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General Pathophysiology of Astroglia

Verkhratsky, Alexei, Ho, Margaret S., Vardjan, Nina, Zorec, Robert, Parpura, Vladimir·2019·Advances in Experimental Medicine and Biology
DOI 10.1007/978-981-13-9913-8_7PMC PMC7188602
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  • Astrocyte reactivity has frequently been associated with neuroinflammation, unfavorable glial scar formation, glutamate dyshomeostasis, altered coverage of synapses and blood vessels, and BBB breakout.

    “Hence, astrocyte reactivity has frequently been associated with neuroinflammation, unfavorable glial scar formation [7, 8, 9, 37, 38, 43, 48, 49], glutamate dyshomeostasis [43, 50, 51], altered coverage of synapses and blood vessels, and BBB breakout [38, 42, 43, 45, 46, 47].”

    From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [43]

    The Reactive Astrogliosis section (page unavailable) links reactivity to scar formation and says reactive astrocytes can become maladaptive under prolonged stress or severe damage. But it describes scars as generally protective and reactivity as helping reconstruct a compromised blood–brain barrier; the Neurotrauma section likewise describes glutamate removal as a protective function. The copy does not establish the claimed association of reactivity with glutamate dyshomeostasis, altered synaptic and vascular coverage, or BBB breakout. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • The astroglial reactive response is a context-specific reaction influenced by brain region, pathology, disease stage, genetics, age, and comorbidities, and is characteristic of multiple brain pathologies including Alzheimer's disease.

    “The astroglial reactive response is far from a uniform process. Rather, it is a context‐specific reaction influenced by brain region, pathology, disease stage, genetics, age, and comorbidities [15, 43, 45, 52], and it is characteristic of multiple brain pathologies, including Alzheimer's disease (AD).”

    From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [43]

    In “Principles of Astrogliopathology,” the paper says astroglial changes vary by disease and stage and are affected by age and comorbidity; “Reactive Astrogliosis” describes varied, disease-specific phenotypes. The paper also reports reactive astrogliosis in many neurological disorders and discusses it in an Alzheimer’s disease model. The passages do not establish genetics as an influence on the reactive response, and the stroke section’s variation with distance from an ischemic core does not establish variation by brain region. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • Atrophied astrocytes fail to maintain the glutamate‐glutamine shuttle and display insufficient glutamate clearance because of reduced synaptic coverage, contributing to synaptic extinction and cognitive deficiency.

    “previous reports have shown that atrophied astrocytes fail to maintain the glutamate‐glutamine shuttle [28, 47] and display insufficient glutamate clearance [43] because of reduced synaptic coverage [45, 46, 47], contributing to synaptic extinction and cognitive deficiency [43].”

    From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [43]

    The “Astroglial Atrophy” section links astrodegeneration to impaired glutamate–glutamine shuttling. It separately describes insufficient glutamate clearance in amyotrophic lateral sclerosis and reduced synaptic coverage contributing to synaptic extinction and cognitive deficiency in Alzheimer’s disease. It does not say that reduced coverage causes the insufficient clearance. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • Hyperactivated astrocytes and microglia support excitotoxicity through the exacerbated release of glutamate in response to Aβ, and GABA‐producing astrocytes are commonly found in AD.

    “hyperactivated astrocytes and microglia, support excitotoxicity through the exacerbated release of glutamate in response to Aβ [37, 38, 40, 43, 50, 51, 117, 118], and even GABA‐producing astrocytes are commonly found in AD [42, 97, 119].”

    From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [43]

    The Hyperammonemia and Hepatic Encephalopathy section says astrocytes release glutamate that exacerbates excitotoxic damage, but attributes this to ammonium exposure, not Aβ. The Reactive Astrogliosis section says Aβ triggers astroglial reactivity; it does not connect that response to glutamate release. The retrieved passages do not establish microglial glutamate release or that GABA-producing astrocytes are common in Alzheimer’s disease (pages unavailable). (LLM, conf=0.79)

    Experimental — accuracy not yet measured

  • Reactive morphological changes are driven by an increase of intermediate filament proteins such as GFAP and vimentin.

    “Finely tuned morphological changes are driven by an increase of intermediate filament proteins, such as GFAP and vimentin [15, 38, 41, 42, 43], which not only provide mechanical sustenance for the maintenance of astrocyte shape, but also support the functional profile of reactive astrocytes through transcriptional modulation of target genes involved in astroglial and microglial responsiveness [44,”

    From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [43]

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Authors
Verkhratsky, A., Ho, M. S., Vardjan, N., Zorec, R., & Parpura, V.
Venue
Advances in Experimental Medicine and Biology
Publisher
Springer Singapore
Published
2019
Pages
149-179
ISSN
  • 0065-2598
  • 2214-8019
DOI
10.1007/978-981-13-9913-8_7
PMC
PMC7188602
Cited by
59
References
18
Language
en
Licence
www.springer.com/tdm (tdm)

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