Cited by 123Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology Research

The DOI matches its Crossref record; 126 of the 127 references it cites were found in a registry or an index.

The Many Faces of Astrocytes in Alzheimer's Disease

Open access
Monterey, Michael D., Wei, Haichao, Wu, Xizi, Wu, Jia Qian·2021·Frontiers in Neurology

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease and is the most common cause of dementia in an aging population. The majority of research effort has focused on the role of neurons in neurodegeneration and current therapies have limited ability to slow disease progression. Recently more attention has been given to the role of astrocytes in the process of neurodegeneration. Specifically, reactive astrocytes have both advantageous and adverse effects during neurodegeneration. The ability to isolate and depict astrocyte phenotype has been challenging. However, with the recent development of single-cell sequencing technologies researchers are provided with the resource to delineate specific biomarkers associated with reactive astrocytes in AD. In this review, we will focus on the role of astrocytes in normal conditions and the pathological development of AD. We will further review recent developments in the understanding of astrocyte heterogeneity and associated biomarkers. A better understanding of astrocyte contributions and phenotypic changes in AD can ultimately lead to more effective therapeutic targets.

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Crossref · 10.3389/fneur.2021.619626

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Figures

Figure 1 Examples of roles of astrocytes in normal condition and in AD. The left half of astrocyte (yellow) depicts normal astrocyte functions, including neurotransmitter recycling (U-turn arrow and brown-outlined circles), synaptogenesis, central nerve system (CNS) homeostasis, and interaction with vasculature. The right half of astrocyte (Pink) depicts a reactive astrocyte in Alzheimer's Disease (AD). The black box contains some examples of the astrocytic signaling pathways related to AD. Green box indicates examples of inducing factors of reactive astrocytes from microglia. Red boxes are the representative intracellular and secretory molecules (red-outlined circles) and astrocytic makers expressed by reactive astrocytes in AD. Blue circles with icons are synapses. K+, potassium; AQP4, aquaporin-4; Kir4.1, inwardly rectifying K+ channel subunit 4.1; APP, amyloid-beta precursor protein; BACE1, β-site APP-cleaving enzyme 1; FFA, free fatty acid; GFAP, glial fibrillary acidic protein; YKL-40, chitinase-3 protein like-1; S100B, S100 calcium-binding protein B; MAOB, monoamine-oxidase-b; GLAST, glutamate aspartate transporter; GLT-1, glutamate transporter 1; Ca2+, calcium; NF-κB, nuclear factor- kappa B; Stat3, signal transducer and activator of transcription 3; AGEs, advance glycation end-products; RAGE, Receptor for advanced glycation end products; TGF-β, transforming growth factor beta; GABA, gamma-aminobutyric acid; IL, interleukin; TNF-α, tumor necrosis factor alpha; C1q, complement component 1q.
Figure 1 Examples of roles of astrocytes in normal condition and in AD. The left half of astrocyte (yellow) depicts normal astrocyte functions, including neurotransmitter recycling (U-turn arrow and brown-outlined circles), synaptogenesis, central nerve system (CNS) homeostasis, and interaction with vasculature. The right half of astrocyte (Pink) depicts a reactive astrocyte in Alzheimer's Disease (AD). The black box contains some examples of the astrocytic signaling pathways related to AD. Green box indicates examples of inducing factors of reactive astrocytes from microglia. Red boxes are the representative intracellular and secretory molecules (red-outlined circles) and astrocytic makers expressed by reactive astrocytes in AD. Blue circles with icons are synapses. K+, potassium; AQP4, aquaporin-4; Kir4.1, inwardly rectifying K+ channel subunit 4.1; APP, amyloid-beta precursor protein; BACE1, β-site APP-cleaving enzyme 1; FFA, free fatty acid; GFAP, glial fibrillary acidic protein; YKL-40, chitinase-3 protein like-1; S100B, S100 calcium-binding protein B; MAOB, monoamine-oxidase-b; GLAST, glutamate aspartate transporter; GLT-1, glutamate transporter 1; Ca2+, calcium; NF-κB, nuclear factor- kappa B; Stat3, signal transducer and activator of transcription 3; AGEs, advance glycation end-products; RAGE, Receptor for advanced glycation end products; TGF-β, transforming growth factor beta; GABA, gamma-aminobutyric acid; IL, interleukin; TNF-α, tumor necrosis factor alpha; C1q, complement component 1q.CC BY · PubMed Central

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Metadata

Authors
Monterey, M. D., Wei, H., Wu, X., & Wu, J. Q.
Affiliations
  • The University of Texas Health Science Center at Houston (US)
  • Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases (US)
  • The University of Texas MD Anderson Cancer Center (US)
Corresponding author
Wu, Jia Qian
Venue
Frontiers in Neurology
Published
2021-08-31
Volume
12
Pages
619626-619626
ISSN
1664-2295 (ISSN-L)
OpenAlex
W3197066362
Cited by
117
References
127
Citations by year
2026: 12 · 2025: 27 · 2024: 34 · 2023: 29 · 2022: 15
FWCI
2.80
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Neurology (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, other-oa)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Institutes of Health
  • National Eye Institute (R21EY028647)
  • National Institute of Neurological Disorders and Stroke (R21NS113068, R01NS088353)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
Alzheimer's disease, astrocytes, reactive astrocytes, astrocyte heterogeneity, neurodegeneration, single-cell sequencing, therapeutic target

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