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Overexpression of miR17 ~ 92 in Myeloid Cells in Mice Increased Bone Mass Through Reduced Bone Resorption and Increased Bone Formation in Sex-Dependent Manner.
Calcif Tissue Int
January 2025
Jerry L. Pettis Memorial VA Medical Center, VA Loma Linda Healthcare System, Loma Linda, CA, USA.
This study assessed the feasibility of miR17 ~ 92-based antiresorptive strategy by determining the effects of conditional transgenic (cTG) overexpression of miR17 ~ 92 in myeloid cells on bone and osteoclasts. Osteoclasts of male and female cTG mutant mice each showed 3- to fivefold overexpression of miR17 ~ 92 cluster genes compared to those of age- and sex-matched wildtype (WT) littermates. Male but not female cTG mutant mice had more trabecular and cortical bones as well as lower bone resorption reflected by reduction in osteoclast number and resorbing surface.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Institute of Neurosciences, University of Barcelona, Barcelona, Catalunya, Spain.
Background: Senescence is a cellular response to stress or damage leading to a state of irreversible growth arrest. As we age, the number of senescent cells increases and directly contributes to age-related conditions including cancer and neurodegenerative diseases. As a result, there is a growing interest to therapeutically target senescence either with drugs eliminating senescent cells (senolytics) or with strategies to modulate their secretory phenotype among others.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Background: Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by hallmark pathologies that affect many brain regions, including the cellular microenvironment with the hippocampus, ultimately leading to profound deficits in cognition. Surprising recent work has shown that factors in the systemic environment regulate the hippocampal cellular niche; age-associated blood-borne factors exacerbate brain aging phenotypes, whereas youth-associated blood-borne factors, including tissue inhibitor of metalloproteinases 2 (TIMP2), reverse or ameliorate features of brain aging. As aging serves as the major risk factor for AD, and recent work shows that systemic factors can regulate AD pathology, we sought to characterize mechanisms by which the systemic environment regulates CNS phenotypes relevant to AD pathology through changes in neuroinflammation.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Institute of Brain Sciene, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Background: Genome-wide association studies demonstrated that immune suppressive receptor CD33 variants are associated with high susceptibility to developing Alzheimer's disease (AD). Human CD33 (hCD33) regulates microglial immune response and clearance ability. However, the differential regulation of phagocytosis by human and mouse CD33 imposes constraints on utilizing the mouse model for investigating the role of CD33 in AD.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Brigham and Women's Hospital; Harvard Medical School, Boston, MA, USA.
Background: Previously, we found that germline C3 deletion protected cognition and hippocampal synapses in aged APP/PS1dE9 mice, despite increasing Aß plaques. Here, we crossed our C3 inducible conditional mouse model to APP knockin mice to determine whether global C3 lowering in an adult amyloid mouse model would be protective.
Methods: C3;Rosa26-Cre-ERT2 (C3iKO) mice were crossed to C3;APP mice to generate APP;C3iKO mice, which received 75 mg/kg tamoxifen (TAM; n = 16) or corn oil (CO; n = 15) for 5 days at 3.
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