Modulating Ageing Anti-Ageing

128 Pages·2017·3.93 MB·English

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Modulating Ageing
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Anti-Ageing
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from Molecular Biology
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to Clinical Perspectives
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Heart Centre Keynote Speaker
University Hospital Halle
Claudio Franceschi
Ernst-Grube-Str. 40
Bologna, Italy
R 06120 Halle (Saale)
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German National Academy of From Friday,
Sciences Leopoldina
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German Society of Gerontology September 1st, 2017, 6 pm
and Geriatrics (DGGG)
Interdisciplinary Centre till Sunday,
T on Ageing Halle (IZAH)
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RTG 2155: ProMoAge September 3rd, 2017, 1:30 pm
N Opening: Lion Building
Universitätsplatz 11, Halle (Saale)
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Conference Site: Steintor-Campus
Adam-Kuckhoff-Straße 35, 06120 Halle (Saale)
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Modulating Ageing /
Anti-Ageing:
from Molecular Biology
to Clinical Perspectives

st rd
September 01 – 03 2017

Heart Centre
University Hospital Halle (Saale)

in cooperation with

German National Academy of Sciences Leopoldina

German Society of Gerontology and Geriatrics
(DGGG)

Interdisciplinary Centre on Ageing Halle
(IZAH)

RTG 2155: ProMoAge
Index

Page

4 Running Program

5 Abstracts Speakers

8 Aging and diseases: common mechanisms but different rates
Claudio Franceschi

10 Defining the target group: risk prediction of ageing trajectories
Andrea Maier

12 Do biomarkers of ageing reflect real age?
Andreas Simm

14 Challenges understanding aging through biomarkers across
populations: the example of calcium
Tamàs Fülöp

16 Motor and cognitive intervention to improve functional mobility and
reduce falls in older adults and patients with neurodegeneration
Anat Mirelman

18 Age-dependent posttranslational protein modification – driving
force in neurodegeneration?
Hans-Ulrich Demuth

20 Protein oxidation and aggregation in aging and senescence
Tilman Grune

22 Proteasome modulation as an anti-aging and antiaggregation
strategy
Niki Chondrogianni

24 Glycated proteins in nutrition: friend or foe
Katarina Sebekova

26 Cardiac ageing enhances atrial fibrillation or vice versa? – Impact of
altered miRNA expressional profile and metabolic signalling for
treatment and persistence of atrial fibrillation?
Bernd Niemann

28 Protective effects of caffeine in the cardiovascular system depend
on mitochondrial p27 – in aging and disease
Judith Haendeler

30 Oral anticoagulation and polypharmacy in older adults with atrial
fibrillation
Markus Gosch

32 Gender related aspects of the cardiovascular system and its impact
on progression and aging
Sandra Eifert
34 Historical overview of research on lifespan extension and its ethical
implications
Georg M. Martin

36 Rejuvenation biotechnology: why age may soon no longer mean
aging
Aubrey de Grey

38 The shape of lives to come
Ian Richard Ground

40 Ethical aspects of biogerontological research
Zoé Rheinsberg

42 Epigenetic stress response and stem cell aging
Lenhard Rudolph

44 Understanding muscle stem cell regenerative decline with aging
Pura Munoz-Cánove

46 Bioengineered matrices to regenerate the heart – The Zurich
LifeMatrix programm
Maximilian Emmert

48 Mesenchymal stem cells-on-chips/organ-on-chips/chips in
mesenchymal organs – monitoring healing kinetics: an ageing
perspective
Günter Lepperdinger

50 Effects of pharmacological inhibition of aging-associated pathways
on Drosophila lifespan
Alexey Moskalev

52 The Path towards translating senolytic drugs and other
interventions targeting aging processes into clinical treatments
James Kirkland

54 Cellular senescence and aging
Judith Campisi

56 DNA damage: impact on aging, neurodegeneration and the effect of
nutritional interventions
Jan Hoeijmakers

58 Posters ( in alphabetical order)

114 List of speakers

118 Organizers

119 Involved Societies

120 Authors Index

125 List of Sponsors

126 Map of Halle (Saale)

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R u n n i n g P r o g r a m

Modulating Ageing / Antiageing:
From Molecular Biology to Clinical Perspectives

- Meeting language English -

Friday September 01st 2017

18:00 Opening

Andreas Simm

Address
M. Gekle, Dean of the Medical Faculty,
Martin-Luther-University Halle-Wittenberg
T. Klöss, Medical Director of the University Hospital Halle (Saale)
H. Treede, Heart Centre of the University Hospital

Keynote lecture and Schober award

Laudation Claudio Franceschi

by Judith Campisi, Novato, USA

Keynote lecture:

Claudio Franceschi
University of Bologna, Bologna, I

“Aging and diseases: common mechanisms but different rates”

20:00 Come Together (Löwengebäude – Lion Building)
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Saturday September 02nd 2017

08:00 – 10:00 Session 1

Setting up the problem, predictors and markers

Chair: Claudio Franceschi, Andreas Simm

Defining the target group: risk prediction of ageing Andrea Maier
trajectories

Do biomarkers of ageing reflect real age? Andreas Simm

Challenges understanding aging through biomarkers Tamás Fülöp
across populations: the example of calcium

Motor-Cognitive Interventions to reduce the risk of falls Anat Mirelman
in older adults and neurodegenerative conditions

10:00 – 10:30 Coffee Break

10:30 – 12:30 Session 2

Protein damage and Aggregation

Chair: Günter Lepperdinger, Lenhard Rudolph

Age-dependent posttranslational protein modification – Hans-Ulrich Demuth
driving force in neurodegeneration?
Protein Oxidation and Aggregation in Aging and Tilman Grune
Senescence

Proteasome modulation as an anti-aging and anti- Niki Chondrogianni
aggregation strategy

Glycated proteins in nutrition: friend or foe Katarina Sebekova

12:30 – 13:30 Lunch Break

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Saturday September 02nd 2017

13:30 – 15:30 Session 3

Cardiovascular System

Chair: Tamàs Fülöp, Maximilian Emmert

Cardiac ageing enhances atrial fibrillation or vice versa? – Bernd Niemann
Impact of altered miRNA expressional profile and
metabolic signalling for treatment and persistence of atrial
fibrillation?

Protective effects of caffeine in the cardiovascular system Judith Haendeler
depend on mitochondrial p27 - in aging and disease

Oral anticoagulation and polypharmacy in older adults Markus Gosch
with atrial fibrillation

Gender related aspects of the cardiovascular system and Sandra Eifert
its impact on progression and aging

15:30 – 16:30 Poster Session / Coffee Break

16:30 – 18:30 Session 4

Panel discussion on ethical issues

Chair: Jutta Schnitzer-Ungefug

Historical overview of research on lifespan extension George M. Martin
and its ethical implications

Rejuvenation biotechnology: Aubrey de Grey
why age may soon no longer mean aging

The shape of lives to come Ian Richard Ground

Ethical aspects of biogerontological research Zoé Rheinsberg

20:00 Conference-Dinner (Halloren- und Salinemuseum)

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Sunday September 03rd 2017

08:30 – 10:30 Session 5

Stem Cells and Regeneration

Chair: Judith Campisi, Judith Haendeler

Epigenetic stress response and stem cell aging Lenhard Rudolph

Understanding muscle stem cell regenerative decline Pura Munoz-Cánove
with aging

Bioengineered matrices to regenerate the heart – Maximilian Emmert
The Zurich LifeMatrix programm

Mesenchymal stem cells-on-chips/organ-on-chips/chips Günter Lepperdinger
in mesenchymal organs – Monitoring healing kinetics:
an ageing perspective

10:30 – 11:30 Poster Session / Coffee Break

11:30 – 11:45 Posterprice

11:45 – 13:45 Session 6

Anti-Aging Therapies

Chair: Andrea Maier, George M. Martin

Effects of pharmacological inhibition of aging-associated Alexey Moskalev
pathways on Drosophila lifespan

The path towards translating senolytic drugs and other James Kirkland
interventions targeting aging processes into clinical
treatments

Cellular senescence and aging Judith Campisi

DNA damage: impact on aging, neurodegeneration and Jan Hoeijmakers
the effect of nutritional interventions

13:45 – 14:15 Farewell
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Aging and diseases: common mechanisms but different rates

Claudio Franceschi

The new GEROSCIENCE is based on the strong epidemiological evidence that aging is the
major risk factor for age-related diseases, and assumes that they share a common set of basic
mechanisms. This assumption is supported by a large panoply of experimental data and its
major consequence is that the primary target of Medicine is to combat aging instead of any
single age-related disease one by one, as favored by the present fragmentation into hundreds
of specialties and sub-specialties. If the same molecular and cellular mechanisms underpin both
aging and age-related diseases, a major question emerges: which is the difference between
aging and diseases? This is an old question that was addressed starting from Terentius and
Cicero who argued pros and cons, respectively, whether “senectus ipsa est morbus”, and
recently this topic was addressed by several scholars. On the basis of a variety of recent
experimental data and of the conceptualizations I proposed in the last years (the “remodeling”
theory of aging; inflammaging and garbaging; liquid immune self and immunobiography) I will
illustrate the hypothesis that age-related diseases - including the not so well-defined geriatric
syndromes and conditions such as frailty, metabolic syndrome and mild cognitive impairment -
can be conceptualized as ACCELERATED aging. Within such a perspective centenarians
represent one extreme (healthy aging/extreme longevity) characterized by DECELERATED
aging. At the other extreme there are patients who suffered one or more severe age-related
pathologies in their sixties, seventies and eighties, and died 20-40 years before people of the
same cohort who reached 100 years or more. These patients can be considered as affected by
ACCELERATED aging. In between these two extremes there is a bunch of intermediate
trajectories representing a sort of grey area. Thus, clinically different, classically-defined age-
related diseases such as diabetes, cardiovascular diseases, cancer, dementia, among others,
are indeed the result of a peculiar combination of alterations regarding the same, above-
mentioned shared, limited set of basic mechanisms. Thus, as anticipated by Lazlo Barabasi
some years ago with the conceptualization of “diseasome”, apparently/clinically different
diseases share common mechanisms and genes. According to this integrated view the question
whether aging is a disease in itself becomes meaningless because aging and age-related
diseases are part of a continuum where precise boundaries do not exist. Whether an individual
will follow a trajectory of accelerated or decelerated aging will depend on his/her genetic
background (population genetics) which will interact lifelong with environmental and lifestyle
factors, in a rapidly changing world. Within this scenario it is easy to understand how important
and critical is the search for biomarkers capable of distinguishing between chronological and
biological age and predict/anticipate the rate/trajectory of aging.
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