Background: We previously demonstrated the normal mouse epididymal lumen contains a non-pathological amyloid matrix that surrounds spermatozoa and plays important roles in sperm maturation and protection.
Objective: The objective herein was to present a review of this work, including studies showing the amyloid structures of four members of the CRES (cystatin-related epididymal spermatogenic) subgroup are integral and essential components of the amyloid matrix.
Methods: We used conformation-dependent reagents that recognize the cross-β-sheet structure characteristic of amyloid, including thioflavin S (ThS), thioflavin T (ThT), anti-amyloid antibodies, and X-ray diffraction, as well as negative-stain transmission electron microscopy (TEM) to visualize amyloid structures in the epididymal lumen. Antibodies that specifically detect each CRES subgroup family member were also used in indirect immunofluorescence analysis.
Results And Discussion: The epididymal lumen contains an amyloid matrix that surrounds maturing spermatozoa and represents a functional amyloid. Alterations in the structure of the amyloid matrix by the loss of the CRES subgroup members or the overexpression of cystatin C result in epididymal pathologies, including infertility. Preliminary data suggest the epididymal amyloid matrix is structurally and functionally similar to bacterial biofilms.
Conclusion: Together, these results suggest the amyloid matrix serves important roles in epididymal function including sperm maturation and protection.
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http://dx.doi.org/10.1111/andr.12586 | DOI Listing |
Bioengineering (Basel)
January 2025
Division of Ultrahigh Field MRI, Iwate Medical University, 1-1-1 Idaidori, Yahaba 028-3694, Japan.
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View Article and Find Full Text PDFBBA Adv
December 2024
Department of Bioscience and Bioengineering, Indian Institute of Technology Jodhpur, NH 65, Nagaur Road, Karwar, Rajasthan 342037, India.
Biofilm is an assemblage of microorganisms embedded within the extracellular matrix that provides mechanical stability, nutrient absorption, antimicrobial resistance, cell-cell interactions, and defence against host immune system. Various biomolecules such as lipids, carbohydrates, protein polymers (amyloid), and eDNA are present in the matrix playing significant role in determining the distinctive properties of biofilm. The formation of biofilms contributes to resistance against antimicrobial therapy in most of the human infections and exacerbates existing diseases.
View Article and Find Full Text PDFActa Neuropathol
January 2025
Department of Neurology, NYU Grossman School of Medicine, New York, NY, USA.
Down syndrome (DS) is strongly associated with Alzheimer's disease (AD) due to APP overexpression, exhibiting Amyloid-β (Aβ) and Tau pathology similar to early-onset (EOAD) and late-onset AD (LOAD). We evaluated the Aβ plaque proteome of DS, EOAD, and LOAD using unbiased localized proteomics on post-mortem paraffin-embedded tissues from four cohorts (n = 20/group): DS (59.8 ± 4.
View Article and Find Full Text PDFNeural Regen Res
January 2025
Department of Developmental Cell Biology, Key Laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, Liaoning Province, China.
Amyloid-beta clearance plays a key role In the pathogenesis of Alzheimer's disease. However, the variation in functional proteins involved in amyloid-beta clearance and their correlation with amyloid-beta levels remain unclear. In this study, we conducted meta-analyses and a systematic review using studies from the PubMed, Embase, Web of Science, and Cochrane Library databases, including journal articles published from inception to June 30, 2023.
View Article and Find Full Text PDFAlzheimer's disease (AD) is the most prevalent neurodegenerative dementia, marked by progressive cognitive decline and memory impairment. Despite advances in therapeutic research, single-target-directed treatments often fall short in addressing the complex, multifactorial nature of AD. This arises from various pathological features, including amyloid-β (Aβ) aggregate deposition, metal ion dysregulation, oxidative stress, impaired neurotransmission, neuroinflammation, mitochondrial dysfunction, and neuronal cell death.
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