Microglial Transforming Growth Factor-β Signaling in Alzheimer’s Disease
Novel technologies such as single-cell RNA and single-nucleus RNA sequencing have shed new light on the complexity of different microglia populations in physiological and pathological states. The transcriptomic profiling of these populations has led to the subclassification of specific disease-assoc...
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| Format: | Article |
| Language: | English |
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MDPI AG
2024-03-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/25/6/3090 |
| _version_ | 1797240770871164928 |
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| author | Natascha Vidovic Björn Spittau |
| author_facet | Natascha Vidovic Björn Spittau |
| author_sort | Natascha Vidovic |
| collection | DOAJ |
| description | Novel technologies such as single-cell RNA and single-nucleus RNA sequencing have shed new light on the complexity of different microglia populations in physiological and pathological states. The transcriptomic profiling of these populations has led to the subclassification of specific disease-associated microglia and microglia clusters in neurodegenerative diseases. A common profile includes the downregulation of homeostasis and the upregulation of inflammatory markers. Furthermore, there is concordance in few clusters between murine and human samples. Apolipoprotein E, which has long been considered a high-risk factor for late-onset Alzheimer’s disease, is strongly regulated in both these murine and human clusters. Transforming growth factor-β plays an essential role during the development and maturation of microglia. In a pathological state, it attenuates their activation and is involved in numerous cell regulatory processes. Transforming growth factor-β also has an influence on the deposition of amyloid-beta, as it is involved in the regulation of key proteins and molecules. Taken together, this review highlights the complex interaction of apolipoprotein E, the triggering receptor on myeloid cells 2, and transforming growth factor-β as part of a regulatory axis in microglia at the onset and over the course of Alzheimer’s disease. |
| first_indexed | 2024-04-24T18:12:43Z |
| format | Article |
| id | doaj.art-b81e14d2052049089c1bce69c3e03cc7 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-04-24T18:12:43Z |
| publishDate | 2024-03-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-b81e14d2052049089c1bce69c3e03cc72024-03-27T13:45:02ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672024-03-01256309010.3390/ijms25063090Microglial Transforming Growth Factor-β Signaling in Alzheimer’s DiseaseNatascha Vidovic0Björn Spittau1Anatomy and Cell Biology, Medical School OWL, Bielefeld University, 33615 Bielefeld, GermanyAnatomy and Cell Biology, Medical School OWL, Bielefeld University, 33615 Bielefeld, GermanyNovel technologies such as single-cell RNA and single-nucleus RNA sequencing have shed new light on the complexity of different microglia populations in physiological and pathological states. The transcriptomic profiling of these populations has led to the subclassification of specific disease-associated microglia and microglia clusters in neurodegenerative diseases. A common profile includes the downregulation of homeostasis and the upregulation of inflammatory markers. Furthermore, there is concordance in few clusters between murine and human samples. Apolipoprotein E, which has long been considered a high-risk factor for late-onset Alzheimer’s disease, is strongly regulated in both these murine and human clusters. Transforming growth factor-β plays an essential role during the development and maturation of microglia. In a pathological state, it attenuates their activation and is involved in numerous cell regulatory processes. Transforming growth factor-β also has an influence on the deposition of amyloid-beta, as it is involved in the regulation of key proteins and molecules. Taken together, this review highlights the complex interaction of apolipoprotein E, the triggering receptor on myeloid cells 2, and transforming growth factor-β as part of a regulatory axis in microglia at the onset and over the course of Alzheimer’s disease.https://www.mdpi.com/1422-0067/25/6/3090neurodegenerative diseasesAlzheimer’s diseaseamyloid betamicrogliaTGFβhippocampus |
| spellingShingle | Natascha Vidovic Björn Spittau Microglial Transforming Growth Factor-β Signaling in Alzheimer’s Disease International Journal of Molecular Sciences neurodegenerative diseases Alzheimer’s disease amyloid beta microglia TGFβ hippocampus |
| title | Microglial Transforming Growth Factor-β Signaling in Alzheimer’s Disease |
| title_full | Microglial Transforming Growth Factor-β Signaling in Alzheimer’s Disease |
| title_fullStr | Microglial Transforming Growth Factor-β Signaling in Alzheimer’s Disease |
| title_full_unstemmed | Microglial Transforming Growth Factor-β Signaling in Alzheimer’s Disease |
| title_short | Microglial Transforming Growth Factor-β Signaling in Alzheimer’s Disease |
| title_sort | microglial transforming growth factor β signaling in alzheimer s disease |
| topic | neurodegenerative diseases Alzheimer’s disease amyloid beta microglia TGFβ hippocampus |
| url | https://www.mdpi.com/1422-0067/25/6/3090 |
| work_keys_str_mv | AT nataschavidovic microglialtransforminggrowthfactorbsignalinginalzheimersdisease AT bjornspittau microglialtransforminggrowthfactorbsignalinginalzheimersdisease |