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  1. Article ; Online: The role of platelet-rich plasma in androgenetic alopecia: A systematic review.

    Donnelly, C / Minty, I / Dsouza, A / Wong, Y Y / Mukhopadhyay, I / Nagarajan, V / Rupra, R / Charles, W N / Khajuria, A

    Journal of cosmetic dermatology

    2024  Volume 23, Issue 5, Page(s) 1551–1559

    Abstract: Background: Androgenetic alopecia (AGA), also referred to as male or female pattern hair loss, is the commonest cause of chronic hair loss and affects up to 80% of men by the age of 70. Despite a high prevalence, there are few approved therapies, which ... ...

    Abstract Background: Androgenetic alopecia (AGA), also referred to as male or female pattern hair loss, is the commonest cause of chronic hair loss and affects up to 80% of men by the age of 70. Despite a high prevalence, there are few approved therapies, which show minimal efficacy.
    Objectives: This systematic review aims to evaluate the efficacy of platelet-rich plasma (PrP) in the treatment of AGA in male patients.
    Methods: MEDLINE, EMBASE, Cochrane (CENTRAL), CINAHL, clinicaltrials.gov, Google Scholar and the Science Citation Index database were searched to identify eligible studies. All randomized controlled trials (RCTs) and prospective cohort studies related to PrP use in AGA were included. Primary outcomes included changes in hair density and hair count. Methodological quality was assessed using bias assessment tools.
    Results: Eight RCTs and one cohort study were included in the review with a total of 291 participants. Six studies reported a statistically significant increase in hair density in the PrP group versus the control. Five studies reported a statistically significant increase in hair count with PrP. Seven studies showed moderate risk and two showed low risk of bias.
    Conclusion: In a methodologically robust review on the effectiveness of PrP on male AGA, PrP demonstrated some potential to be used therapeutically. However, the low quality of evidence, moderate risk of bias, and high heterogeneity of included studies limit inferences and call for more robust designs to investigate this further.
    MeSH term(s) Humans ; Male ; Alopecia/therapy ; Hair/growth & development ; Platelet-Rich Plasma ; Randomized Controlled Trials as Topic ; Treatment Outcome
    Language English
    Publishing date 2024-01-29
    Publishing country England
    Document type Journal Article ; Systematic Review
    ZDB-ID 2280551-5
    ISSN 1473-2165 ; 1473-2130
    ISSN (online) 1473-2165
    ISSN 1473-2130
    DOI 10.1111/jocd.16185
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Regulatory T cells decrease C3-positive reactive astrocytes in Alzheimer-like pathology.

    Stym-Popper, Grégoire / Matta, Karen / Chaigneau, Thomas / Rupra, Roshan / Demetriou, Alexandros / Fouquet, Stéphane / Dansokho, Cira / Toly-Ndour, Cécile / Dorothée, Guillaume

    Journal of neuroinflammation

    2023  Volume 20, Issue 1, Page(s) 64

    Abstract: Background: Increasing evidence supports a key role for peripheral immune processes in the pathophysiology of Alzheimer's disease (AD), highlighting an intricate interplay between brain resident glial cells and both innate and adaptive peripheral immune ...

    Abstract Background: Increasing evidence supports a key role for peripheral immune processes in the pathophysiology of Alzheimer's disease (AD), highlighting an intricate interplay between brain resident glial cells and both innate and adaptive peripheral immune effectors. We previously showed that regulatory T cells (Tregs) have a beneficial impact on disease progression in AD-like pathology, notably by modulating the microglial response associated with Aβ deposits in a mouse model of amyloid pathology. Besides microglia, reactive astrocytes also play a critical role in neuroinflammatory processes associated with AD. Different phenotypes of reactive astrocytes have previously been characterized, including A1-like neurotoxic and A2-like neuroprotective subtypes. However, the precise impact of Tregs on astrocyte reactivity and phenotypes in AD still remains poorly defined.
    Methods: We assessed the impact of Treg immunomodulation on astrocyte reactivity in a mouse model of AD-like amyloid pathology. Using 3D imaging, we carried out extensive morphological analyses of astrocytes following either depletion or amplification of Tregs. We further assessed the expression of several A1- and A2-like markers by immunofluorescence and RT-qPCR.
    Results: Modulation of Tregs did not significantly impact the magnitude of global astrocyte reactivity in the brain nor in the close vicinity of cortical amyloid deposits. We did not observe changes in the number, morphology, or branching complexity of astrocytes according to immunomodulation of Tregs. However, early transient depletion of Tregs modulated the balance of reactive astrocyte subtypes, resulting in increased C3-positive A1-like phenotypes associated with amyloid deposits. Conversely, early depletion of Tregs decreased markers of A2-like phenotypes of reactive astrocytes associated with larger amyloid deposits. Intriguingly, modulation of Tregs also impacted the cerebral expression of several markers of A1-like subsets in healthy mice.
    Conclusions: Our study suggests that Tregs contribute to modulate and fine-tune the balance of reactive astrocyte subtypes in AD-like amyloid pathology, by dampening C3-positive astrocytes in favor of A2-like phenotypes. This effect of Tregs may partly relate to their capacity at modulating steady state astrocyte reactivity and homeostasis. Our data further highlight the need for refined markers of astrocytes subsets and strategy of analysis for better deciphering the complexity of astrocyte reactivity in neurodegeneration.
    MeSH term(s) Mice ; Animals ; Alzheimer Disease/pathology ; Amyloid beta-Protein Precursor/genetics ; Astrocytes/metabolism ; T-Lymphocytes, Regulatory ; Mice, Transgenic ; Plaque, Amyloid/pathology ; Amyloid beta-Peptides/metabolism
    Chemical Substances Amyloid beta-Protein Precursor ; Amyloid beta-Peptides
    Language English
    Publishing date 2023-03-08
    Publishing country England
    Document type Journal Article
    ZDB-ID 2156455-3
    ISSN 1742-2094 ; 1742-2094
    ISSN (online) 1742-2094
    ISSN 1742-2094
    DOI 10.1186/s12974-023-02702-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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