Multi-transcriptomic analysis points to early organelle dysfunction in human astrocytes in Alzheimer's disease
The phenotypic transformation of astrocytes in Alzheimer's disease (AD) is still not well understood. Recent analyses based on single-nucleus RNA sequencing of postmortem Alzheimer's disease (AD) samples are limited by the low number of sequenced astrocytes, small cohort sizes, and low num...
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| Published in | Neurobiology of disease Vol. 166; p. 105655 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
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United States
Elsevier Inc
01.05.2022
Elsevier |
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| Abstract | The phenotypic transformation of astrocytes in Alzheimer's disease (AD) is still not well understood. Recent analyses based on single-nucleus RNA sequencing of postmortem Alzheimer's disease (AD) samples are limited by the low number of sequenced astrocytes, small cohort sizes, and low number of differentially expressed genes detected. To optimize the detection of astrocytic genes, we employed a novel strategy consisting of the localization of pre-determined astrocyte and neuronal gene clusters in publicly available whole-brain transcriptomes. Specifically, we used cortical transcriptomes from 766 individuals, including cognitively normal subjects (Controls), and people diagnosed with mild cognitive impairment (MCI) or dementia due to AD. Samples came from three independent cohorts organized by the Mount Sinai Hospital, the Mayo Clinic, and the Religious Order Study/Memory and Aging Project (ROSMAP). Astrocyte- and neuron-specific gene clusters were generated from human brain cell-type specific RNAseq data using hierarchical clustering and cell-type enrichment scoring. Genes from each cluster were manually annotated according to cell-type specific functional Categories. Gene Set Variation Analysis (GSVA) and Principal Component Analysis (PCA) were used to establish changes in these functional categories among clinical cohorts. We highlight three novel findings of the study. First, individuals with the same clinical diagnosis were molecularly heterogeneous. Particularly in the Mayo Clinic and ROSMAP cohorts, over 50% of Controls presented down-regulation of genes encoding synaptic proteins typical of AD, whereas 30% of patients diagnosed with dementia due to AD presented Control-like transcriptomic profiles. Second, down-regulation of neuronal genes related to synaptic proteins coincided, in astrocytes, with up-regulation of genes related to perisynaptic astrocytic processes (PAP) and down-regulation of genes encoding endolysosomal and mitochondrial proteins. Third, down-regulation of astrocytic mitochondrial genes inversely correlated with the disease stages defined by Braak and CERAD scoring. Finally, we interpreted these changes as maladaptive or adaptive from the point of view of astrocyte biology in a model of the phenotypical transformation of astrocytes in AD. The main prediction is that early malfunction of the astrocytic endolysosomal system, associated with progressive mitochondrial dysfunction, contribute to Alzheimer's disease. If this prediction is correct, therapies preventing organelle dysfunction in astrocytes may be beneficial in preclinical and clinical AD.
[Display omitted]
•Detection of two molecular profiles in both control subjects and AD patients•Use of astrocyte-specific annotations and pre-clustered gene sets•Downregulation of endolysosome-related genes in early Braak/CERAD stages•Progressive downregulation of mitochondrion genes along Braak/CERAD stages•Astrocytic endolysosomes and mitochondria as therapeutic targets in AD |
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| AbstractList | The phenotypic transformation of astrocytes in Alzheimer's disease (AD) is still not well understood. Recent analyses based on single-nucleus RNA sequencing of postmortem Alzheimer's disease (AD) samples are limited by the low number of sequenced astrocytes, small cohort sizes, and low number of differentially expressed genes detected. To optimize the detection of astrocytic genes, we employed a novel strategy consisting of the localization of pre-determined astrocyte and neuronal gene clusters in publicly available whole-brain transcriptomes. Specifically, we used cortical transcriptomes from 766 individuals, including cognitively normal subjects (Controls), and people diagnosed with mild cognitive impairment (MCI) or dementia due to AD. Samples came from three independent cohorts organized by the Mount Sinai Hospital, the Mayo Clinic, and the Religious Order Study/Memory and Aging Project (ROSMAP). Astrocyte- and neuron-specific gene clusters were generated from human brain cell-type specific RNAseq data using hierarchical clustering and cell-type enrichment scoring. Genes from each cluster were manually annotated according to cell-type specific functional Categories. Gene Set Variation Analysis (GSVA) and Principal Component Analysis (PCA) were used to establish changes in these functional categories among clinical cohorts. We highlight three novel findings of the study. First, individuals with the same clinical diagnosis were molecularly heterogeneous. Particularly in the Mayo Clinic and ROSMAP cohorts, over 50% of Controls presented down-regulation of genes encoding synaptic proteins typical of AD, whereas 30% of patients diagnosed with dementia due to AD presented Control-like transcriptomic profiles. Second, down-regulation of neuronal genes related to synaptic proteins coincided, in astrocytes, with up-regulation of genes related to perisynaptic astrocytic processes (PAP) and down-regulation of genes encoding endolysosomal and mitochondrial proteins. Third, down-regulation of astrocytic mitochondrial genes inversely correlated with the disease stages defined by Braak and CERAD scoring. Finally, we interpreted these changes as maladaptive or adaptive from the point of view of astrocyte biology in a model of the phenotypical transformation of astrocytes in AD. The main prediction is that early malfunction of the astrocytic endolysosomal system, associated with progressive mitochondrial dysfunction, contribute to Alzheimer's disease. If this prediction is correct, therapies preventing organelle dysfunction in astrocytes may be beneficial in preclinical and clinical AD. The phenotypic transformation of astrocytes in Alzheimer’s disease (AD) is still not well understood. Recent analyses based on single-nucleus RNA sequencing of postmortem Alzheimer’s disease (AD) samples are limited by the low number of sequenced astrocytes, small cohort sizes, and low number of differentially expressed genes detected. To optimize the detection of astrocytic genes, we employed a novel strategy consisting of the localization of pre-determined astrocyte and neuronal gene clusters in publicly available whole-brain transcriptomes. Specifically, we used cortical transcriptomes from 766 individuals, including cognitively normal subjects (Controls), and people diagnosed with mild cognitive impairment (MCI) or dementia due to AD. Samples came from three independent cohorts organized by the Mount Sinai Hospital, the Mayo Clinic, and the Religious Order Study/Memory and Aging Project (ROSMAP). Astrocyte- and neuron-specific gene clusters were generated from human brain cell-type specific RNAseq data using hierarchical clustering and cell-type enrichment scoring. Genes from each cluster were manually annotated according to cell-type specific functional categories. Gene Set Variation Analysis (GSVA) and Principal Component Analysis (PCA) were used to establish changes in these functional categories among clinical cohorts. We highlight three novel findings of the study. First, individuals with the same clinical diagnosis were molecularly heterogeneous. Particularly in the Mayo Clinic and ROSMAP cohorts, over 50% of Controls presented down-regulation of genes encoding synaptic proteins typical of AD, whereas 30% of patients diagnosed with dementia due to AD presented Control-like transcriptomic profiles. Second, down-regulation of neuronal genes related to synaptic proteins coincided, in astrocytes, with up-regulation of genes related to perisynaptic astrocytic processes (PAP) and down-regulation of genes encoding endolysosomal and mitochondrial proteins. Third, down-regulation of astrocytic mitochondrial genes inversely correlated with the disease stages defined by Braak and CERAD scoring. Finally, we interpreted these changes as maladaptive or adaptive from the point of view of astrocyte biology in a model of the phenotypical transformation of astrocytes in AD. The main prediction is that early malfunction of the astrocytic endolysosomal system, associated with progressive mitochondrial dysfunction, contribute to Alzheimer’s disease. If this prediction is correct, therapies preventing organelle dysfunction in astrocytes may be beneficial in preclinical and clinical AD. The phenotypic transformation of astrocytes in Alzheimer's disease (AD) is still not well understood. Recent analyses based on single-nucleus RNA sequencing of postmortem Alzheimer's disease (AD) samples are limited by the low number of sequenced astrocytes, small cohort sizes, and low number of differentially expressed genes detected. To optimize the detection of astrocytic genes, we employed a novel strategy consisting of the localization of pre-determined astrocyte and neuronal gene clusters in publicly available whole-brain transcriptomes. Specifically, we used cortical transcriptomes from 766 individuals, including cognitively normal subjects (Controls), and people diagnosed with mild cognitive impairment (MCI) or dementia due to AD. Samples came from three independent cohorts organized by the Mount Sinai Hospital, the Mayo Clinic, and the Religious Order Study/Memory and Aging Project (ROSMAP). Astrocyte- and neuron-specific gene clusters were generated from human brain cell-type specific RNAseq data using hierarchical clustering and cell-type enrichment scoring. Genes from each cluster were manually annotated according to cell-type specific functional Categories. Gene Set Variation Analysis (GSVA) and Principal Component Analysis (PCA) were used to establish changes in these functional categories among clinical cohorts. We highlight three novel findings of the study. First, individuals with the same clinical diagnosis were molecularly heterogeneous. Particularly in the Mayo Clinic and ROSMAP cohorts, over 50% of Controls presented down-regulation of genes encoding synaptic proteins typical of AD, whereas 30% of patients diagnosed with dementia due to AD presented Control-like transcriptomic profiles. Second, down-regulation of neuronal genes related to synaptic proteins coincided, in astrocytes, with up-regulation of genes related to perisynaptic astrocytic processes (PAP) and down-regulation of genes encoding endolysosomal and mitochondrial proteins. Third, down-regulation of astrocytic mitochondrial genes inversely correlated with the disease stages defined by Braak and CERAD scoring. Finally, we interpreted these changes as maladaptive or adaptive from the point of view of astrocyte biology in a model of the phenotypical transformation of astrocytes in AD. The main prediction is that early malfunction of the astrocytic endolysosomal system, associated with progressive mitochondrial dysfunction, contribute to Alzheimer's disease. If this prediction is correct, therapies preventing organelle dysfunction in astrocytes may be beneficial in preclinical and clinical AD. [Display omitted] •Detection of two molecular profiles in both control subjects and AD patients•Use of astrocyte-specific annotations and pre-clustered gene sets•Downregulation of endolysosome-related genes in early Braak/CERAD stages•Progressive downregulation of mitochondrion genes along Braak/CERAD stages•Astrocytic endolysosomes and mitochondria as therapeutic targets in AD The phenotypic transformation of astrocytes in Alzheimer's disease (AD) is still not well understood. Recent analyses based on single-nucleus RNA sequencing of postmortem Alzheimer's disease (AD) samples are limited by the low number of sequenced astrocytes, small cohort sizes, and low number of differentially expressed genes detected. To optimize the detection of astrocytic genes, we employed a novel strategy consisting of the localization of pre-determined astrocyte and neuronal gene clusters in publicly available whole-brain transcriptomes. Specifically, we used cortical transcriptomes from 766 individuals, including cognitively normal subjects (Controls), and people diagnosed with mild cognitive impairment (MCI) or dementia due to AD. Samples came from three independent cohorts organized by the Mount Sinai Hospital, the Mayo Clinic, and the Religious Order Study/Memory and Aging Project (ROSMAP). Astrocyte- and neuron-specific gene clusters were generated from human brain cell-type specific RNAseq data using hierarchical clustering and cell-type enrichment scoring. Genes from each cluster were manually annotated according to cell-type specific functional Categories. Gene Set Variation Analysis (GSVA) and Principal Component Analysis (PCA) were used to establish changes in these functional categories among clinical cohorts. We highlight three novel findings of the study. First, individuals with the same clinical diagnosis were molecularly heterogeneous. Particularly in the Mayo Clinic and ROSMAP cohorts, over 50% of Controls presented down-regulation of genes encoding synaptic proteins typical of AD, whereas 30% of patients diagnosed with dementia due to AD presented Control-like transcriptomic profiles. Second, down-regulation of neuronal genes related to synaptic proteins coincided, in astrocytes, with up-regulation of genes related to perisynaptic astrocytic processes (PAP) and down-regulation of genes encoding endolysosomal and mitochondrial proteins. Third, down-regulation of astrocytic mitochondrial genes inversely correlated with the disease stages defined by Braak and CERAD scoring. Finally, we interpreted these changes as maladaptive or adaptive from the point of view of astrocyte biology in a model of the phenotypical transformation of astrocytes in AD. The main prediction is that early malfunction of the astrocytic endolysosomal system, associated with progressive mitochondrial dysfunction, contribute to Alzheimer's disease. If this prediction is correct, therapies preventing organelle dysfunction in astrocytes may be beneficial in preclinical and clinical AD.The phenotypic transformation of astrocytes in Alzheimer's disease (AD) is still not well understood. Recent analyses based on single-nucleus RNA sequencing of postmortem Alzheimer's disease (AD) samples are limited by the low number of sequenced astrocytes, small cohort sizes, and low number of differentially expressed genes detected. To optimize the detection of astrocytic genes, we employed a novel strategy consisting of the localization of pre-determined astrocyte and neuronal gene clusters in publicly available whole-brain transcriptomes. Specifically, we used cortical transcriptomes from 766 individuals, including cognitively normal subjects (Controls), and people diagnosed with mild cognitive impairment (MCI) or dementia due to AD. Samples came from three independent cohorts organized by the Mount Sinai Hospital, the Mayo Clinic, and the Religious Order Study/Memory and Aging Project (ROSMAP). Astrocyte- and neuron-specific gene clusters were generated from human brain cell-type specific RNAseq data using hierarchical clustering and cell-type enrichment scoring. Genes from each cluster were manually annotated according to cell-type specific functional Categories. Gene Set Variation Analysis (GSVA) and Principal Component Analysis (PCA) were used to establish changes in these functional categories among clinical cohorts. We highlight three novel findings of the study. First, individuals with the same clinical diagnosis were molecularly heterogeneous. Particularly in the Mayo Clinic and ROSMAP cohorts, over 50% of Controls presented down-regulation of genes encoding synaptic proteins typical of AD, whereas 30% of patients diagnosed with dementia due to AD presented Control-like transcriptomic profiles. Second, down-regulation of neuronal genes related to synaptic proteins coincided, in astrocytes, with up-regulation of genes related to perisynaptic astrocytic processes (PAP) and down-regulation of genes encoding endolysosomal and mitochondrial proteins. Third, down-regulation of astrocytic mitochondrial genes inversely correlated with the disease stages defined by Braak and CERAD scoring. Finally, we interpreted these changes as maladaptive or adaptive from the point of view of astrocyte biology in a model of the phenotypical transformation of astrocytes in AD. The main prediction is that early malfunction of the astrocytic endolysosomal system, associated with progressive mitochondrial dysfunction, contribute to Alzheimer's disease. If this prediction is correct, therapies preventing organelle dysfunction in astrocytes may be beneficial in preclinical and clinical AD. The phenotypic transformation of astrocytes in Alzheimer’s disease (AD) is still not well understood. Recentanalyses based on single-nucleus RNA sequencing of postmortem Alzheimer’s disease (AD) samples are limited bythe low number of sequenced astrocytes, small cohort sizes, and low number of differentially expressed genesdetected. To optimize the detection of astrocytic genes, we employed a novel strategy consisting of the localization of pre-determined astrocyte and neuronal gene clusters in publicly available whole-brain transcriptomes.Specifically, we used cortical transcriptomes from 766 individuals, including cognitively normal subjects(Controls), and people diagnosed with mild cognitive impairment (MCI) or dementia due to AD. Samples camefrom three independent cohorts organized by the Mount Sinai Hospital, the Mayo Clinic, and the Religious OrderStudy/Memory and Aging Project (ROSMAP). Astrocyte- and neuron-specific gene clusters were generated fromhuman brain cell-type specific RNAseq data using hierarchical clustering and cell-type enrichment scoring. Genesfrom each cluster were manually annotated according to cell-type specific functional Categories. Gene SetVariation Analysis (GSVA) and Principal Component Analysis (PCA) were used to establish changes in thesefunctional categories among clinical cohorts. We highlight three novel findings of the study. First, individualswith the same clinical diagnosis were molecularly heterogeneous. Particularly in the Mayo Clinic and ROSMAPcohorts, over 50% of Controls presented down-regulation of genes encoding synaptic proteins typical of AD,whereas 30% of patients diagnosed with dementia due to AD presented Control-like transcriptomic profiles.Second, down-regulation of neuronal genes related to synaptic proteins coincided, in astrocytes, with upregulation of genes related to perisynaptic astrocytic processes (PAP) and down-regulation of genes encoding endolysosomal and mitochondrial proteins. Third, down-regulation of astrocytic mitochondrial genes inverselycorrelated with the disease stages defined by Braak and CERAD scoring. Finally, we interpreted these changes asmaladaptive or adaptive from the point of view of astrocyte biology in a model of the phenotypical transformation of astrocytes in AD. The main prediction is that early malfunction of the astrocytic endolysosomal system, associated with progressive mitochondrial dysfunction, contribute to Alzheimer’s disease. If this prediction is correct, therapies preventing organelle dysfunction in astrocytes may be beneficial in preclinical and clinical AD. |
| ArticleNumber | 105655 |
| Author | Escartin, Carole Weinstock, Laura D. Pybus, Alyssa F. Galea, Elena Larramona-Arcas, Raquel Wood, Levi B. Giménez-Llort, Lydia |
| AuthorAffiliation | e. Departament de Psiquiatria i Medicina Forense, Universitat Autònoma de Barcelona, Bellaterra, 08193 Barcelona, Spain b. Departament de Bioquímica, Unitat de Bioquímica, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain f. Université Paris-Saclay, CEA, CNRS, MIRCen, Laboratoire des Maladies Neurodégénératives, 92265, Fontenay-aux-Roses, France a. Institut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra, 08193 Barcelona, Spain d. Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta, 30332 USA g. George W. Woodruff School of Mechanical Engineering and Parker H. Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, 30332 USA c. ICREA, 08010 Barcelona, Spain |
| AuthorAffiliation_xml | – name: b. Departament de Bioquímica, Unitat de Bioquímica, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain – name: c. ICREA, 08010 Barcelona, Spain – name: a. Institut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra, 08193 Barcelona, Spain – name: d. Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta, 30332 USA – name: e. Departament de Psiquiatria i Medicina Forense, Universitat Autònoma de Barcelona, Bellaterra, 08193 Barcelona, Spain – name: f. Université Paris-Saclay, CEA, CNRS, MIRCen, Laboratoire des Maladies Neurodégénératives, 92265, Fontenay-aux-Roses, France – name: g. George W. Woodruff School of Mechanical Engineering and Parker H. Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, 30332 USA |
| Author_xml | – sequence: 1 givenname: Elena surname: Galea fullname: Galea, Elena email: Elena.Galea@uab.es organization: Institut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra 08193, Barcelona, Spain – sequence: 2 givenname: Laura D. surname: Weinstock fullname: Weinstock, Laura D. organization: Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta 30332, USA – sequence: 3 givenname: Raquel surname: Larramona-Arcas fullname: Larramona-Arcas, Raquel organization: Institut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra 08193, Barcelona, Spain – sequence: 4 givenname: Alyssa F. surname: Pybus fullname: Pybus, Alyssa F. organization: Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta 30332, USA – sequence: 5 givenname: Lydia surname: Giménez-Llort fullname: Giménez-Llort, Lydia organization: Institut de Neurociències, Universitat Autònoma de Barcelona, Bellaterra 08193, Barcelona, Spain – sequence: 6 givenname: Carole surname: Escartin fullname: Escartin, Carole organization: Université Paris-Saclay, CEA, CNRS, MIRCen, Laboratoire des Maladies Neurodégénératives, 92265 Fontenay-aux-Roses, France – sequence: 7 givenname: Levi B. surname: Wood fullname: Wood, Levi B. email: levi.wood@me.gatech.edu organization: Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta 30332, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35143967$$D View this record in MEDLINE/PubMed https://cea.hal.science/cea-03872733$$DView record in HAL |
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| Keywords | MCI Mitochondria Astrocytes Perisynaptic astrocyte processes RNA seq Hierarchical clustering Alzheimer's disease |
| Language | English |
| License | This is an open access article under the CC BY-NC-ND license. Copyright © 2021. Published by Elsevier Inc. Distributed under a Creative Commons Attribution 4.0 International License: http://creativecommons.org/licenses/by/4.0 |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Current address R. Larramona: Celltec-UB, Departament de Biologia Cel.lular, Fisiologia i Immunologia, Universitat de Barcelona, 08028; Institut de Neurociències, Universitat de Barcelona, 08035, Barcelona, Spain. |
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| Snippet | The phenotypic transformation of astrocytes in Alzheimer's disease (AD) is still not well understood. Recent analyses based on single-nucleus RNA sequencing of... The phenotypic transformation of astrocytes in Alzheimer’s disease (AD) is still not well understood. Recentanalyses based on single-nucleus RNA sequencing of... The phenotypic transformation of astrocytes in Alzheimer’s disease (AD) is still not well understood. Recent analyses based on single-nucleus RNA sequencing of... |
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| SubjectTerms | Alzheimer Disease - metabolism Alzheimer's disease Astrocytes Astrocytes - metabolism Cognitive Dysfunction - complications Gene Expression Profiling Hierarchical clustering Humans Life Sciences MCI Mitochondria Neurons and Cognition Organelles - metabolism Perisynaptic astrocyte processes RNA seq Transcriptome |
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| Title | Multi-transcriptomic analysis points to early organelle dysfunction in human astrocytes in Alzheimer's disease |
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