TY  - JOUR
AU  - Mladenović, Aleksandra
AU  - Kapetanou, Marianna
AU  - Lončarević Vasiljković, Nataša
AU  - Todorović, Smilja
AU  - Athanasopoulou, Sofia
AU  - Jović, Milena
AU  - Prvulović, Milica
AU  - Taoufik, Era
AU  - Matsas, Rebecca
AU  - Kanazir, Selma
AU  - Gonos, Efstathios S.
PY  - 2021
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4074
AB  - Alzheimer's disease (AD) is the most common form of dementia worldwide, characterized by a progressive decline in a variety of cognitive and non-cognitive functions. The amyloid beta protein cascade hypothesis places the formation of amyloid beta protein aggregates on the first position in the complex pathological cascade leading to neurodegeneration, and therefore AD might be considered to be a protein-misfolding disease. The Ubiquitin Proteasome System (UPS), being the primary protein degradation mechanism with a fundamental role in the maintenance of proteostasis, has been identified as a putative therapeutic target to delay and/or to decelerate the progression of neurodegenerative disorders that are characterized by accumulated/aggregated proteins. The purpose of this study was to test if the activation of proteasome in vivo can alleviate AD pathology. Specifically by using two compounds with complementary modes of proteasome activation and documented antioxidant and redox regulating properties in the 5xFAD transgenic mice model of AD, we ameliorated a number of AD related deficits. Shortly after proteasome activation we detected significantly reduced amyloid-beta load correlated with improved motor functions, reduced anxiety and frailty level. Essentially, to our knowledge this is the first report to demonstrate a dual activation of the proteasome and its downstream effects. In conclusion, these findings open up new directions for future therapeutic potential of proteasome-mediated proteolysis enhancement.
PB  - Elsevier Inc.
T2  - Free Radical Biology and Medicine
T1  - Pharmacological intervention in a transgenic mouse model improves Alzheimer's-associated pathological phenotype: Involvement of proteasome activation
VL  - 162
DO  - 10.1016/j.freeradbiomed.2020.11.038
SP  - 88
EP  - 103
ER  - 

@article{
author = "Mladenović, Aleksandra and Kapetanou, Marianna and Lončarević Vasiljković, Nataša and Todorović, Smilja and Athanasopoulou, Sofia and Jović, Milena and Prvulović, Milica and Taoufik, Era and Matsas, Rebecca and Kanazir, Selma and Gonos, Efstathios S.",
year = "2021",
abstract = "Alzheimer's disease (AD) is the most common form of dementia worldwide, characterized by a progressive decline in a variety of cognitive and non-cognitive functions. The amyloid beta protein cascade hypothesis places the formation of amyloid beta protein aggregates on the first position in the complex pathological cascade leading to neurodegeneration, and therefore AD might be considered to be a protein-misfolding disease. The Ubiquitin Proteasome System (UPS), being the primary protein degradation mechanism with a fundamental role in the maintenance of proteostasis, has been identified as a putative therapeutic target to delay and/or to decelerate the progression of neurodegenerative disorders that are characterized by accumulated/aggregated proteins. The purpose of this study was to test if the activation of proteasome in vivo can alleviate AD pathology. Specifically by using two compounds with complementary modes of proteasome activation and documented antioxidant and redox regulating properties in the 5xFAD transgenic mice model of AD, we ameliorated a number of AD related deficits. Shortly after proteasome activation we detected significantly reduced amyloid-beta load correlated with improved motor functions, reduced anxiety and frailty level. Essentially, to our knowledge this is the first report to demonstrate a dual activation of the proteasome and its downstream effects. In conclusion, these findings open up new directions for future therapeutic potential of proteasome-mediated proteolysis enhancement.",
publisher = "Elsevier Inc.",
journal = "Free Radical Biology and Medicine",
title = "Pharmacological intervention in a transgenic mouse model improves Alzheimer's-associated pathological phenotype: Involvement of proteasome activation",
volume = "162",
doi = "10.1016/j.freeradbiomed.2020.11.038",
pages = "88-103"
}

Mladenović, A., Kapetanou, M., Lončarević Vasiljković, N., Todorović, S., Athanasopoulou, S., Jović, M., Prvulović, M., Taoufik, E., Matsas, R., Kanazir, S.,& Gonos, E. S.. (2021). Pharmacological intervention in a transgenic mouse model improves Alzheimer's-associated pathological phenotype: Involvement of proteasome activation. in Free Radical Biology and Medicine
Elsevier Inc.., 162, 88-103.
https://doi.org/10.1016/j.freeradbiomed.2020.11.038

Mladenović A, Kapetanou M, Lončarević Vasiljković N, Todorović S, Athanasopoulou S, Jović M, Prvulović M, Taoufik E, Matsas R, Kanazir S, Gonos ES. Pharmacological intervention in a transgenic mouse model improves Alzheimer's-associated pathological phenotype: Involvement of proteasome activation. in Free Radical Biology and Medicine. 2021;162:88-103.
doi:10.1016/j.freeradbiomed.2020.11.038 .

Mladenović, Aleksandra, Kapetanou, Marianna, Lončarević Vasiljković, Nataša, Todorović, Smilja, Athanasopoulou, Sofia, Jović, Milena, Prvulović, Milica, Taoufik, Era, Matsas, Rebecca, Kanazir, Selma, Gonos, Efstathios S., "Pharmacological intervention in a transgenic mouse model improves Alzheimer's-associated pathological phenotype: Involvement of proteasome activation" in Free Radical Biology and Medicine, 162 (2021):88-103,
https://doi.org/10.1016/j.freeradbiomed.2020.11.038 . .

TY  - JOUR
AU  - Mladenović, Aleksandra
AU  - Lončarević Vasiljković, Nataša
AU  - Gonos, Efstathios S.
PY  - 2021
UR  - https://pubmed.ncbi.nlm.nih.gov/32242468/
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4208
AB  - Significance: It is well established that lifestyle and dietary habits have a tremendous impact on life span, the rate of aging, and the onset/progression of age-related diseases. Specifically, dietary restriction (DR) and other healthy dietary patterns are usually accompanied by physical activity and differ from Western diet that is rich in fat and sugars. Moreover, as the generation of reactive oxidative species is the major causative factor of aging, while DR could modify the level of oxidative stress, it has been proposed that DR increases both survival and longevity. Recent Advances: Despite the documented links between DR, aging, and oxidative stress, many issues remain to be addressed. For instance, the free radical theory of aging is under "re-evaluation,"while DR as a golden standard for prolonging life span and ameliorating the effects of aging is also under debate. Critical Issues: This review article pays special attention to highlight the link between DR and oxidative stress in both aging and age-related diseases. We discuss in particular DR's capability to counteract the consequences of oxidative stress and the molecular mechanisms involved in these processes. Future Directions: Although DR is undoubtedly beneficial, several considerations must be taken into account when designing the best dietary intervention. Use of intermittent fasting, daily food reduction, or DR mimetics? Future research should unravel the pros and cons of all these processes. Antioxid. Redox Signal. 34, 421-438.
PB  - Mary Ann Liebert Inc.
T2  - Antioxidants and Redox Signaling
T1  - Dietary Restriction and Oxidative Stress: Friends or Enemies?
IS  - 5
VL  - 34
DO  - 10.1089/ars.2019.7959
SP  - 421
EP  - 438
ER  - 

@article{
author = "Mladenović, Aleksandra and Lončarević Vasiljković, Nataša and Gonos, Efstathios S.",
year = "2021",
abstract = "Significance: It is well established that lifestyle and dietary habits have a tremendous impact on life span, the rate of aging, and the onset/progression of age-related diseases. Specifically, dietary restriction (DR) and other healthy dietary patterns are usually accompanied by physical activity and differ from Western diet that is rich in fat and sugars. Moreover, as the generation of reactive oxidative species is the major causative factor of aging, while DR could modify the level of oxidative stress, it has been proposed that DR increases both survival and longevity. Recent Advances: Despite the documented links between DR, aging, and oxidative stress, many issues remain to be addressed. For instance, the free radical theory of aging is under "re-evaluation,"while DR as a golden standard for prolonging life span and ameliorating the effects of aging is also under debate. Critical Issues: This review article pays special attention to highlight the link between DR and oxidative stress in both aging and age-related diseases. We discuss in particular DR's capability to counteract the consequences of oxidative stress and the molecular mechanisms involved in these processes. Future Directions: Although DR is undoubtedly beneficial, several considerations must be taken into account when designing the best dietary intervention. Use of intermittent fasting, daily food reduction, or DR mimetics? Future research should unravel the pros and cons of all these processes. Antioxid. Redox Signal. 34, 421-438.",
publisher = "Mary Ann Liebert Inc.",
journal = "Antioxidants and Redox Signaling",
title = "Dietary Restriction and Oxidative Stress: Friends or Enemies?",
number = "5",
volume = "34",
doi = "10.1089/ars.2019.7959",
pages = "421-438"
}

Mladenović, A., Lončarević Vasiljković, N.,& Gonos, E. S.. (2021). Dietary Restriction and Oxidative Stress: Friends or Enemies?. in Antioxidants and Redox Signaling
Mary Ann Liebert Inc.., 34(5), 421-438.
https://doi.org/10.1089/ars.2019.7959

Mladenović A, Lončarević Vasiljković N, Gonos ES. Dietary Restriction and Oxidative Stress: Friends or Enemies?. in Antioxidants and Redox Signaling. 2021;34(5):421-438.
doi:10.1089/ars.2019.7959 .

Mladenović, Aleksandra, Lončarević Vasiljković, Nataša, Gonos, Efstathios S., "Dietary Restriction and Oxidative Stress: Friends or Enemies?" in Antioxidants and Redox Signaling, 34, no. 5 (2021):421-438,
https://doi.org/10.1089/ars.2019.7959 . .

TY  - JOUR
AU  - Xie, Kan
AU  - Kapetanou, Marianna
AU  - Sidiropoulou, Kyriaki
AU  - Bano, Daniele
AU  - Gonos, Efstathios S.
AU  - Mladenović, Aleksandra
AU  - Ehninger, Dan
PY  - 2020
UR  - https://radar.ibiss.bg.ac.rs/123456789/3912
AB  - Several laboratory animal models have shown that dietary energy restriction (ER) can promote longevity and improve various health aspects in old age. However, whether the entire spectrum of ER-induced short- and long-term physiological and metabolic adaptions is translatable to humans remains to be determined. In this review article, we present recent evidence towards the elucidation of the impact of ER on brain physiology and in age-related neurodegenerative diseases. We also discuss modulatory influences of ER on metabolism and overall on human health, limitations of current experimental designs as well as future perspectives for ER trials in humans. Finally, we summarize signaling pathways and processes known to be affected by both aging and ER with a special emphasis on the link between ER and cellular proteostasis.
PB  - Elsevier B.V.
T2  - Mechanisms of Ageing and Development
T1  - Signaling pathways of dietary energy restriction and metabolism on brain physiology and in age-related neurodegenerative diseases
VL  - 192
DO  - 10.1016/j.mad.2020.111364
SP  - 111364
ER  - 

@article{
author = "Xie, Kan and Kapetanou, Marianna and Sidiropoulou, Kyriaki and Bano, Daniele and Gonos, Efstathios S. and Mladenović, Aleksandra and Ehninger, Dan",
year = "2020",
abstract = "Several laboratory animal models have shown that dietary energy restriction (ER) can promote longevity and improve various health aspects in old age. However, whether the entire spectrum of ER-induced short- and long-term physiological and metabolic adaptions is translatable to humans remains to be determined. In this review article, we present recent evidence towards the elucidation of the impact of ER on brain physiology and in age-related neurodegenerative diseases. We also discuss modulatory influences of ER on metabolism and overall on human health, limitations of current experimental designs as well as future perspectives for ER trials in humans. Finally, we summarize signaling pathways and processes known to be affected by both aging and ER with a special emphasis on the link between ER and cellular proteostasis.",
publisher = "Elsevier B.V.",
journal = "Mechanisms of Ageing and Development",
title = "Signaling pathways of dietary energy restriction and metabolism on brain physiology and in age-related neurodegenerative diseases",
volume = "192",
doi = "10.1016/j.mad.2020.111364",
pages = "111364"
}

Xie, K., Kapetanou, M., Sidiropoulou, K., Bano, D., Gonos, E. S., Mladenović, A.,& Ehninger, D.. (2020). Signaling pathways of dietary energy restriction and metabolism on brain physiology and in age-related neurodegenerative diseases. in Mechanisms of Ageing and Development
Elsevier B.V.., 192, 111364.
https://doi.org/10.1016/j.mad.2020.111364

Xie K, Kapetanou M, Sidiropoulou K, Bano D, Gonos ES, Mladenović A, Ehninger D. Signaling pathways of dietary energy restriction and metabolism on brain physiology and in age-related neurodegenerative diseases. in Mechanisms of Ageing and Development. 2020;192:111364.
doi:10.1016/j.mad.2020.111364 .

Xie, Kan, Kapetanou, Marianna, Sidiropoulou, Kyriaki, Bano, Daniele, Gonos, Efstathios S., Mladenović, Aleksandra, Ehninger, Dan, "Signaling pathways of dietary energy restriction and metabolism on brain physiology and in age-related neurodegenerative diseases" in Mechanisms of Ageing and Development, 192 (2020):111364,
https://doi.org/10.1016/j.mad.2020.111364 . .

TY  - JOUR
AU  - Gonos, Efstathios S.
AU  - Chondrogianni, Niki
AU  - Mladenović, Aleksandra
PY  - 2019
UR  - https://www.sciencedirect.com/science/article/pii/S0047637418302562?via%3Dihub
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3228
T2  - Mechanisms of Ageing and Development
T1  - Where ageing goes nowadays: Mechanisms, pathways, biomarkers and anti-ageing strategies
VL  - 177
DO  - 10.1016/j.mad.2018.12.002
SP  - 1
EP  - 3
ER  - 

@article{
author = "Gonos, Efstathios S. and Chondrogianni, Niki and Mladenović, Aleksandra",
year = "2019",
journal = "Mechanisms of Ageing and Development",
title = "Where ageing goes nowadays: Mechanisms, pathways, biomarkers and anti-ageing strategies",
volume = "177",
doi = "10.1016/j.mad.2018.12.002",
pages = "1-3"
}

Gonos, E. S., Chondrogianni, N.,& Mladenović, A.. (2019). Where ageing goes nowadays: Mechanisms, pathways, biomarkers and anti-ageing strategies. in Mechanisms of Ageing and Development, 177, 1-3.
https://doi.org/10.1016/j.mad.2018.12.002

Gonos ES, Chondrogianni N, Mladenović A. Where ageing goes nowadays: Mechanisms, pathways, biomarkers and anti-ageing strategies. in Mechanisms of Ageing and Development. 2019;177:1-3.
doi:10.1016/j.mad.2018.12.002 .

Gonos, Efstathios S., Chondrogianni, Niki, Mladenović, Aleksandra, "Where ageing goes nowadays: Mechanisms, pathways, biomarkers and anti-ageing strategies" in Mechanisms of Ageing and Development, 177 (2019):1-3,
https://doi.org/10.1016/j.mad.2018.12.002 . .

TY  - JOUR
AU  - Gonos, Efstathios S.
AU  - Chondrogianni, Niki
AU  - Mladenović, Aleksandra
PY  - 2019
UR  - https://www.sciencedirect.com/science/article/pii/S0047637418302562?via%3Dihub
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3235
T2  - Mechanisms of Ageing and Development
T1  - Where ageing goes nowadays: Mechanisms, pathways, biomarkers and anti-ageing strategies.
VL  - 177
DO  - 10.1016/j.mad.2018.12.002
SP  - 1
EP  - 3
ER  - 

@article{
author = "Gonos, Efstathios S. and Chondrogianni, Niki and Mladenović, Aleksandra",
year = "2019",
journal = "Mechanisms of Ageing and Development",
title = "Where ageing goes nowadays: Mechanisms, pathways, biomarkers and anti-ageing strategies.",
volume = "177",
doi = "10.1016/j.mad.2018.12.002",
pages = "1-3"
}

Gonos, E. S., Chondrogianni, N.,& Mladenović, A.. (2019). Where ageing goes nowadays: Mechanisms, pathways, biomarkers and anti-ageing strategies.. in Mechanisms of Ageing and Development, 177, 1-3.
https://doi.org/10.1016/j.mad.2018.12.002

Gonos ES, Chondrogianni N, Mladenović A. Where ageing goes nowadays: Mechanisms, pathways, biomarkers and anti-ageing strategies.. in Mechanisms of Ageing and Development. 2019;177:1-3.
doi:10.1016/j.mad.2018.12.002 .

Gonos, Efstathios S., Chondrogianni, Niki, Mladenović, Aleksandra, "Where ageing goes nowadays: Mechanisms, pathways, biomarkers and anti-ageing strategies." in Mechanisms of Ageing and Development, 177 (2019):1-3,
https://doi.org/10.1016/j.mad.2018.12.002 . .

TY  - CONF
AU  - Mladenović, Aleksandra
AU  - Jović, Milena
AU  - Lončarević-Vasiljković, Nataša
AU  - Athanasopoulou, Sofia
AU  - Gonos, Efstathios S
AU  - Kanazir, Selma
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5809
AB  - Introduction. Aging represents the most important risk factor for Alzheimer’s
disease (AD), the most common neurodegenerative disorders worldwide. One of 
the hallmarks of AD is the accumulation of plaques composed of aggregated 
amyloid-β peptides (Aβ) which are formed by sequential proteolytic processing 
of the amyloid-precursor protein (APP).It is well known that different factors 
can influence amyloidogenic pathway and/or clearance of already formed Aβ. 
Growing evidence suggest that ubiquitin proteasomal system represents an 
important factor in AD development and a potential target for the management 
of disease. Recently it has been shown that several natural compounds, 
including 18α-glycyrrhetinic acid (18α-GA) protects from protein aggregation related pathology in AD model system. Methods. In order to investigate the 
protective effect of 18α-GA, we used 5xFAD transgenic mouse AD model, 
characterized by early amyloid deposition and intra-neuronal Aβ42 aggregation. 
Both female and male mice were exposed to 18α-GA treatment for one month, 
started at 2-months of age. This is considered as an early phase of AD pathology, 
known to be suitable for therapeutics application. In the cortex and 
hippocampus CT-L, T-L, and PGPH proteasome activities were assayed by 
hydrolysis of Suc-LLVY-AMC, Boc-LRR-AMC, and Z-LLE-AMC fluorogenic 
peptides. The number and size of amyloid plaques were determined in these 
structures. Results. This study revealed that 18α-GA treatment influence 
neuritic dystrophy, increase proteasome activity, decrease Aβ content and 
number of amyloid plaques in 5xFAD mice. Conclusion. These preliminary 
intriguing data open up new directions using natural compounds for the most 
efficient treatment of neurodegenerative disorders.
PB  - Belgrade: Serbian Neuroscience Society
C3  - Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia
T1  - Proteasome activation plays role in 18α-glycyrrhetinic acid protectiveeffect in 5XFAD animal model of Alzheimer’s disease
SP  - 109
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5809
ER  - 

@conference{
author = "Mladenović, Aleksandra and Jović, Milena and Lončarević-Vasiljković, Nataša and Athanasopoulou, Sofia and Gonos, Efstathios S and Kanazir, Selma",
year = "2017",
abstract = "Introduction. Aging represents the most important risk factor for Alzheimer’s
disease (AD), the most common neurodegenerative disorders worldwide. One of 
the hallmarks of AD is the accumulation of plaques composed of aggregated 
amyloid-β peptides (Aβ) which are formed by sequential proteolytic processing 
of the amyloid-precursor protein (APP).It is well known that different factors 
can influence amyloidogenic pathway and/or clearance of already formed Aβ. 
Growing evidence suggest that ubiquitin proteasomal system represents an 
important factor in AD development and a potential target for the management 
of disease. Recently it has been shown that several natural compounds, 
including 18α-glycyrrhetinic acid (18α-GA) protects from protein aggregation related pathology in AD model system. Methods. In order to investigate the 
protective effect of 18α-GA, we used 5xFAD transgenic mouse AD model, 
characterized by early amyloid deposition and intra-neuronal Aβ42 aggregation. 
Both female and male mice were exposed to 18α-GA treatment for one month, 
started at 2-months of age. This is considered as an early phase of AD pathology, 
known to be suitable for therapeutics application. In the cortex and 
hippocampus CT-L, T-L, and PGPH proteasome activities were assayed by 
hydrolysis of Suc-LLVY-AMC, Boc-LRR-AMC, and Z-LLE-AMC fluorogenic 
peptides. The number and size of amyloid plaques were determined in these 
structures. Results. This study revealed that 18α-GA treatment influence 
neuritic dystrophy, increase proteasome activity, decrease Aβ content and 
number of amyloid plaques in 5xFAD mice. Conclusion. These preliminary 
intriguing data open up new directions using natural compounds for the most 
efficient treatment of neurodegenerative disorders.",
publisher = "Belgrade: Serbian Neuroscience Society",
journal = "Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia",
title = "Proteasome activation plays role in 18α-glycyrrhetinic acid protectiveeffect in 5XFAD animal model of Alzheimer’s disease",
pages = "109",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5809"
}

Mladenović, A., Jović, M., Lončarević-Vasiljković, N., Athanasopoulou, S., Gonos, E. S.,& Kanazir, S.. (2017). Proteasome activation plays role in 18α-glycyrrhetinic acid protectiveeffect in 5XFAD animal model of Alzheimer’s disease. in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia
Belgrade: Serbian Neuroscience Society., 109.
https://hdl.handle.net/21.15107/rcub_ibiss_5809

Mladenović A, Jović M, Lončarević-Vasiljković N, Athanasopoulou S, Gonos ES, Kanazir S. Proteasome activation plays role in 18α-glycyrrhetinic acid protectiveeffect in 5XFAD animal model of Alzheimer’s disease. in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia. 2017;:109.
https://hdl.handle.net/21.15107/rcub_ibiss_5809 .

Mladenović, Aleksandra, Jović, Milena, Lončarević-Vasiljković, Nataša, Athanasopoulou, Sofia, Gonos, Efstathios S, Kanazir, Selma, "Proteasome activation plays role in 18α-glycyrrhetinic acid protectiveeffect in 5XFAD animal model of Alzheimer’s disease" in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia (2017):109,
https://hdl.handle.net/21.15107/rcub_ibiss_5809 .

TY  - JOUR
AU  - Figueira, Inês
AU  - Fernandes, Adelaide
AU  - Mladenović, Aleksandra
AU  - Lopez-Contreras, Andres
AU  - Henriques, Catarina M.
AU  - Selman, Colin
AU  - Ferreiro, Elisabete
AU  - Gonos, Efstathios S.
AU  - Trejo, José Luis
AU  - Misra, Juhi
AU  - Rasmussen, Lene Juel
AU  - Xapelli, Sara
AU  - Ellam, Timothy
AU  - Bellantuono, Ilaria
PY  - 2016
UR  - http://linkinghub.elsevier.com/retrieve/pii/S0047637416301816
UR  - https://www.scopus.com/record/display.uri?eid=2-s2.0-84999035290&origin=SingleRecordEmailAlert&dgcid=scalert_sc_search_email&txGid=BC81928C1802E221B1A9A8D8F9963BDB.wsnAw8kcdt7IPYLO0V48gA%3A1#
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2479
AB  - Over 60% of people aged over 65 are affected by multiple morbidities, which are more difficult to treat, generate increased healthcare costs and lead to poor quality of life compared to individual diseases. With the number of older people steadily increasing this presents a societal challenge. Age is the major risk factor for age-related diseases and recent research developments have led to the proposal that pharmacological interventions targeting common mechanisms of ageing may be able to delay the onset of multimorbidity. Here we review the state of the knowledge of multimorbidity, appraise the available evidence supporting the role of mechanisms of ageing in the development of the most common age-related diseases and assess potential molecules that may successfully target those key mechanisms.
T2  - Mechanisms of Ageing and Development
T1  - Interventions for age-related diseases: Shifting the paradigm
VL  - 160
DO  - 10.1016/j.mad.2016.09.009
SP  - 69
EP  - 92
ER  - 

@article{
author = "Figueira, Inês and Fernandes, Adelaide and Mladenović, Aleksandra and Lopez-Contreras, Andres and Henriques, Catarina M. and Selman, Colin and Ferreiro, Elisabete and Gonos, Efstathios S. and Trejo, José Luis and Misra, Juhi and Rasmussen, Lene Juel and Xapelli, Sara and Ellam, Timothy and Bellantuono, Ilaria",
year = "2016",
abstract = "Over 60% of people aged over 65 are affected by multiple morbidities, which are more difficult to treat, generate increased healthcare costs and lead to poor quality of life compared to individual diseases. With the number of older people steadily increasing this presents a societal challenge. Age is the major risk factor for age-related diseases and recent research developments have led to the proposal that pharmacological interventions targeting common mechanisms of ageing may be able to delay the onset of multimorbidity. Here we review the state of the knowledge of multimorbidity, appraise the available evidence supporting the role of mechanisms of ageing in the development of the most common age-related diseases and assess potential molecules that may successfully target those key mechanisms.",
journal = "Mechanisms of Ageing and Development",
title = "Interventions for age-related diseases: Shifting the paradigm",
volume = "160",
doi = "10.1016/j.mad.2016.09.009",
pages = "69-92"
}

Figueira, I., Fernandes, A., Mladenović, A., Lopez-Contreras, A., Henriques, C. M., Selman, C., Ferreiro, E., Gonos, E. S., Trejo, J. L., Misra, J., Rasmussen, L. J., Xapelli, S., Ellam, T.,& Bellantuono, I.. (2016). Interventions for age-related diseases: Shifting the paradigm. in Mechanisms of Ageing and Development, 160, 69-92.
https://doi.org/10.1016/j.mad.2016.09.009

Figueira I, Fernandes A, Mladenović A, Lopez-Contreras A, Henriques CM, Selman C, Ferreiro E, Gonos ES, Trejo JL, Misra J, Rasmussen LJ, Xapelli S, Ellam T, Bellantuono I. Interventions for age-related diseases: Shifting the paradigm. in Mechanisms of Ageing and Development. 2016;160:69-92.
doi:10.1016/j.mad.2016.09.009 .

Figueira, Inês, Fernandes, Adelaide, Mladenović, Aleksandra, Lopez-Contreras, Andres, Henriques, Catarina M., Selman, Colin, Ferreiro, Elisabete, Gonos, Efstathios S., Trejo, José Luis, Misra, Juhi, Rasmussen, Lene Juel, Xapelli, Sara, Ellam, Timothy, Bellantuono, Ilaria, "Interventions for age-related diseases: Shifting the paradigm" in Mechanisms of Ageing and Development, 160 (2016):69-92,
https://doi.org/10.1016/j.mad.2016.09.009 . .