Microglia changes associated to Alzheimer's disease pathology in aged chimpanzees
In Alzheimer's disease (AD), the brain's primary immune cells, microglia, become activated and are found in close apposition to amyloid beta (Aβ) protein plaques and neurofibrillary tangles (NFT). The present study evaluated microglia density and morphology in a large group of aged chimpan...
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| Published in: | Journal of comparative neurology (1911) Vol. 526; no. 18; pp. 2921 - 2936 |
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| Main Authors: | , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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15-12-2018
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| Abstract | In Alzheimer's disease (AD), the brain's primary immune cells, microglia, become activated and are found in close apposition to amyloid beta (Aβ) protein plaques and neurofibrillary tangles (NFT). The present study evaluated microglia density and morphology in a large group of aged chimpanzees (n = 20, ages 37–62 years) with varying degrees of AD‐like pathology. Using immunohistochemical and stereological techniques, we quantified the density of activated microglia and morphological variants (ramified, intermediate, and amoeboid) in postmortem chimpanzee brain samples from prefrontal cortex, middle temporal gyrus, and hippocampus, areas that show a high degree of AD pathology in humans. Microglia measurements were compared to pathological markers of AD in these cases. Activated microglia were consistently present across brain areas. In the hippocampus, CA3 displayed a higher density than CA1. Aβ42 plaque volume was positively correlated with higher microglial activation and with an intermediate morphology in the hippocampus. Aβ42‐positive vessel volume was associated with increased hippocampal microglial activation. Activated microglia density and morphology were not associated with age, sex, pretangle density, NFT density, or tau neuritic cluster density. Aged chimpanzees displayed comparable patterns of activated microglia phenotypes as well as an association of increased microglial activation and morphological changes with Aβ deposition similar to AD patients. In contrast to human AD brains, activated microglia density was not significantly correlated with tau lesions. This evidence suggests that the chimpanzee brain may be relatively preserved during normal aging processes but not entirely protected from neurodegeneration as previously assumed.
In Alzheimer's disease, microglia activation occurs near amyloid beta (Aβ) protein plaques and neurofibrillary tangles. Analyses of microglia densities in aged chimpanzee brains revealed increased microglial activation with greater Aβ42 plaque and vessel volumes, but not tau lesions, in the hippocampus, indicating chimpanzees are not entirely protected from neurodegeneration. |
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| AbstractList | In Alzheimer's disease (AD), the brain's primary immune cells, microglia, become activated and are found in close apposition to amyloid beta (Aβ) protein plaques and neurofibrillary tangles (NFT). The present study evaluated microglia density and morphology in a large group of aged chimpanzees (n = 20, ages 37–62 years) with varying degrees of AD‐like pathology. Using immunohistochemical and stereological techniques, we quantified the density of activated microglia and morphological variants (ramified, intermediate, and amoeboid) in postmortem chimpanzee brain samples from prefrontal cortex, middle temporal gyrus, and hippocampus, areas that show a high degree of AD pathology in humans. Microglia measurements were compared to pathological markers of AD in these cases. Activated microglia were consistently present across brain areas. In the hippocampus, CA3 displayed a higher density than CA1. Aβ42 plaque volume was positively correlated with higher microglial activation and with an intermediate morphology in the hippocampus. Aβ42‐positive vessel volume was associated with increased hippocampal microglial activation. Activated microglia density and morphology were not associated with age, sex, pretangle density, NFT density, or tau neuritic cluster density. Aged chimpanzees displayed comparable patterns of activated microglia phenotypes as well as an association of increased microglial activation and morphological changes with Aβ deposition similar to AD patients. In contrast to human AD brains, activated microglia density was not significantly correlated with tau lesions. This evidence suggests that the chimpanzee brain may be relatively preserved during normal aging processes but not entirely protected from neurodegeneration as previously assumed. In Alzheimer's disease (AD), the brain's primary immune cells, microglia, become activated and are found in close apposition to amyloid beta (Aβ) protein plaques and neurofibrillary tangles (NFT). The present study evaluated microglia density and morphology in a large group of aged chimpanzees (n = 20, ages 37–62 years) with varying degrees of AD‐like pathology. Using immunohistochemical and stereological techniques, we quantified the density of activated microglia and morphological variants (ramified, intermediate, and amoeboid) in postmortem chimpanzee brain samples from prefrontal cortex, middle temporal gyrus, and hippocampus, areas that show a high degree of AD pathology in humans. Microglia measurements were compared to pathological markers of AD in these cases. Activated microglia were consistently present across brain areas. In the hippocampus, CA3 displayed a higher density than CA1. Aβ42 plaque volume was positively correlated with higher microglial activation and with an intermediate morphology in the hippocampus. Aβ42‐positive vessel volume was associated with increased hippocampal microglial activation. Activated microglia density and morphology were not associated with age, sex, pretangle density, NFT density, or tau neuritic cluster density. Aged chimpanzees displayed comparable patterns of activated microglia phenotypes as well as an association of increased microglial activation and morphological changes with Aβ deposition similar to AD patients. In contrast to human AD brains, activated microglia density was not significantly correlated with tau lesions. This evidence suggests that the chimpanzee brain may be relatively preserved during normal aging processes but not entirely protected from neurodegeneration as previously assumed. In Alzheimer's disease, microglia activation occurs near amyloid beta (Aβ) protein plaques and neurofibrillary tangles. Analyses of microglia densities in aged chimpanzee brains revealed increased microglial activation with greater Aβ42 plaque and vessel volumes, but not tau lesions, in the hippocampus, indicating chimpanzees are not entirely protected from neurodegeneration. In Alzheimer's disease (AD), the brain's primary immune cells, microglia, become activated and are found in close apposition to amyloid beta (Aβ) protein plaques and neurofibrillary tangles (NFT). The present study evaluated microglia density and morphology in a large group of aged chimpanzees ( n = 20, ages 37–62 years) with varying degrees of AD‐like pathology. Using immunohistochemical and stereological techniques, we quantified the density of activated microglia and morphological variants (ramified, intermediate, and amoeboid) in postmortem chimpanzee brain samples from prefrontal cortex, middle temporal gyrus, and hippocampus, areas that show a high degree of AD pathology in humans. Microglia measurements were compared to pathological markers of AD in these cases. Activated microglia were consistently present across brain areas. In the hippocampus, CA3 displayed a higher density than CA1. Aβ42 plaque volume was positively correlated with higher microglial activation and with an intermediate morphology in the hippocampus. Aβ42‐positive vessel volume was associated with increased hippocampal microglial activation. Activated microglia density and morphology were not associated with age, sex, pretangle density, NFT density, or tau neuritic cluster density. Aged chimpanzees displayed comparable patterns of activated microglia phenotypes as well as an association of increased microglial activation and morphological changes with Aβ deposition similar to AD patients. In contrast to human AD brains, activated microglia density was not significantly correlated with tau lesions. This evidence suggests that the chimpanzee brain may be relatively preserved during normal aging processes but not entirely protected from neurodegeneration as previously assumed. In Alzheimer’s disease (AD), the brain’s primary immune cells microglia become activated and are found in close apposition to amyloid beta (Aβ) protein plaques and neurofibrillary tangles (NFT). The present study evaluated microglia density and morphology in a large group of aged chimpanzees (n = 20, ages 37-62 years) with varying degrees of AD-like pathology. Using immunohistochemical and stereological techniques, we quantified the density of activated microglia and morphological variants (ramified, intermediate, and amoeboid) in postmortem chimpanzee brain samples from prefrontal cortex, middle temporal gyrus, and hippocampus, areas that show a high degree of AD pathology in humans. Microglia measurements were compared to pathological markers of AD in these cases. Activated microglia densities were consistently present across brain areas. In the hippocampus, CA3 displayed a higher density than CA1. Aβ42 plaque volume was positively correlated with higher microglial activation and with an intermediate morphology in the hippocampus. Aβ42-positive vessel volume was associated with increased hippocampal microglial activation. Activated microglia density and morphology were not associated with age, sex, pretangle density, NFT density, or tau neuritic cluster density. Aged chimpanzees displayed comparable patterns of activated microglia phenotypes as well as an association of increased microglial activation and morphological changes similar to AD patients. In contrast to human AD brains, activated microglia density was not significantly correlated with tau lesions. This evidence suggests that the chimpanzee brain may be relatively preserved during normal aging processes but not entirely protected from neurodegeneration as previously assumed. In Alzheimer’s disease, microglia activation occurs near amyloid beta (Aβ) protein plaques and neurofibrillary tangles. Analyses of microglia densities in aged chimpanzee brains revealed increased microglial activation with greater Aβ42 plaque and vessel volumes, but not tau lesions, in the hippocampus, indicating chimpanzees are not entirely protected from neurodegeneration. |
| Author | Mufson, Elliott J. Raghanti, Mary Ann Munger, Emily L. Meindl, Richard S. Erwin, Joseph M. Hof, Patrick R. Edler, Melissa K. Sherwood, Chet C. Ely, John J. Hopkins, William D. Perl, Daniel P. |
| AuthorAffiliation | g MAEBIOS, Alamogordo, NM 88310 i Departments of Neurobiology and Neurology, Barrow Neurological Institute, Phoenix, AZ 85013 a School of Biomedical Sciences, Kent State University, Kent, OH 44242 f Neuroscience Institute, Georgia State University, Atlanta, GA 30302 e Division of Developmental and Cognitive Neuroscience, Yerkes National Primate Research Center, Atlanta, GA 30322 k New York Consortium for Evolutionary Primatology, New York, NY 10468 d Department of Anthropology, Kent State University, Kent, OH 44242 c Department of Anthropology and Center for the Advanced Study of Human Paleobiology, The George Washington University, Washington, DC 20052 h Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814 b Department of Pharmaceutical Sciences, Northeast Ohio Medical University, Rootstown, OH 44272 j Fishberg Department of Neuroscience, Ronald M. Loeb Center for Alzheimer’s Disease, and Friedman Brain Institute, Icahn School of Medicine at Mount Si |
| AuthorAffiliation_xml | – name: a School of Biomedical Sciences, Kent State University, Kent, OH 44242 – name: c Department of Anthropology and Center for the Advanced Study of Human Paleobiology, The George Washington University, Washington, DC 20052 – name: k New York Consortium for Evolutionary Primatology, New York, NY 10468 – name: b Department of Pharmaceutical Sciences, Northeast Ohio Medical University, Rootstown, OH 44272 – name: h Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814 – name: d Department of Anthropology, Kent State University, Kent, OH 44242 – name: g MAEBIOS, Alamogordo, NM 88310 – name: i Departments of Neurobiology and Neurology, Barrow Neurological Institute, Phoenix, AZ 85013 – name: f Neuroscience Institute, Georgia State University, Atlanta, GA 30302 – name: j Fishberg Department of Neuroscience, Ronald M. Loeb Center for Alzheimer’s Disease, and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029 – name: e Division of Developmental and Cognitive Neuroscience, Yerkes National Primate Research Center, Atlanta, GA 30322 |
| Author_xml | – sequence: 1 givenname: Melissa K. surname: Edler fullname: Edler, Melissa K. email: medler@neomed.edu organization: Northeast Ohio Medical University – sequence: 2 givenname: Chet C. surname: Sherwood fullname: Sherwood, Chet C. organization: The George Washington University – sequence: 3 givenname: Richard S. surname: Meindl fullname: Meindl, Richard S. organization: Kent State University – sequence: 4 givenname: Emily L. surname: Munger fullname: Munger, Emily L. organization: Kent State University – sequence: 5 givenname: William D. surname: Hopkins fullname: Hopkins, William D. organization: Georgia State University – sequence: 6 givenname: John J. surname: Ely fullname: Ely, John J. organization: MAEBIOS – sequence: 7 givenname: Joseph M. surname: Erwin fullname: Erwin, Joseph M. organization: The George Washington University – sequence: 8 givenname: Daniel P. surname: Perl fullname: Perl, Daniel P. organization: Uniformed Services University of the Health Sciences – sequence: 9 givenname: Elliott J. surname: Mufson fullname: Mufson, Elliott J. organization: Barrow Neurological Institute – sequence: 10 givenname: Patrick R. surname: Hof fullname: Hof, Patrick R. organization: New York Consortium for Evolutionary Primatology – sequence: 11 givenname: Mary Ann surname: Raghanti fullname: Raghanti, Mary Ann organization: Kent State University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30069930$$D View this record in MEDLINE/PubMed |
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| Keywords | RRID: AB_2313952 amyloid beta protein RRID: AB_223647 neuroinflammation neurofibrillary tangle RRID: AB_2313890 chimpanzee RRID: AB_839504 Alzheimer's disease RRID: AB_2315150 microglia |
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| Snippet | In Alzheimer's disease (AD), the brain's primary immune cells, microglia, become activated and are found in close apposition to amyloid beta (Aβ) protein... In Alzheimer’s disease (AD), the brain’s primary immune cells microglia become activated and are found in close apposition to amyloid beta (Aβ) protein plaques... |
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| SubjectTerms | Aging Aging - pathology Alzheimer Disease - pathology Alzheimer's disease amyloid beta protein Animals Apposition Autopsy Brain Brain - pathology chimpanzee Cortex (temporal) Female Hippocampus Male Microglia Microglia - pathology Morphology Neurodegeneration Neurodegenerative diseases neurofibrillary tangle Neurofibrillary tangles Neurofibrillary Tangles - pathology neuroinflammation Pan troglodytes Pathology Phenotypes Plaque, Amyloid - pathology Plaques Prefrontal cortex RRID: AB_223647 RRID: AB_2313890 RRID: AB_2313952 RRID: AB_2315150 RRID: AB_839504 Tau protein Temporal gyrus |
| Title | Microglia changes associated to Alzheimer's disease pathology in aged chimpanzees |
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