Astrocytes in Alzheimer's Disease: Pathological Significance and Molecular Pathways.
|
IF: 7.666
|
Cited by: 18
|
Abstract
Astrocytes perform a wide variety of essential functions defining normal operation of the nervous system and are active contributors to the pathogenesis of neurodegenerative disorders such as Alzheimer's among others. Recent data provide compelling evidence that distinct astrocyte states are associated with specific stages of Alzheimer´s disease. The advent of transcriptomics technologies enables rapid progress in the characterisation of such pathological astrocyte states. In this review, we provide an overview of the origin, main functions, molecular and morphological features of astrocytes in physiological as well as pathological conditions related to Alzheimer´s disease. We will also explore the main roles of astrocytes in the pathogenesis of Alzheimer´s disease and summarize main transcriptional changes and altered molecular pathways observed in astrocytes during the course of the disease.
Recommend literature
1. The Many Faces of Astrocytes in Alzheimer's Disease.
2. An Overview of Astrocyte Responses in Genetically Induced Alzheimer's Disease Mouse Models.
3. Different Flavors of Astrocytes: Revising the Origins of Astrocyte Diversity and Epigenetic Signatures to Understand Heterogeneity after Injury.
4. Protective Functions of Reactive Astrocytes Following Central Nervous System Insult.
5. Astrocytes in Alzheimer's Disease: Pathological Significance and Molecular Pathways.
Similar data
1. Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and -independent cellular responses in Alzheimer’s disease
2. Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and -independent cellular responses in Alzheimer’s disease [15 months]
3. Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and -independent cellular responses in Alzheimer’s disease [7 months]
4. Microarray analysis of the astrocyte transcriptome in the ageing brain: relationship to Alzheimer's pathology and ApoE genotype
5. LPS and brain inflammation