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The gliocentric brain = phenotype plasticity of the damaged brain /

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	The gliocentric brain/ by Wolfgang Walz.
其他題名:	phenotype plasticity of the damaged brain /
作者:	Walz, Wolfgang.
出版者:	Cham :Springer International Publishing : : 2023.,
面頁冊數:	ix, 249 p. :ill., digital ; : 24 cm.;
Contained By:	Springer Nature eBook
標題:	Neuroglia. -
電子資源:	https://doi.org/10.1007/978-3-031-48105-5
ISBN:	9783031481055

The gliocentric brain = phenotype plasticity of the damaged brain /
Walz, Wolfgang.

The gliocentric brainphenotype plasticity of the damaged brain /[electronic resource] :by Wolfgang Walz. - Cham :Springer International Publishing :2023. - ix, 249 p. :ill., digital ;24 cm.

1. Introduction -- 2. The Brain as an Organ -- 3. Life Cycle -- 4. Reactive Microglia and Astrocyte Phenotype Transitions. 5. Transition of Microglia to Reactive States -- 6. Reactive Astrocytes -- 7. Neuroinflammation -- 8. The Brain and the Immune System -- 9. Viral and Bacterial Infections -- 10. Autoimmune Reactions -- 11. Adult Glial Cell Proliferation and Neurogenesis -- 12. Glioma -- 13. Neurodegenerative Disorders -- 14. Vascular Diseases -- 15. Seizures -- 16. Traumatic Brain Injury -- 17. Major Psychiatric Disorders -- 18. Glia in Recovery Processes and Repair -- 19. Glial Phenotype Plasticity.

The brain is the body's most vulnerable organ due to the defined roles of neurons within circuits. Neurons are vastly outnumbered by microglia, astrocytes, oligodendrocytes, macrophages, cells of the blood brain barrier and invading immune cells. These cells display different grades of reactivities and interactions. They integrate their responses and not only change phenotypes but can also completely reprogram after damage to protect the neuronal complexity. The interactions of these satellite cells in the healthy brain are described as well as their roles in all major brain diseases. Special emphasis is put on immune system - brain interactions and regenerative and repair processes. The gliotic response is compared with the reactions to injuries of the skin and other organs. A final chapter addresses the definition of a cell type. It concludes that cell types can no longer be regarded as defined entities over the body's lifetime but are prone to phenotype plasticity and even complete reprograming.

ISBN: 9783031481055

Standard No.: 10.1007/978-3-031-48105-5doiSubjects--Topical Terms:

582989
Neuroglia.

LC Class. No.: QP363.2

Dewey Class. No.: 612.81046

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505 0 $a 1. Introduction -- 2. The Brain as an Organ -- 3. Life Cycle -- 4. Reactive Microglia and Astrocyte Phenotype Transitions. 5. Transition of Microglia to Reactive States -- 6. Reactive Astrocytes -- 7. Neuroinflammation -- 8. The Brain and the Immune System -- 9. Viral and Bacterial Infections -- 10. Autoimmune Reactions -- 11. Adult Glial Cell Proliferation and Neurogenesis -- 12. Glioma -- 13. Neurodegenerative Disorders -- 14. Vascular Diseases -- 15. Seizures -- 16. Traumatic Brain Injury -- 17. Major Psychiatric Disorders -- 18. Glia in Recovery Processes and Repair -- 19. Glial Phenotype Plasticity.
520 $a The brain is the body's most vulnerable organ due to the defined roles of neurons within circuits. Neurons are vastly outnumbered by microglia, astrocytes, oligodendrocytes, macrophages, cells of the blood brain barrier and invading immune cells. These cells display different grades of reactivities and interactions. They integrate their responses and not only change phenotypes but can also completely reprogram after damage to protect the neuronal complexity. The interactions of these satellite cells in the healthy brain are described as well as their roles in all major brain diseases. Special emphasis is put on immune system - brain interactions and regenerative and repair processes. The gliotic response is compared with the reactions to injuries of the skin and other organs. A final chapter addresses the definition of a cell type. It concludes that cell types can no longer be regarded as defined entities over the body's lifetime but are prone to phenotype plasticity and even complete reprograming.
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