Assessment of age‐related morphological changes in the testes of post‐hatch light ecotype Nigerian indigenous chicken

Background: Oxidative stress is caused by free radicals or oxidant productions, including lipid peroxidation, protein modification, DNA damage and apoptosis or cell death and results in cellular degeneration and neurodegeneration from damage to macromolecules. Results: Accumulation of the DNA damage (8HOdG) products and the end products of LPO (including aldehyde, diene, triene conjugates and Schiff’s bases) were noted in the research studies. Significantly higher levels of these products in comparison with the controls were observed. Oxidative stress induced changes to ocular cells and tissues. Typical changes include ECM accumulation, cell dysfunction, cell death, advanced senescence, disarrangement or rearrangement of the cytoskeleton and released inflammatory cytokines. It is involved in ocular diseases, including keratoconus, Fuchs endothelial corneal dystrophy, and granular corneal dystrophy type 2, cataract, age-related macular degeneration, primary open-angle glaucoma, retinal light damage, and retinopathy of prematurity. These ocular diseases are the cause of irreversible blindness worldwide. Conclusions: Oxidative stress, inflammation and autophagy are implicated in biochemical and morphological changes in these ocular tissues. The development of therapy is a major target for the management care of these ocular diseases.

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Age-Related Changes in the Primary Motor Cortex of Newborn to Adult Domestic Pig Sus scrofa domesticus

Animals ◽

10.3390/ani11072019 ◽

2021 ◽

Vol 11 (7) ◽

pp. 2019

Author(s):

Salvatore Desantis ◽

Serena Minervini ◽

Lorenzo Zallocco ◽

Bruno Cozzi ◽

Andrea Pirone

Keyword(s):

Animal Model ◽

Motor Cortex ◽

Calcium Binding ◽

Sus Scrofa ◽

Primary Motor Cortex ◽

Morphological Changes ◽

Neural Cells ◽

Age Related ◽

Cell Layers ◽

Sus Scrofa Domesticus

The pig has been increasingly used as a suitable animal model in translational neuroscience. However, several features of the fast-growing, immediately motor-competent cerebral cortex of this species have been adequately described. This study analyzes the cytoarchitecture of the primary motor cortex (M1) of newborn, young and adult pigs (Sus scrofa domesticus). Moreover, we investigated the distribution of the neural cells expressing the calcium-binding proteins (CaBPs) (calretinin, CR; parvalbumin, PV) throughout M1. The primary motor cortex of newborn piglets was characterized by a dense neuronal arrangement that made the discrimination of the cell layers difficult, except for layer one. The absence of a clearly recognizable layer four, typical of the agranular cortex, was noted in young and adult pigs. The morphometric and immunohistochemical analyses revealed age-associated changes characterized by (1) thickness increase and neuronal density (number of cells/mm2 of M1) reduction during the first year of life; (2) morphological changes of CR-immunoreactive neurons in the first months of life; (3) higher density of CR- and PV-immunopositive neurons in newborns when compared to young and adult pigs. Since most of the present findings match with those of the human M1, this study strengthens the growing evidence that the brain of the pig can be used as a potentially valuable translational animal model during growth and development.

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Physiological and Pathological Ageing of Astrocytes in the Human Brain

Neurochemical Research ◽

10.1007/s11064-021-03256-7 ◽

2021 ◽

Author(s):

Marloes Verkerke ◽

Elly M. Hol ◽

Jinte Middeldorp

Keyword(s):

Risk Factor ◽

Morphological Changes ◽

Ion Homeostasis ◽

Brain Functioning ◽

Physiological Ageing ◽

Human Astrocytes ◽

Age Related ◽

Technical Issues ◽

Neuronal Transmission ◽

Ageing Brain

AbstractAgeing is the greatest risk factor for dementia, although physiological ageing by itself does not lead to cognitive decline. In addition to ageing, APOE ε4 is genetically the strongest risk factor for Alzheimer’s disease and is highly expressed in astrocytes. There are indications that human astrocytes change with age and upon expression of APOE4. As these glial cells maintain water and ion homeostasis in the brain and regulate neuronal transmission, it is likely that age- and APOE4-related changes in astrocytes have a major impact on brain functioning and play a role in age-related diseases. In this review, we will discuss the molecular and morphological changes of human astrocytes in ageing and the contribution of APOE4. We conclude this review with a discussion on technical issues, innovations, and future perspectives on how to gain more knowledge on astrocytes in the human ageing brain.

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Chronic senescent human mesenchymal stem cells as possible contributor to the wound healing disorder after exposure to the alkylating agent sulfur mustard

Archives of Toxicology ◽

10.1007/s00204-020-02946-5 ◽

2021 ◽

Vol 95 (2) ◽

pp. 727-747

Author(s):

Simone Rothmiller ◽

Niklas Jäger ◽

Nicole Meier ◽

Thimo Meyer ◽

Adrian Neu ◽

...

Keyword(s):

Stem Cells ◽

Wound Healing ◽

Mesenchymal Stem Cells ◽

Alkylating Agent ◽

Chronic Wounds ◽

Sulfur Mustard ◽

Morphological Changes ◽

Human Mesenchymal Stem Cells ◽

Age Related

AbstractWound healing is a complex process, and disturbance of even a single mechanism can result in chronic ulcers developing after exposure to the alkylating agent sulfur mustard (SM). A possible contributor may be SM-induced chronic senescent mesenchymal stem cells (MSCs), unable to fulfil their regenerative role, by persisting over long time periods and creating a proinflammatory microenvironment. Here we show that senescence induction in human bone marrow derived MSCs was time- and concentration-dependent, and chronic senescence could be verified 3 weeks after exposure to between 10 and 40 µM SM. Morphological changes, reduced clonogenic and migration potential, longer scratch closure times, differences in senescence, motility and DNA damage response associated genes as well as increased levels of proinflammatory cytokines were revealed. Selective removal of these cells by senolytic drugs, in which ABT-263 showed initial potential in vitro, opens the possibility for an innovative treatment strategy for chronic wounds, but also tumors and age-related diseases.

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Effects of innate immune receptor stimulation on extracellular α-synuclein uptake and degradation by brain resident cells

Experimental & Molecular Medicine ◽

10.1038/s12276-021-00562-6 ◽

2021 ◽

Author(s):

Changyoun Kim ◽

Somin Kwon ◽

Michiyo Iba ◽

Brian Spencer ◽

Edward Rockenstein ◽

...

Keyword(s):

Degradation Kinetics ◽

Morphological Changes ◽

Direct Interaction ◽

Innate Immune ◽

Pathological Feature ◽

Tlr2 Expression ◽

Immune Receptors ◽

Age Related ◽

Stimulation Of

AbstractSynucleinopathies are age-related neurological disorders characterized by the progressive deposition of α-synuclein (α-syn) aggregates and include Parkinson’s disease (PD) and dementia with Lewy bodies (DLB). Although cell-to-cell α-syn transmission is thought to play a key role in the spread of α-syn pathology, the detailed mechanism is still unknown. Neuroinflammation is another key pathological feature of synucleinopathies. Previous studies have identified several immune receptors that mediate neuroinflammation in synucleinopathies, such as Toll-like receptor 2 (TLR2). However, the species of α-syn aggregates varies from study to study, and how different α-syn aggregate species interact with innate immune receptors has yet to be addressed. Therefore, we investigated whether innate immune receptors can facilitate the uptake of different species of α-syn aggregates. Here, we examined whether stimulation of TLRs could modulate the cellular uptake and degradation of α-syn fibrils despite a lack of direct interaction. We observed that stimulation of TLR2 in vitro accelerated α-syn fibril uptake in neurons and glia while delaying the degradation of α-syn in neurons and astrocytes. Internalized α-syn was rapidly degraded in microglia regardless of whether TLR2 was stimulated. However, cellular α-syn uptake and degradation kinetics were not altered by TLR4 stimulation. In addition, upregulation of TLR2 expression in a synucleinopathy mouse model increased the density of Lewy-body-like inclusions and induced morphological changes in microglia. Together, these results suggest that cell type-specific modulation of TLR2 may be a multifaceted and promising therapeutic strategy for synucleinopathies; inhibition of neuronal and astroglial TLR2 decreases pathogenic α-syn transmission, but activation of microglial TLR2 enhances microglial extracellular α-syn clearance.

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FUNCTIONAL METHODS OF EARLY DIAGNOSTICS OF AGE MACULAR DEGENERATION.(LITERATURE REVIEW)

UZBEK MEDICAL JOURNAL ◽

10.26739/2181-0664-2021-si-2-10 ◽

2021 ◽

Vol Special issue (2) ◽

pp. 61-67

Author(s):

Azamat Yusupov ◽

◽

Mukhiddin Ziyoviddinov ◽

Shavkat Mukhanov ◽

O.O. Sobirov

Keyword(s):

Literature Review ◽

Macular Degeneration ◽

Contrast Sensitivity ◽

Morphological Changes ◽

Pigment Epithelium ◽

Sensitivity Study ◽

Age Related Macular Degeneration ◽

Functional Diagnostics ◽

Advantages And Disadvantages ◽

Age Related

This article provides an unsystematic literature review devoted to analyzing the currently existing methods of functional diagnostics for age-related macular degeneration.The essence, advantages and disadvantages, and literature data on the use of such methods asphotostresstest, electrooculography, dark adaptation study, contrast sensitivity function assessment, light and color sensitivity study,electroretinographyand critical flicker fusion frequencyare described.Based on the analysis of literature data, itis shownthat currently, there is a need to searchfor informative and accessible methods of functional diagnostics in age-related macular degeneration, especially for its early diagnosis. The analysis has shown that the existing methods are mainly aimed either at fixing secondary morphological changes in the layer of pigment epithelial cells, at identifying the pathology of the pigment epithelium in conjunction with determining the function of photoreceptor elements, or at a comprehensive assessment of the structures of several layers of the retina. Keywords:age-related macular degeneration; methods of functional diagnostics; photostress test; electrooculography; contrast sensitivity

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Senescent Accelerated Prone 8 (SAMP8) Mice as A Model of Age Dependent Neuroinflammation

10.21203/rs.3.rs-72160/v1 ◽

2020 ◽

Author(s):

Andrés Fernández ◽

Elena Quintana ◽

Patricia Velasco ◽

Belén de Andrés ◽

Maria Luisa Gaspar ◽

...

Keyword(s):

Choroid Plexus ◽

Inflammatory Cytokines ◽

Hippocampal Formation ◽

Morphological Changes ◽

Interleukin 1 ◽

Brain Parenchyma ◽

Age Related ◽

Inflammatory Changes ◽

Samp8 Mice ◽

The Brain

Abstract Background: Aging and age related diseases are strong risk factors for the development of neurodegenerative diseases. Neuroinflammation (NIF), as the brain's immune response, plays an important role in aged associated degeneration of central nervous system (CNS). The need of animal models that will allow us to understand and modulate this process is required for the scientific community. Methods: We have analyzed aging-phenotypical and inflammatory changes of brain myeloid cells (bMyC) in a senescent accelerated prone aged (SAMP8) mouse model, and compared with their resistant to senescence control (SAMR1). We have performed morphometric methods to evaluate the architecture of cellular prolongations and analyzed Iba1+ clustered cells with aging. To analyse specific constant brain areas we have performed stereology measurements of Iba1+ cells in the hippocampal formation. We have isolated bMyC from brain parenchyma (BP) and choroid plexus and meningeal membranes (m/Ch), and analyzed their response to systemic LPS- driven inflammation.Results: Aged 10 month old SAMP8 mice presents many of the hallmarks of aging-dependent neuroinflammation when compared with their senescence resistant control (SAMR1); ie, increase of protein aggregates, presence of Iba1+ clusters, but not increase in the number of Iba1+ cells. We have further observed and increased of main inflammatory mediator IL-1β, and augment of border MHCII+Iba1+ cells. Isolated CD45+ bMyC from brain parenchyma (BP) and choroid plexus and meningeal membranes (m/Ch) have been analyzed showing that there is not significant increase of CD45+ from the periphery. Our data support that aged-driven pro-inflammatory cytokine interleukin 1 beta (IL1β) transcription is mainly enhanced in CD45+BP cells. Furthermore, we are showing that LPS-driven systemic inflammation produces inflammatory cytokines mainly in the border bMyC, sensed to a lesser extent by the BP bMyC, and is enhanced in aged SAMP8 compared to control SAMR1.Conclusion: Our data validate the SAMP8 model to study age-associated neuroinflammatory events, but careful controls for age and strain are required. These animals show morphological changes in their bMyC cell repertoires associated to age, corresponding to an increase in the production of main pro inflammatory cytokines such as IL-1β, which predispose the brain to an enhanced inflammatory response after LPS-systemic challenge.

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A Report of Two Cases of Age-Related Changes in Cervical Morphology in Postmenopausal Women with Vaginal Adenosis

Case Reports in Obstetrics and Gynecology ◽

10.1155/2017/9523853 ◽

2017 ◽

Vol 2017 ◽

pp. 1-4

Author(s):

Marguerite B. Vigliani

Keyword(s):

Middle Age ◽

Morphological Changes ◽

Pap Smears ◽

Squamocolumnar Junction ◽

Age Related ◽

Normal Cervix ◽

Vaginal Canal ◽

Endocervical Canal ◽

Over Time ◽

Age Related Changes

This paper presents two cases of women who had extensive vaginal adenosis from prenatal DES exposure, extending almost halfway down the vaginal canal. Both women were followed for decades with annual exams and Pap smears until after menopause. Clinical examination in both cases initially showed an absent pars vaginalis of the cervix, vaginal adenosis, and shallowness of the fornices. Several decades of annual exams showed these stigmata of DES exposure gradually disappear as the upper vagina progressively contracted. After menopause the upper vagina in both cases transformed into what appeared to be a normal cervix with all adenosis involuted into a normal endocervical canal. A timeline was created to show the morphological changes that were observed over time. This timeline illustrates how severe vaginal stenosis above the level of the squamocolumnar junction developed in middle age and was followed in the postmenopause by fusion of the upper vaginal walls in the midline resulting in the appearance of a normal, but prolapsed, cervix.

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