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  1. Article: Gut-Brain Axis Impact on Canine Anxiety Disorders: New Challenges for Behavioral Veterinary Medicine.

    Sacoor, Carina / Marugg, John D / Lima, Nuno R / Empadinhas, Nuno / Montezinho, Liliana

    Veterinary medicine international

    2024  Volume 2024, Page(s) 2856759

    Abstract: Anxiety disorders in dogs are ever-growing and represent an important concern in the veterinary behavior field. These disorders are often disregarded in veterinary clinical practice, negatively impacting the animal's and owner's quality of life. Moreover, ...

    Abstract Anxiety disorders in dogs are ever-growing and represent an important concern in the veterinary behavior field. These disorders are often disregarded in veterinary clinical practice, negatively impacting the animal's and owner's quality of life. Moreover, these anxiety disorders can potentially result in the abandonment or euthanasia of dogs. Growing evidence shows that the gut microbiota is a central player in the gut-brain axis. A variety of microorganisms inhabit the intestines of dogs, which are essential in maintaining intestinal homeostasis. These microbes can impact mental health through several mechanisms, including metabolic, neural, endocrine, and immune-mediated pathways. The disruption of a balanced composition of resident commensal communities, or dysbiosis, is implicated in several pathological conditions, including mental disorders such as anxiety. Studies carried out in rodent models and humans demonstrate that the intestinal microbiota can influence mental health through these mechanisms, including anxiety disorders. Furthermore, novel therapeutic strategies using prebiotics and probiotics have been shown to ameliorate anxiety-related symptoms. However, regarding the canine veterinary behavior field, there is still a lack of insightful research on this topic. In this review, we explore the few but relevant studies performed on canine anxiety disorders. We agree that innovative bacterial therapeutical approaches for canine anxiety disorders will become a promising field of investigation and certainly pave the way for new approaches to these behavioral conditions.
    Language English
    Publishing date 2024-01-23
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2536385-2
    ISSN 2042-0048 ; 2090-8113
    ISSN (online) 2042-0048
    ISSN 2090-8113
    DOI 10.1155/2024/2856759
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Neurodegenerative Microbially-Shaped Diseases: Oxidative Stress Meets Neuroinflammation.

    Silva, Diana Filipa / Empadinhas, Nuno / Cardoso, Sandra Morais / Esteves, Ana Raquel

    Antioxidants (Basel, Switzerland)

    2022  Volume 11, Issue 11

    Abstract: Inflammation and oxidative stress characterize a number of chronic conditions including neurodegenerative diseases and aging. Inflammation is a key component of the innate immune response in Alzheimer's disease and Parkinson's disease of which oxidative ... ...

    Abstract Inflammation and oxidative stress characterize a number of chronic conditions including neurodegenerative diseases and aging. Inflammation is a key component of the innate immune response in Alzheimer's disease and Parkinson's disease of which oxidative stress is an important hallmark. Immune dysregulation and mitochondrial dysfunction with concomitant reactive oxygen species accumulation have also been implicated in both diseases, both systemically and within the Central Nervous System. Mitochondria are a centrally positioned signalling hub for inflammatory responses and inflammatory cells can release reactive species at the site of inflammation often leading to exaggerated oxidative stress. A growing body of evidence suggests that disruption of normal gut microbiota composition may induce increased permeability of the gut barrier leading to chronic systemic inflammation, which may, in turn, impair the blood-brain barrier function and promote neuroinflammation and neurodegeneration. The gastrointestinal tract is constantly exposed to myriad exogenous substances and microbial pathogens, which are abundant sources of reactive oxygen species, oxidative damage and pro-inflammatory events. Several studies have demonstrated that microbial infections may also affect the balance in gut microbiota composition (involving oxidant and inflammatory processes by the host and indigenous microbiota) and influence downstream Alzheimer's disease and Parkinson's disease pathogenesis, in which blood-brain barrier damage ultimately occurs. Therefore, the oxidant/inflammatory insults triggered by a disrupted gut microbiota and chronic dysbiosis often lead to compromised gut barrier function, allowing inflammation to "escape" as well as uncontrolled immune responses that may ultimately disrupt mitochondrial function upwards the brain. Future therapeutic strategies should be designed to "restrain" gut inflammation, a goal that could ideally be attained by microbiota modulation strategies, in alternative to classic anti-inflammatory agents with unpredictable effects on the microbiota architecture itself.
    Language English
    Publishing date 2022-10-28
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox11112141
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  3. Article ; Online: The Role of Bacteria-Mitochondria Communication in the Activation of Neuronal Innate Immunity: Implications to Parkinson's Disease.

    Magalhães, João D / Esteves, Ana Raquel / Candeias, Emanuel / Silva, Diana F / Empadinhas, Nuno / Cardoso, Sandra Morais

    International journal of molecular sciences

    2023  Volume 24, Issue 5

    Abstract: Mitochondria play a key role in regulating host metabolism, immunity and cellular homeostasis. Remarkably, these organelles are proposed to have evolved from an endosymbiotic association between an alphaproteobacterium and a primitive eukaryotic host ... ...

    Abstract Mitochondria play a key role in regulating host metabolism, immunity and cellular homeostasis. Remarkably, these organelles are proposed to have evolved from an endosymbiotic association between an alphaproteobacterium and a primitive eukaryotic host cell or an archaeon. This crucial event determined that human cell mitochondria share some features with bacteria, namely cardiolipin, N-formyl peptides, mtDNA and transcription factor A, that can act as mitochondrial-derived damage-associated molecular patterns (DAMPs). The impact of extracellular bacteria on the host act largely through the modulation of mitochondrial activities, and often mitochondria are themselves immunogenic organelles that can trigger protective mechanisms through DAMPs mobilization. In this work, we demonstrate that mesencephalic neurons exposed to an environmental alphaproteobacterium activate innate immunity through toll-like receptor 4 and Nod-like receptor 3. Moreover, we show that mesencephalic neurons increase the expression and aggregation of alpha-synuclein that interacts with mitochondria, leading to their dysfunction. Mitochondrial dynamic alterations also affect mitophagy which favors a positive feedback loop on innate immunity signaling. Our results help to elucidate how bacteria and neuronal mitochondria interact and trigger neuronal damage and neuroinflammation and allow us to discuss the role of bacterial-derived pathogen-associated molecular patterns (PAMPs) in Parkinson's disease etiology.
    MeSH term(s) Humans ; Parkinson Disease/metabolism ; Mitochondria/metabolism ; Immunity, Innate ; Alarmins/metabolism ; Bacteria ; Neurons/metabolism
    Chemical Substances Alarmins
    Language English
    Publishing date 2023-02-22
    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/ijms24054339
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  4. Article ; Online: Parkinson's Disease: A Multisystem Disorder.

    Costa, Helena Nunes / Esteves, Ana Raquel / Empadinhas, Nuno / Cardoso, Sandra Morais

    Neuroscience bulletin

    2022  Volume 39, Issue 1, Page(s) 113–124

    Abstract: The way sporadic Parkinson's disease (PD) is perceived has undergone drastic changes in recent decades. For a long time, PD was considered a brain disease characterized by motor disturbances; however, the identification of several risk factors and the ... ...

    Abstract The way sporadic Parkinson's disease (PD) is perceived has undergone drastic changes in recent decades. For a long time, PD was considered a brain disease characterized by motor disturbances; however, the identification of several risk factors and the hypothesis that PD has a gastrointestinal onset have shed additional light. Today, after recognition of prodromal non-motor symptoms and the pathological processes driving their evolution, there is a greater understanding of the involvement of other organ systems. For this reason, PD is increasingly seen as a multiorgan and multisystemic pathology that arises from the interaction of susceptible genetic factors with a challenging environment during aging-related decline.
    MeSH term(s) Humans ; Parkinson Disease/genetics ; Parkinson Disease/pathology ; Gastrointestinal Tract ; Risk Factors ; Gastrointestinal Microbiome ; Prodromal Symptoms ; alpha-Synuclein
    Chemical Substances alpha-Synuclein
    Language English
    Publishing date 2022-08-22
    Publishing country Singapore
    Document type Journal Article ; Review
    ZDB-ID 2419741-5
    ISSN 1995-8218 ; 1673-7067
    ISSN (online) 1995-8218
    ISSN 1673-7067
    DOI 10.1007/s12264-022-00934-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6734: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: The neuromicrobiology of Parkinson's disease: A unifying theory.

    Munoz-Pinto, Mario F / Empadinhas, Nuno / Cardoso, Sandra M

    Ageing research reviews

    2021  Volume 70, Page(s) 101396

    Abstract: Recent evidence confirms that PD is indeed a multifactorial disease with different aetiologies and prodromal symptomatology that likely depend on the initial trigger. New players with important roles as triggers, facilitators and aggravators of the PD ... ...

    Abstract Recent evidence confirms that PD is indeed a multifactorial disease with different aetiologies and prodromal symptomatology that likely depend on the initial trigger. New players with important roles as triggers, facilitators and aggravators of the PD neurodegenerative process have re-emerged in the last few years, the microbes. Having evolved in association with humans for ages, microbes and their products are now seen as fundamental regulators of human physiology with disturbances in their balance being increasingly accepted to have a relevant impact on the progression of disease in general and on PD in particular. In this review, we comprehensively address early studies that have directly or indirectly linked bacteria or other infectious agents to the onset and progression of PD, from the earliest suspects to the most recent culprits, the gut microbiota. The quest for effective treatments to arrest PD progression must inevitably address the different interactions between microbiota and human cells, and naturally consider the gut-brain axis. The comprehensive characterization of such mechanisms will help design innovative bacteriotherapeutic approaches to selectively shape the gut microbiota profile ultimately to halt PD progression. The present review describes our current understanding of the role of microorganisms and their endosymbiotic relatives, the mitochondria, in inducing, facilitating, or aggravating PD pathogenesis.
    MeSH term(s) Brain ; Gastrointestinal Microbiome ; Humans ; Microbiota ; Parkinson Disease/therapy
    Language English
    Publishing date 2021-06-23
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2075672-0
    ISSN 1872-9649 ; 1568-1637
    ISSN (online) 1872-9649
    ISSN 1568-1637
    DOI 10.1016/j.arr.2021.101396
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5579: 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)

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  6. Article ; Online: Neuronal control of microglia through the mitochondria.

    Pereira-Santos, A R / Candeias, Emanuel / Magalhães, J D / Empadinhas, Nuno / Esteves, A Raquel / Cardoso, Sandra M

    Biochimica et biophysica acta. Molecular basis of disease

    2024  Volume 1870, Issue 5, Page(s) 167167

    Abstract: The microbial toxin β-N-methylamino-L-alanine (BMAA), which is derived from cyanobacteria, targets neuronal mitochondria, leading to the activation of neuronal innate immunity and, consequently, neurodegeneration. Although known to modulate brain ... ...

    Abstract The microbial toxin β-N-methylamino-L-alanine (BMAA), which is derived from cyanobacteria, targets neuronal mitochondria, leading to the activation of neuronal innate immunity and, consequently, neurodegeneration. Although known to modulate brain inflammation, the precise role of aberrant microglial function in the neurodegenerative process remains elusive. To determine if neurons signal microglial cells, we treated primary cortical neurons with BMAA and then co-cultured them with the N9 microglial cell line. Our observations indicate that microglial cell activation requires initial neuronal priming. Contrary to what was observed in cortical neurons, BMAA was not able to activate inflammatory pathways in N9 cells. We observed that microglial activation is dependent on mitochondrial dysfunction signaled by BMAA-treated neurons. In this scenario, the NLRP3 pro-inflammatory pathway is activated due to mitochondrial impairment in N9 cells. These results demonstrate that microglia activation in the presence of BMAA is dependent on neuronal signaling. This study provides evidence that neurons may trigger microglia activation and subsequent neuroinflammation. In addition, we demonstrate that microglial activation may have a protective role in ameliorating neuronal innate immune activation, at least in the initial phase. This work challenges the current understanding of neuroinflammation by assigning the primary role to neurons.
    Language English
    Publishing date 2024-04-16
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 60-7
    ISSN 1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbadis.2024.167167
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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.247: Show issues Location:
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  7. Article: The Microbiome-Mitochondria Dance in Prodromal Parkinson's Disease.

    Cardoso, Sandra M / Empadinhas, Nuno

    Frontiers in physiology

    2018  Volume 9, Page(s) 471

    Abstract: The brain is an immunologically active organ where neurons and glia cells orchestrate complex innate immune responses against infections and injuries. Neuronal responses involve Toll-like or Nod-like receptors and the secretion of antimicrobial peptides ... ...

    Abstract The brain is an immunologically active organ where neurons and glia cells orchestrate complex innate immune responses against infections and injuries. Neuronal responses involve Toll-like or Nod-like receptors and the secretion of antimicrobial peptides and cytokines. The endosymbiotic theory for the evolutionary origin of mitochondria from primitive bacteria, suggests that they may have also retained the capacity to activate neuronal innate immunity. In fact, it was shown that mitochondrial damage-associated molecular patterns could signal and activate innate immunity and inflammation. Moreover, the mitochondrial cascade hypothesis for sporadic Parkinson's disease (PD) argues that altered mitochondrial metabolism and function can drive neurodegeneration. Additionally, a neuroinflammatory signature with increased levels of pro-inflammatory mediators in PD affected brain areas was recently detected. Herein, we propose that a cascade of events initiating in a dysbiotic gut microbiome drive the production of toxins or antibiotics that target and damage mitochondria. This in turn activates neuronal innate immunity and triggers sterile inflammation phenomena that culminate in the neurodegenerative processes observed in the enteric and in the central nervous systems and that ultimately lead to Parkinson's disease.
    Language English
    Publishing date 2018-05-09
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2018.00471
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  8. Article ; Online: Editorial: Interplay Between Nutrition, the Intestinal Microbiota and the Immune System.

    Oriá, Reinaldo B / Empadinhas, Nuno / Malva, João O

    Frontiers in immunology

    2020  Volume 11, Page(s) 1758

    MeSH term(s) Animals ; Bacteria/immunology ; Bacteria/metabolism ; Diet/adverse effects ; Dysbiosis ; Gastrointestinal Microbiome ; Host-Pathogen Interactions ; Humans ; Immune System/immunology ; Immune System/physiopathology ; Immune System Diseases/immunology ; Immune System Diseases/microbiology ; Immune System Diseases/physiopathology ; Nutritional Status
    Language English
    Publishing date 2020-08-06
    Publishing country Switzerland
    Document type Editorial ; Introductory Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2020.01758
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  9. Article: Enzyme Promiscuity in Serotonin Biosynthesis, From Bacteria to Plants and Humans.

    Gonçalves, Sara / Nunes-Costa, Daniela / Cardoso, Sandra Morais / Empadinhas, Nuno / Marugg, John David

    Frontiers in microbiology

    2022  Volume 13, Page(s) 873555

    Abstract: Serotonin is a phylogenetically ancient compound found in animals, plants, and some bacteria. In eukaryotes, serotonin is synthesized from the aromatic amino acid ... ...

    Abstract Serotonin is a phylogenetically ancient compound found in animals, plants, and some bacteria. In eukaryotes, serotonin is synthesized from the aromatic amino acid tryptophan
    Language English
    Publishing date 2022-04-14
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2587354-4
    ISSN 1664-302X
    ISSN 1664-302X
    DOI 10.3389/fmicb.2022.873555
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  10. Article ; Online: Effect of ScCO

    Bento, Cristiana S A / Carrelo, Henrique / Alarico, Susana / Empadinhas, Nuno / de Sousa, Hermínio C / Teresa Cidade, Maria / Braga, Mara E M

    International journal of pharmaceutics

    2023  Volume 646, Page(s) 123451

    Abstract: Biopolymers present ideal properties to be used in wound dressing solutions. By mixing two oppositely charged macromolecules it is possible to form polyelectrolyte complex (PEC) based cryogels using lyophilization. Their application in the biomedical ... ...

    Abstract Biopolymers present ideal properties to be used in wound dressing solutions. By mixing two oppositely charged macromolecules it is possible to form polyelectrolyte complex (PEC) based cryogels using lyophilization. Their application in the biomedical field is limited due to their sterilization requirements, as conventional methods compromise their physicochemical properties. ScCO
    Language English
    Publishing date 2023-09-27
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 428962-6
    ISSN 1873-3476 ; 0378-5173
    ISSN (online) 1873-3476
    ISSN 0378-5173
    DOI 10.1016/j.ijpharm.2023.123451
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1409: 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)
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