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Book ; Online: Software Architecture for Operation and Use of Quantum Communications Networks

Verma, Dinesh / Figueroa, Eden / Carini, Gabriella / Ritter, Mark

2023

Abstract: Quantum Communications Networks using the properties of qubits, namely state superposition, no-cloning and entanglement, can enable the exchange of information in a very secure manner across optical links or free space. New innovations enable the use of ... ...

Abstract	Quantum Communications Networks using the properties of qubits, namely state superposition, no-cloning and entanglement, can enable the exchange of information in a very secure manner across optical links or free space. New innovations enable the use of optical repeaters as well as multi-cast communication in the networks. Some types of quantum communications mechanisms can be implemented at room-temperature instead of requiring super-cooled systems. This makes it likely that business impact from quantum communications will be realized sooner than that from quantum computers. Quantum networks need to be integrated into the ecosystem of currently deployed classical networks and augment them with new capabilities. Classical computers and networks need to be able to use the new secure communication capabilities offered by quantum networks. To provide this interoperability, appropriate software abstractions on the usage of quantum networks need to be developed. In this paper, we examine what the type of software abstractions quantum networks can provide, and the type of applications that the new abstractions can support.
Keywords	Quantum Physics ; Computer Science - Networking and Internet Architecture
Subject code	303
Publishing date	2023-05-31
Publishing country	us
Document type	Book ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: LRRK2 Kinase Inhibition Attenuates Neuroinflammation and Cytotoxicity in Animal Models of Alzheimer's and Parkinson's Disease-Related Neuroinflammation.

Mutti, Veronica / Carini, Giulia / Filippini, Alice / Castrezzati, Stefania / Giugno, Lorena / Gennarelli, Massimo / Russo, Isabella

Cells

2023 Volume 12, Issue 13

Abstract: Chronic neuroinflammation plays a crucial role in the progression of several neurodegenerative diseases (NDDs), including Parkinson's disease (PD) and Alzheimer's disease (AD). Intriguingly, in the last decade, leucine-rich repeat kinase-2 ( ...

Abstract	Chronic neuroinflammation plays a crucial role in the progression of several neurodegenerative diseases (NDDs), including Parkinson's disease (PD) and Alzheimer's disease (AD). Intriguingly, in the last decade, leucine-rich repeat kinase-2 (
MeSH term(s)	Mice ; Animals ; Parkinson Disease/pathology ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Neuroinflammatory Diseases ; Alzheimer Disease/drug therapy ; Models, Animal
Chemical Substances	Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1)
Language	English
Publishing date	2023-07-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12131799
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Article ; Online: Phenotypic Frailty Assessment in SAMP8 Mice: Sex Differences and Potential Role of miRNAs as Peripheral Biomarkers.

Musazzi, Laura / Carini, Giulia / Barbieri, Silvia S / Maggi, Stefania / Veronese, Nicola / Popoli, Maurizio / Barbon, Alessandro / Ieraci, Alessandro

The journals of gerontology. Series A, Biological sciences and medical sciences

2023 Volume 78, Issue 11, Page(s) 1935–1943

Abstract: Frailty is a geriatric syndrome characterized by age-related decline in physiological reserves and functions in multiple organ systems, including the musculoskeletal, neuroendocrine/metabolic, and immune systems. Animal models are essential to study the ... ...

Abstract	Frailty is a geriatric syndrome characterized by age-related decline in physiological reserves and functions in multiple organ systems, including the musculoskeletal, neuroendocrine/metabolic, and immune systems. Animal models are essential to study the biological basis of aging and potential ways to delay the onset of age-related phenotypes. Unfortunately, validated animal models of frailty are still lacking in preclinical research. The senescence-accelerated prone-8 (SAMP8) mouse strain exhibits early cognitive loss that mimics the deterioration of learning and memory in the elderly and is widely used as a model of aging and neurodegenerative diseases. Here, we examined the frailty phenotype, which includes body weight, strength, endurance, activity, and slow walking speed, in male and female SAMP8 and senescence-accelerated mouse resistant (SAMR1) mice at 6- and 9-months of age. We found that the prevalence of frailty was higher in SAMP8 mice compared with SAMR1 mice, regardless of sex. The overall percentage of prefrail and frail mice was similar in male and female SAMP8 mice, although the percentage of frail mice was slightly higher in males than in females. In addition, we found sex- and frailty-specific changes in selected miRNAs blood levels. In particular, the levels of miR-34a-5p and miR-331-3p were higher in both prefrail and frail mice, whereas miR-26b-5p was increased only in frail mice compared with robust mice. Finally, levels of miR-331-3p were also increased in whole blood from a small group of frail patients. Overall, these results suggest that SAMP8 mice may be a useful mouse model for identifying potential biomarkers and studying biological mechanisms of frailty.
MeSH term(s)	Humans ; Mice ; Male ; Female ; Animals ; Aged ; MicroRNAs/genetics ; Frailty/genetics ; Sex Characteristics ; Aging/physiology ; Phenotype ; Biomarkers ; Disease Models, Animal
Chemical Substances	MicroRNAs ; Biomarkers
Language	English
Publishing date	2023-07-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1223643-3
ISSN	1758-535X ; 1079-5006
ISSN (online)	1758-535X
ISSN	1079-5006
DOI	10.1093/gerona/glad160
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Article ; Online: Involvement of miR-135a-5p Downregulation in Acute and Chronic Stress Response in the Prefrontal Cortex of Rats.

Mingardi, Jessica / Paoli, Caterina / La Via, Luca / Carini, Giulia / Misztak, Paulina / Cifani, Carlo / Popoli, Maurizio / Barbon, Alessandro / Musazzi, Laura

International journal of molecular sciences

2023 Volume 24, Issue 2

Abstract: Stress is a key risk factor in the onset of neuropsychiatric disorders. The study of the mechanisms underlying stress response is important to understand the etiopathogenetic mechanisms and identify new putative therapeutic targets. In this context, ... ...

Abstract	Stress is a key risk factor in the onset of neuropsychiatric disorders. The study of the mechanisms underlying stress response is important to understand the etiopathogenetic mechanisms and identify new putative therapeutic targets. In this context, microRNAs (miRNAs) have emerged as key regulators of the complex patterns of gene/protein expression changes in the brain, where they have a crucial role in the regulation of neuroplasticity, neurogenesis, and neuronal differentiation. Among them, miR-135a-5p has been associated with stress response, synaptic plasticity, and the antidepressant effect in different brain areas. Here, we used acute unavoidable foot-shock stress (FS) and chronic mild stress (CMS) on male rats to study whether miR-135a-5p was involved in stress-induced changes in the prefrontal cortex (PFC). Both acute and chronic stress decreased miR-135a-5p levels in the PFC, although after CMS the reduction was induced only in animals vulnerable to CMS, according to a sucrose preference test. MiR-135a-5p downregulation in the primary neurons reduced dendritic spine density, while its overexpression exerted the opposite effect. Two bioinformatically predicted target genes, Kif5c and Cplx1/2, were increased in FS rats 24 h after stress. Altogether, we found that miR-135a-5p might play a role in stress response in PFC involving synaptic mechanisms.
MeSH term(s)	Animals ; Male ; Rats ; Down-Regulation/genetics ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Neurons/metabolism ; Neurons/pathology ; Prefrontal Cortex/metabolism ; Prefrontal Cortex/pathology ; Prefrontal Cortex/physiology ; Acute Disease/psychology ; Chronic Disease/psychology ; Stress, Physiological/genetics ; Stress, Psychological/genetics ; Stress, Psychological/psychology ; Synapses/genetics ; Synapses/metabolism ; Synapses/pathology ; Dendritic Spines/genetics ; Dendritic Spines/metabolism ; Dendritic Spines/pathology
Chemical Substances	MicroRNAs ; MIRN135 microRNA, rat ; KIF5C protein, rat (EC 3.6.1.-) ; complexin I ; complexin II
Language	English
Publishing date	2023-01-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24021552
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Article ; Online: Molecular insights in the pathogenesis of classical Ehlers-Danlos syndrome from transcriptome-wide expression profiling of patients' skin fibroblasts.

Chiarelli, Nicola / Carini, Giulia / Zoppi, Nicoletta / Ritelli, Marco / Colombi, Marina

PloS one

2019 Volume 14, Issue 2, Page(s) e0211647

Abstract: Classical Ehlers-Danlos syndrome (cEDS) is a dominant inherited connective tissue disorder mainly caused by mutations in the COL5A1 and COL5A2 genes encoding type V collagen (COLLV), which is a fibrillar COLL widely distributed in a variety of connective ...

Abstract	Classical Ehlers-Danlos syndrome (cEDS) is a dominant inherited connective tissue disorder mainly caused by mutations in the COL5A1 and COL5A2 genes encoding type V collagen (COLLV), which is a fibrillar COLL widely distributed in a variety of connective tissues. cEDS patients suffer from skin hyperextensibility, abnormal wound healing/atrophic scars, and joint hypermobility. Most of the causative variants result in a non-functional COL5A1 allele and COLLV haploinsufficiency, whilst COL5A2 mutations affect its structural integrity. To shed light into disease mechanisms involved in cEDS, we performed gene expression profiling in skin fibroblasts from four patients harboring haploinsufficient and structural mutations in both disease genes. Transcriptome profiling revealed significant changes in the expression levels of different extracellular matrix (ECM)-related genes, such as SPP1, POSTN, EDIL3, IGFBP2, and C3, which encode both matricellular and soluble proteins that are mainly involved in cell proliferation and migration, and cutaneous wound healing. These gene expression changes are consistent with our previous protein findings on in vitro fibroblasts from other cEDS patients, which exhibited reduced migration and poor wound repair owing to COLLV disorganization, altered deposition of fibronectin into ECM, and an abnormal integrin pattern. Microarray analysis also indicated the decreased expression of DNAJB7, VIPAS39, CCPG1, ATG10, SVIP, which encode molecular chaperones facilitating protein folding, enzymes regulating post-Golgi COLLs processing, and proteins acting as cargo receptors required for endoplasmic reticulum (ER) proteostasis and implicated in the autophagy process. Patients' cells also showed altered mRNA levels of many cell cycle regulating genes including CCNE2, KIF4A, MKI67, DTL, and DDIAS. Protein studies showed that aberrant COLLV expression causes the disassembly of itself and many structural ECM constituents including COLLI, COLLIII, fibronectin, and fibrillins. Our findings provide the first molecular evidence of significant gene expression changes in cEDS skin fibroblasts highlighting that defective ECM remodeling, ER homeostasis and autophagy might play a role in the pathogenesis of this connective tissue disorder.
MeSH term(s)	Adult ; Alleles ; Case-Control Studies ; Cell Cycle/genetics ; Cells, Cultured ; Collagen/genetics ; Connective Tissue/physiology ; Ehlers-Danlos Syndrome/genetics ; Ehlers-Danlos Syndrome/pathology ; Endoplasmic Reticulum/genetics ; Extracellular Matrix/genetics ; Female ; Fibroblasts/physiology ; Fibronectins/genetics ; Gene Expression Profiling/methods ; Haploinsufficiency/genetics ; Humans ; Male ; Middle Aged ; Mutation/genetics ; RNA, Messenger/genetics ; Skin/pathology ; Skin Abnormalities/genetics ; Skin Abnormalities/pathology ; Transcriptome/genetics
Chemical Substances	Fibronectins ; RNA, Messenger ; Collagen (9007-34-5)
Language	English
Publishing date	2019-02-04
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0211647
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Observation of directional leaky polaritons at anisotropic crystal interfaces.

Ni, Xiang / Carini, Giulia / Ma, Weiliang / Renzi, Enrico Maria / Galiffi, Emanuele / Wasserroth, Sören / Wolf, Martin / Li, Peining / Paarmann, Alexander / Alù, Andrea

Nature communications

2023 Volume 14, Issue 1, Page(s) 2845

Abstract: Extreme anisotropy in some polaritonic materials enables light propagation with a hyperbolic dispersion, leading to enhanced light-matter interactions and directional transport. However, these features are typically associated with large momenta that ... ...

Abstract	Extreme anisotropy in some polaritonic materials enables light propagation with a hyperbolic dispersion, leading to enhanced light-matter interactions and directional transport. However, these features are typically associated with large momenta that make them sensitive to loss and poorly accessible from far-field, being bound to the material interface or volume-confined in thin films. Here, we demonstrate a new form of directional polaritons, leaky in nature and featuring lenticular dispersion contours that are neither elliptical nor hyperbolic. We show that these interface modes are strongly hybridized with propagating bulk states, sustaining directional, long-range, sub-diffractive propagation at the interface. We observe these features using polariton spectroscopy, far-field probing and near-field imaging, revealing their peculiar dispersion, and - despite their leaky nature - long modal lifetime. Our leaky polaritons (LPs) nontrivially merge sub-diffractive polaritonics with diffractive photonics onto a unified platform, unveiling opportunities that stem from the interplay of extreme anisotropic responses and radiation leakage.
Language	English
Publishing date	2023-05-18
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-38326-7
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Article ; Online: Transcriptional Profiling of Rat Prefrontal Cortex after Acute Inescapable Footshock Stress.

Martini, Paolo / Mingardi, Jessica / Carini, Giulia / Mattevi, Stefania / Ndoj, Elona / La Via, Luca / Magri, Chiara / Gennarelli, Massimo / Russo, Isabella / Popoli, Maurizio / Musazzi, Laura / Barbon, Alessandro

Genes

2023 Volume 14, Issue 3

Abstract: Stress is a primary risk factor for psychiatric disorders such as Major Depressive Disorder (MDD) and Post Traumatic Stress Disorder (PTSD). The response to stress involves the regulation of transcriptional programs, which is supposed to play a role in ... ...

Abstract	Stress is a primary risk factor for psychiatric disorders such as Major Depressive Disorder (MDD) and Post Traumatic Stress Disorder (PTSD). The response to stress involves the regulation of transcriptional programs, which is supposed to play a role in coping with stress. To evaluate transcriptional processes implemented after exposure to unavoidable traumatic stress, we applied microarray expression analysis to the PFC of rats exposed to acute footshock (FS) stress that were sacrificed immediately after the 40 min session or 2 h or 24 h after. While no substantial changes were observed at the single gene level immediately after the stress session, gene set enrichment analysis showed alterations in neuronal pathways associated with glia development, glia-neuron networking, and synaptic function. Furthermore, we found alterations in the expression of gene sets regulated by specific transcription factors that could represent master regulators of the acute stress response. Of note, these pathways and transcriptional programs are activated during the early stress response (immediately after FS) and are already turned off after 2 h-while at 24 h, the transcriptional profile is largely unaffected. Overall, our analysis provided a transcriptional landscape of the early changes triggered by acute unavoidable FS stress in the PFC of rats, suggesting that the transcriptional wave is fast and mild, but probably enough to activate a cellular response to acute stress.
MeSH term(s)	Rats ; Animals ; Rats, Sprague-Dawley ; Depressive Disorder, Major/metabolism ; Prefrontal Cortex/metabolism ; Adaptation, Psychological ; Stress Disorders, Post-Traumatic
Language	English
Publishing date	2023-03-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes14030740
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Article ; Online: Dopamine-Dependent Ketamine Modulation of Glutamatergic Synaptic Plasticity in the Prelimbic Cortex of Adult Rats Exposed to Acute Stress.

Forti, Lia / Ndoj, Elona / Mingardi, Jessica / Secchi, Emanuele / Bonifacino, Tiziana / Schiavon, Emanuele / Carini, Giulia / La Via, Luca / Russo, Isabella / Milanese, Marco / Gennarelli, Massimo / Bonanno, Giambattista / Popoli, Maurizio / Barbon, Alessandro / Musazzi, Laura

International journal of molecular sciences

2023 Volume 24, Issue 10

Abstract: Traumatic stress is the main environmental risk factor for the development of psychiatric disorders. We have previously shown that acute footshock (FS) stress in male rats induces rapid and long-lasting functional and structural changes in the prefrontal ...

Abstract	Traumatic stress is the main environmental risk factor for the development of psychiatric disorders. We have previously shown that acute footshock (FS) stress in male rats induces rapid and long-lasting functional and structural changes in the prefrontal cortex (PFC), which are partly reversed by acute subanesthetic ketamine. Here, we asked if acute FS may also induce any changes in glutamatergic synaptic plasticity in the PFC 24 h after stress exposure and whether ketamine administration 6 h after stress may have any effect. We found that the induction of long-term potentiation (LTP) in PFC slices of both control and FS animals is dependent on dopamine and that dopamine-dependent LTP is reduced by ketamine. We also found selective changes in ionotropic glutamate receptor subunit expression, phosphorylation, and localization at synaptic membranes induced by both acute stress and ketamine. Although more studies are needed to understand the effects of acute stress and ketamine on PFC glutamatergic plasticity, this first report suggests a restoring effect of acute ketamine, supporting the potential benefit of ketamine in limiting the impact of acute traumatic stress.
MeSH term(s)	Rats ; Male ; Animals ; Ketamine/pharmacology ; Dopamine/pharmacology ; Neuronal Plasticity ; Long-Term Potentiation ; Prefrontal Cortex
Chemical Substances	Ketamine (690G0D6V8H) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2023-05-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24108718
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Article ; Online: Transcriptome analysis of skin fibroblasts with dominant negative COL3A1 mutations provides molecular insights into the etiopathology of vascular Ehlers-Danlos syndrome.

Chiarelli, Nicola / Carini, Giulia / Zoppi, Nicoletta / Ritelli, Marco / Colombi, Marina

PloS one

2018 Volume 13, Issue 1, Page(s) e0191220

Abstract: Vascular Ehlers-Danlos syndrome (vEDS) is a dominantly inherited connective tissue disorder caused by mutations in the COL3A1 gene that encodes type III collagen (COLLIII), which is the major expressed collagen in blood vessels and hollow organs. The ... ...

Abstract	Vascular Ehlers-Danlos syndrome (vEDS) is a dominantly inherited connective tissue disorder caused by mutations in the COL3A1 gene that encodes type III collagen (COLLIII), which is the major expressed collagen in blood vessels and hollow organs. The majority of disease-causing variants in COL3A1 are glycine substitutions and in-frame splice mutations in the triple helix domain that through a dominant negative effect are associated with the severe clinical spectrum potentially lethal of vEDS, characterized by fragility of soft connective tissues with arterial and organ ruptures. To shed lights into molecular mechanisms underlying vEDS, we performed gene expression profiling in cultured skin fibroblasts from three patients with different structural COL3A1 mutations. Transcriptome analysis revealed significant changes in the expression levels of several genes involved in maintenance of cell redox and endoplasmic reticulum (ER) homeostasis, COLLs folding and extracellular matrix (ECM) organization, formation of the proteasome complex, and cell cycle regulation. Protein analyses showed that aberrant COLLIII expression is associated with the disassembly of many structural ECM constituents, such as fibrillins, EMILINs, and elastin, as well as with the reduction of the proteoglycans perlecan, decorin, and versican, all playing an important role in the vascular system. Furthermore, the altered distribution of the ER marker protein disulfide isomerase PDI and the strong reduction of the COLLs-modifying enzyme FKBP22 are consistent with the disturbance of ER-related homeostasis and COLLs biosynthesis and post-translational modifications, indicated by microarray analysis. Our findings add new insights into the pathophysiology of this severe vascular disorder, since they provide a picture of the gene expression changes in vEDS skin fibroblasts and highlight that dominant negative mutations in COL3A1 also affect post-translational modifications and deposition into the ECM of several structural proteins crucial to the integrity of soft connective tissues.
MeSH term(s)	Amino Acid Substitution ; Cell Cycle/genetics ; Cells, Cultured ; Collagen Type III/chemistry ; Collagen Type III/genetics ; Collagen Type III/metabolism ; Ehlers-Danlos Syndrome/etiology ; Ehlers-Danlos Syndrome/genetics ; Ehlers-Danlos Syndrome/metabolism ; Extracellular Matrix/metabolism ; Fibroblasts/metabolism ; Gene Expression Profiling ; Humans ; Mutant Proteins/chemistry ; Mutant Proteins/genetics ; Mutant Proteins/metabolism ; Mutation ; Mutation, Missense ; Protein Folding ; Protein Processing, Post-Translational ; Skin/metabolism
Chemical Substances	COL3A1 protein, human ; Collagen Type III ; Mutant Proteins
Language	English
Publishing date	2018
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0191220
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: The Potential Role of miRNAs in Cognitive Frailty.

Carini, Giulia / Musazzi, Laura / Bolzetta, Francesco / Cester, Alberto / Fiorentini, Chiara / Ieraci, Alessandro / Maggi, Stefania / Popoli, Maurizio / Veronese, Nicola / Barbon, Alessandro

Frontiers in aging neuroscience

2021 Volume 13, Page(s) 763110

Abstract: Frailty is an aging related condition, which has been defined as a state of enhanced vulnerability to stressors, leading to a limited capacity to meet homeostatic demands. Cognitive impairment is also frequent in older people, often accompanying frailty. ...

Abstract	Frailty is an aging related condition, which has been defined as a state of enhanced vulnerability to stressors, leading to a limited capacity to meet homeostatic demands. Cognitive impairment is also frequent in older people, often accompanying frailty. Age is the main independent risk factor for both frailty and cognitive impairment, and compelling evidence suggests that similar age-associated mechanisms could underlie both clinical conditions. Accordingly, it has been suggested that frailty and cognitive impairment share common pathways, and some authors proposed "cognitive frailty" as a single complex phenotype. Nevertheless, so far, no clear common underlying pathways have been discovered for both conditions. microRNAs (miRNAs) have emerged as key fine-tuning regulators in most physiological processes, as well as pathological conditions. Importantly, miRNAs have been proposed as both peripheral biomarkers and potential molecular factors involved in physiological and pathological aging. In this review, we discuss the evidence linking changes of selected miRNAs expression with frailty and cognitive impairment. Overall, miR-92a-5p and miR-532-5p, as well as other miRNAs implicated in pathological aging, should be investigated as potential biomarkers (and putative molecular effectors) of cognitive frailty.
Language	English
Publishing date	2021-11-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2021.763110
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