LIVIVO - Search results -

Search results

Result 1 - 10 of total 112

Search options

Article ; Online: Ageing-associated phenotypes in mice.

Xie, Kan / Ehninger, Dan

2023 Volume 214, Page(s) 111852

Abstract: Ageing is a continuous process in life featuring progressive damage accumulation that leads to physiological decline, functional deterioration and ultimately death of an organism. Based on the relatively close anatomical and physiological similarity to ... ...

Abstract	Ageing is a continuous process in life featuring progressive damage accumulation that leads to physiological decline, functional deterioration and ultimately death of an organism. Based on the relatively close anatomical and physiological similarity to humans, the mouse has been proven as a valuable model organism in ageing research over the last decades. In this review, we survey methods and tools currently in use to assess ageing phenotypes in mice. We summarize a range of ageing-associated alterations detectable at two major levels of analysis: (1) physiology and pathophysiology and (2) molecular biomarkers. Age-sensitive phenotypes provided in this article may serve to inform future studies targeting various aspects of organismal ageing in mice. In addition, we discuss conceptual and technical challenges faced by previous ageing studies in mice and, where possible, provide recommendations on how to resolve some of these issues.
MeSH term(s)	Humans ; Mice ; Animals ; Aging/physiology ; Biomarkers ; Phenotype
Chemical Substances	Biomarkers
Language	English
Publishing date	2023-07-14
Publishing country	Ireland
Document type	Review ; Journal Article
ZDB-ID	183915-9
ISSN	1872-6216 ; 0047-6374
ISSN (online)	1872-6216
ISSN	0047-6374
DOI	10.1016/j.mad.2023.111852
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1012: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article: Decoding metabolic signatures in Alzheimer's disease: a mitochondrial perspective.

Bano, Daniele / Ehninger, Dan / Bagetta, Giacinto

Cell death discovery

2023 Volume 9, Issue 1, Page(s) 432

Abstract: Alzheimer's disease (AD) is one of the most prevalent age-related neurodegenerative diseases and accounts for the majority of dementia cases worldwide. Tremendous ongoing efforts of basic and clinical research have expanded our knowledge on AD and its ... ...

Abstract	Alzheimer's disease (AD) is one of the most prevalent age-related neurodegenerative diseases and accounts for the majority of dementia cases worldwide. Tremendous ongoing efforts of basic and clinical research have expanded our knowledge on AD and its complex multifactorial pathogenesis. For sporadic AD, it is widely assumed that silent and early symptomatic stages initiate decades before the irreversible decline in cognitive abilities that ultimately lead to debilitating conditions. In addition to amyloid plaques and tau-containing neurofibrillary tangles as the most prominent hallmarks of AD lesions within the affected brain areas, we now possess a broader collection of pathological signatures that are associated with AD development and progression. In this regard, there is a substantial body of evidence suggesting that hypometabolism occurs in the brains of individuals at the prodromal stage before dementia is diagnosed, which may reflect an early role of metabolic dysfunction in AD. This perspective surveys the vast literature and critically assesses the current evidence demonstrating a mitochondrial contribution to AD. Additionally, we discuss our interpretations of the reported mitochondrial signatures and consider how altered mitochondrial bioenergetics may be an additional risk factor for AD pathogenesis.
Language	English
Publishing date	2023-12-01
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-023-01732-3
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Aging - What it is and how to measure it.

Keshavarz, Maryam / Xie, Kan / Bano, Daniele / Ehninger, Dan

Mechanisms of ageing and development

2023 Volume 213, Page(s) 111837

Abstract: The current understanding of the biology of aging is largely based on research aimed at identifying factors that influence lifespan. However, lifespan as a sole proxy measure of aging has limitations because it can be influenced by specific pathologies ( ... ...

Abstract	The current understanding of the biology of aging is largely based on research aimed at identifying factors that influence lifespan. However, lifespan as a sole proxy measure of aging has limitations because it can be influenced by specific pathologies (not generalized physiological deterioration in old age). Hence, there is a great need to discuss and design experimental approaches that are well-suited for studies targeting the biology of aging, rather than the biology of specific pathologies that restrict the lifespan of a given species. For this purpose, we here review various perspectives on aging, discuss agreement and disagreement among researchers on the definition of aging, and show that while slightly different aspects are emphasized, a widely accepted feature, shared across many definitions, is that aging is accompanied by phenotypic changes that occur in a population over the course of an average lifespan. We then discuss experimental approaches that are in line with these considerations, including multidimensional analytical frameworks as well as designs that facilitate the proper assessment of intervention effects on aging rate. The proposed framework can guide discovery approaches to aging mechanisms in all key model organisms (e.g., mouse, fish models, D. melanogaster, C. elegans) as well as in humans.
MeSH term(s)	Animals ; Humans ; Mice ; Aging/physiology ; Caenorhabditis elegans ; Drosophila melanogaster ; Longevity
Language	English
Publishing date	2023-06-09
Publishing country	Ireland
Document type	Journal Article ; Review
ZDB-ID	183915-9
ISSN	1872-6216 ; 0047-6374
ISSN (online)	1872-6216
ISSN	0047-6374
DOI	10.1016/j.mad.2023.111837
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1012: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: AIFM1 beyond cell death: An overview of this OXPHOS-inducing factor in mitochondrial diseases.

Wischhof, Lena / Scifo, Enzo / Ehninger, Dan / Bano, Daniele

EBioMedicine

2022 Volume 83, Page(s) 104231

Abstract: Apoptosis-inducing factor (AIF) is a mitochondrial intermembrane space flavoprotein with diverse functions in cellular physiology. In this regard, a large number of studies have elucidated AIF's participation to chromatin condensation during cell death ... ...

Abstract	Apoptosis-inducing factor (AIF) is a mitochondrial intermembrane space flavoprotein with diverse functions in cellular physiology. In this regard, a large number of studies have elucidated AIF's participation to chromatin condensation during cell death in development, cancer, cardiovascular and brain disorders. However, the discovery of rare AIFM1 mutations in patients has shifted the interest of biomedical researchers towards AIF's contribution to pathogenic mechanisms underlying inherited AIFM1-linked metabolic diseases. The functional characterization of AIF binding partners has rapidly advanced our understanding of AIF biology within the mitochondria and beyond its widely reported role in cell death. At the present time, it is reasonable to assume that AIF contributes to cell survival by promoting biogenesis and maintenance of the mitochondrial oxidative phosphorylation (OXPHOS) system. With this review, we aim to outline the current knowledge around the vital role of AIF by primarily focusing on currently reported human diseases that have been linked to AIFM1 deficiency.
MeSH term(s)	Apoptosis/genetics ; Apoptosis Inducing Factor/genetics ; Apoptosis Inducing Factor/metabolism ; Cell Death/genetics ; Chromatin ; Humans ; Mitochondrial Diseases/genetics ; Oxidative Phosphorylation
Chemical Substances	AIFM1 protein, human ; Apoptosis Inducing Factor ; Chromatin
Language	English
Publishing date	2022-08-19
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2022.104231
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 7090: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Tsc2 Haploinsufficiency Has Limited Effects on Fetal Brain Cytokine Levels during Gestational Immune Activation.

Ehninger, Dan

Autism research and treatment

2014 Volume 2014, Page(s) 761279

Abstract: Dysregulated TSC/mTOR signaling may play a pathogenetic role in forms of syndromic autism, such as autism associated with tuberous sclerosis, a genetic disorder caused by heterozygous TSC1 or TSC2 mutations. Environmental risk factors, such as ... ...

Abstract	Dysregulated TSC/mTOR signaling may play a pathogenetic role in forms of syndromic autism, such as autism associated with tuberous sclerosis, a genetic disorder caused by heterozygous TSC1 or TSC2 mutations. Environmental risk factors, such as gestational viral infections, may, in some cases, also contribute to the pathogenesis of autism and related neuropsychiatric disorders. We have recently found that a heterozygous Tsc2 mutation and the poly I:C model of maternal immune activation (MIA) interactively perturb fetal development and adult social behavior in mice, suggesting that these factors converge on shared pathways. TSC/mTOR signaling plays an important role in the modulation of immune responses, raising the possibility that the damage caused by MIA was greater in Tsc2(+/-) than in wildtype fetuses because of an exacerbated immune response in the mutants. Here, cytokine antibody arrays were employed to measure relative cytokine abundances in the fetal brain and the placenta during MIA. Cytokines were induced by gestational poly I:C but there was no obvious modulatory effect of Tsc2 haploinsufficiency. The data indicate that cytokine exposure during MIA is comparable in Tsc2 haploinsufficient and wildtype control fetuses, suggesting that downstream molecular and cellular processes may account for the interactive effects of Tsc2 haploinsufficiency and MIA.
Language	English
Publishing date	2014-07-09
Publishing country	Egypt
Document type	Journal Article
ZDB-ID	2626622-2
ISSN	2090-1933 ; 2090-1925
ISSN (online)	2090-1933
ISSN	2090-1925
DOI	10.1155/2014/761279
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Article ; Online: AIFM1 beyond cell death

Lena Wischhof / Enzo Scifo / Dan Ehninger / Daniele Bano

EBioMedicine, Vol 83, Iss , Pp 104231- (2022)

An overview of this OXPHOS-inducing factor in mitochondrial diseases

2022

Abstract: Summary: Apoptosis-inducing factor (AIF) is a mitochondrial intermembrane space flavoprotein with diverse functions in cellular physiology. In this regard, a large number of studies have elucidated AIF's participation to chromatin condensation during ... ...

Abstract	Summary: Apoptosis-inducing factor (AIF) is a mitochondrial intermembrane space flavoprotein with diverse functions in cellular physiology. In this regard, a large number of studies have elucidated AIF's participation to chromatin condensation during cell death in development, cancer, cardiovascular and brain disorders. However, the discovery of rare AIFM1 mutations in patients has shifted the interest of biomedical researchers towards AIF's contribution to pathogenic mechanisms underlying inherited AIFM1-linked metabolic diseases. The functional characterization of AIF binding partners has rapidly advanced our understanding of AIF biology within the mitochondria and beyond its widely reported role in cell death. At the present time, it is reasonable to assume that AIF contributes to cell survival by promoting biogenesis and maintenance of the mitochondrial oxidative phosphorylation (OXPHOS) system. With this review, we aim to outline the current knowledge around the vital role of AIF by primarily focusing on currently reported human diseases that have been linked to AIFM1 deficiency.
Keywords	Aapoptosis-inducing factor (AIF) ; CHCHD4 ; Mitochondria ; Mitochondrial diseases ; Oxidative phosphorylation (OXPHOS) ; Medicine ; R ; Medicine (General) ; R5-920
Subject code	610
Language	English
Publishing date	2022-09-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: The histone code in dementia: Transcriptional and chromatin plasticity fades away.

Bano, Daniele / Salomoni, Paolo / Ehninger, Dan / Nicotera, Pierluigi

Current opinion in pharmacology

2021 Volume 60, Page(s) 117–122

Abstract: With the aging of the population, Alzheimer's disease and other forms of dementia represent major challenges for health care systems globally. To date, the molecular mechanisms underlying the pathophysiology of dementia remain elusive, with a consequent ... ...

Abstract	With the aging of the population, Alzheimer's disease and other forms of dementia represent major challenges for health care systems globally. To date, the molecular mechanisms underlying the pathophysiology of dementia remain elusive, with a consequent negative impact in developing efficient disease modifiers. New exciting findings suggest that modulation of the histone code may influence transcriptional networks at the root of neuronal plasticity and cognitive performance. Although most of the current conclusions require further mechanistic evidence, it appears that chromatin perturbations actually correlate with Alzheimer's disease onset and progression. Thus, a better understanding of the epigenetic contribution to normal brain function and dementia pathogenesis may help to identify new epigenetic targets for the inhibition of disease trajectories associated with cognitive decline.
MeSH term(s)	Aging/genetics ; Alzheimer Disease/genetics ; Chromatin/genetics ; Cognitive Dysfunction ; Histone Code ; Humans
Chemical Substances	Chromatin
Language	English
Publishing date	2021-08-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2021.07.014
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 5608: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Targeting the "hallmarks of aging" to slow aging and treat age-related disease: fact or fiction?

Keshavarz, Maryam / Xie, Kan / Schaaf, Kristina / Bano, Daniele / Ehninger, Dan

Molecular psychiatry

2022 Volume 28, Issue 1, Page(s) 242–255

Abstract: Aging is a major risk factor for a number of chronic diseases, including neurodegenerative and cerebrovascular disorders. Aging processes have therefore been discussed as potential targets for the development of novel and broadly effective preventatives ... ...

Abstract	Aging is a major risk factor for a number of chronic diseases, including neurodegenerative and cerebrovascular disorders. Aging processes have therefore been discussed as potential targets for the development of novel and broadly effective preventatives or therapeutics for age-related diseases, including those affecting the brain. Mechanisms thought to contribute to aging have been summarized under the term the "hallmarks of aging" and include a loss of proteostasis, mitochondrial dysfunction, altered nutrient sensing, telomere attrition, genomic instability, cellular senescence, stem cell exhaustion, epigenetic alterations and altered intercellular communication. We here examine key claims about the "hallmarks of aging". Our analysis reveals important weaknesses that preclude strong and definitive conclusions concerning a possible role of these processes in shaping organismal aging rate. Significant ambiguity arises from the overreliance on lifespan as a proxy marker for aging, the use of models with unclear relevance for organismal aging, and the use of study designs that do not allow to properly estimate intervention effects on aging rate. We also discuss future research directions that should be taken to clarify if and to what extent putative aging regulators do in fact interact with aging. These include multidimensional analytical frameworks as well as designs that facilitate the proper assessment of intervention effects on aging rate.
MeSH term(s)	Epigenesis, Genetic ; Cellular Senescence ; Stem Cells ; Longevity
Language	English
Publishing date	2022-07-15
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-022-01680-x
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 4812: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: From genes to cognition in tuberous sclerosis: implications for mTOR inhibitor-based treatment approaches.

Ehninger, Dan

Neuropharmacology

2013 Volume 68, Page(s) 97–105

Abstract: Tuberous sclerosis (TSC) is a neurocutaneous disorder with an autosomal-dominant pattern of inheritance and is caused by heterozygous mutations in the TSC1 or TSC2 gene. Neuropsychiatric conditions, including intellectual disability, autism and epilepsy, ...

Abstract	Tuberous sclerosis (TSC) is a neurocutaneous disorder with an autosomal-dominant pattern of inheritance and is caused by heterozygous mutations in the TSC1 or TSC2 gene. Neuropsychiatric conditions, including intellectual disability, autism and epilepsy, are highly prevalent in TSC populations. Here, I review recent findings that shed light on some of the neurobiological mechanisms that may contribute to the pathogenesis of TSC-associated neuropsychiatric impairments. Emerging intervention studies in animal models show striking effects of mTORC1 inhibitors on TSC-related CNS manifestations. Translational studies that assess the effects of mTORC1 inhibitors on neuropsychiatric phenotypes in human TSC individuals are underway. This article is part of the Special Issue entitled 'Neurodevelopmental Disorders'.
MeSH term(s)	Animals ; Cognition ; Disease Models, Animal ; Humans ; Phenotype ; Protein Kinase Inhibitors/therapeutic use ; TOR Serine-Threonine Kinases/antagonists & inhibitors ; Tuberous Sclerosis/drug therapy ; Tuberous Sclerosis/genetics ; Tuberous Sclerosis/psychology
Chemical Substances	Protein Kinase Inhibitors ; TOR Serine-Threonine Kinases (EC 2.7.1.1)
Language	English
Publishing date	2013-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2012.05.015
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ui I Zs.242: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Impact of paternal nutrition on epigenetic patterns.

Pearson, Brandon L / Ehninger, Dan

Epigenomics

2018 Volume 10, Issue 2, Page(s) 115–117

MeSH term(s)	Animals ; Diet ; Epigenesis, Genetic ; Humans ; Male ; Mice ; Nutrigenomics ; Paternal Inheritance
Language	English
Publishing date	2018-01-15
Publishing country	England
Document type	Journal Article
ISSN	1750-192X
ISSN (online)	1750-192X
DOI	10.2217/epi-2017-0134
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾
- Full text online
- Order with fees

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

Inter-library loan at ZB MED