المؤلفون: Hee Kyung Jin, Ji Woong Shin, Hyun Ju Lee, Janet Carter, Jae-sung Bae, Hyun Lee, Jong Kil Lee, Toshiro Sakamoto

المصدر: Neuroscience letters. 481(1)

مصطلحات موضوعية: Pathology, medicine.medical_specialty, Programmed cell death, Indoles, Hippocampus, Apoptosis, Hippocampal formation, medicine.disease_cause, Mesenchymal Stem Cell Transplantation, Mice, Fetus, Alzheimer Disease, medicine, In Situ Nick-End Labeling, Animals, Humans, Cells, Cultured, Neurons, Analysis of Variance, Amyloid beta-Peptides, Behavior, Animal, business.industry, General Neuroscience, Mesenchymal stem cell, Mesenchymal Stem Cells, medicine.disease, Embryo, Mammalian, Fetal Blood, Coculture Techniques, Transplantation, Mice, Inbred C57BL, Disease Models, Animal, Alzheimer's disease, Stem cell, business, Oxidative stress

الوصف: The neuropathological hallmarks of Alzheimer's disease (AD) include the presence of extracellular amyloid-beta peptide (Abeta) in the form of amyloid plaques in the brain parenchyma and neuronal loss. The mechanism associated with neuronal death by amyloid plaques is unclear but oxidative stress and glial activation has been implicated. Human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSCs) are being scrutinized as a potential therapeutic tool to prevent various neurodegenerative diseases including AD. However, the therapeutic impact of hUCB-MSCs in AD has not yet been reported. Here we undertook in vitro work to examine the potential impact of hUCB-MSCs treatment on neuronal loss using a paradigm of cultured hippocampal neurons treated with Abeta. We confirmed that hUCB-MSCs co-culture reduced the hippocampal apoptosis induced by Abeta treatment. Moreover, in an acute AD mouse model to directly test the efficacy of hUCB-MSCs treatment on AD-related cognitive and neuropathological outcomes, we demonstrated that markers of glial activation, oxidative stress and apoptosis levels were decreased in AD mouse brain. Interestingly, hUCB-MSCs treated AD mice demonstrated cognitive rescue with restoration of learning/memory function. These data suggest that hUCB-MSCs warrant further investigation as a potential therapeutic agent in AD.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b04512012daa5468a3695f1cf010c943Test
https://pubmed.ncbi.nlm.nih.gov/20600610Test

المؤلفون: Hee Kyung Jin, Jong Kil Lee, Jae-sung Bae

المصدر: Neuroscience letters. 450(2)

مصطلحات موضوعية: Pathology, medicine.medical_specialty, Central nervous system, Hippocampus, Cell Count, Mesenchymal Stem Cell Transplantation, Mice, Alzheimer Disease, Medicine, Animals, Bone Marrow Transplantation, Amyloid beta-Peptides, Microglia, business.industry, General Neuroscience, Dentate gyrus, Mesenchymal stem cell, Calcium-Binding Proteins, Microfilament Proteins, Brain, Transplantation, Mice, Inbred C57BL, Disease Models, Animal, medicine.anatomical_structure, Neuroglia, Stem cell, business

الوصف: The therapeutic potential of bone marrow-derived mesenchymal stem cells (BM-MSCs) has recently been explored in various pathological conditions of the central nervous system (CNS). However, the application of BM-MSCs in acutely induced Alzheimer's disease (AD) has not yet been reported. Herein the feasibility of using the BM-MSCs, as a therapeutic agent for AD has been tested. To assess this possibility, an acutely induced AD model induced by injecting amyloid-beta (Abeta) into the dentate gyrus (DG) of hippocampus of C57BL/6 mice was used. Intracerebral transplantation of BM-MSCs into the brain of an induced AD model reduced their Abeta levels when compared to sham-transplanted animals. The diminution of Abeta deposits was accompanied by the activation of microglia. In addition, the activated microglia was located near the Abeta deposits, and their morphology was changed from ramified to ameboid as a sign of microglial phagocytosis. This study provides evidence that BM-MSCs can promote the reduction of Abeta through the microglial activation in this acutely induced AD brain, suggesting a potential therapeutic agent against AD.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3d0b9457e9df01c050ad4905d84c30e0Test
https://pubmed.ncbi.nlm.nih.gov/19084047Test