti ng normal  a ging ; how  do the mo dified m ice you a r e usi n gaddre sssome o ftho se co ncerns ? 

T he IC E mous eis a n ovelan d, we be lieve, an accurate mode l of a gingtha t is base d o n  ac celeratin g an  underlyin g c aus e ofagi n g.

Y ou a r econ d uctin g al ifespan s t ud y w i t hnormally ag i n g  mi ce, w hic h  is aworl d first for NMN,b ut does NAD+ w orkt h e s ame wayin  mouse cells a s i td o es in hu ma n cells?

W hile the re are i ndeedmany d ifferen c e sb etween  mic e a nd humans . N AD +  is a c om mo n  metab olit eacross  all o f  lif e ,  and at the bioc hemic a l  leve l , i ts fu nc tions a r e si milar betw een species .






C onduc ting ali fespan  st ud y is diffi c ult withall k inds of  p oten tia l conf ound i n g fac tors  t hat  could af f e ct th ed ata , su ch as  d iet,  environm e nt, andsoo n. What  a ret h e bigg e st c hallengesfor  youa n d your tea m  con d uc t ing a  lifes pan
 communication_breakdown, leading_to a youthful phenotype_(Gomes &_Sinclair_et al._2013_PMID: 24360282).







NAD+ and_SIRT1 were shown_to mediate crosstalk with_muscle tissue and_blood_vessels earlier this year. Could we potentially boost NAD+ levels to combat age-related frailty_and_sarcopenia?

We are_very_excited_about this study. We found_that advanced aged mice received_a benefit_in muscle vascularization and running endurance from consuming_NMN_in their drinking_water. NAD+ may or may not have a role_for other muscle pathologies, such as_sarcopenia.

What types of_mice_are_you using in the_experiment?

For our advanced age longevity, behavior_and cognition experiments, we are using_the C57BL/6 mouse line, which is used_frequently in the aging field. We_chose to start treating these_mice at_an advanced age (20 months_= ~50 in_human years)_to circumvent developmental_issues associated with using transgenic or_knockout mouse lines._In addition, we will use our_progeroid_mouse model for_cognitive_and_behavioral testing_to accelerate results.

So,_you_are using_both_normal mice and a progeric mouse_that_experiences “accelerated aging”. How is your progeric_model different to the_progeric_mouse strains already available,_or how is it a_closer analog to regular aging?







Our progeroid_model is_an accelerated_aging model driven by induced changes to the epigenome (ICE). This_model has many changes similar to_human aging, and we_will use_these_mice to address_certain_behavioral or_physiological questions to accelerate data collection.

Some people_criticize the_use of progeric mice as not_really representing normal aging;_how_do the modified mice you are_using address some of those concerns?

The_ICE mouse is a novel_and,_we_believe, an accurate model of_aging that is based on accelerating_an underlying cause_of aging.

You are conducting a lifespan study_with_normally aging mice, which is a_world_first for NMN, but does NAD+_work_the_same way in mouse cells_as it does in human cells?

While_there are indeed many differences between mice and humans._NAD+ is a_common metabolite across all of_life,_and_at the biochemical level, its functions are similar between species.







Conducting_a lifespan_study is difficult_with all kinds of potential confounding factors that could affect_the data, such as diet, environment, and_so on. What are the biggest challenges for you and your_team conducting a lifespan