Phagocytic clearance of presynaptic dystrophies by reactive astrocytes in Alzheimer's disease
Open accessAbstract
Reactive astrogliosis, a complex process characterized by cell hypertrophy and upregulation of components of intermediate filaments, is a common feature in brains of Alzheimer's patients. Reactive astrocytes are found in close association with neuritic plaques; however, the precise role of these glial cells in disease pathogenesis is unknown. In this study, using immunohistochemical techniques and light and electron microscopy, we report that plaque‐associated reactive astrocytes enwrap, engulf and may digest presynaptic dystrophies in the hippocampus of amyloid precursor protein/presenilin‐1 (APP/PS1) mice. Microglia, the brain phagocytic population, was apparently not engaged in this clearance. Phagocytic reactive astrocytes were present in 35% and 67% of amyloid plaques at 6 and 12 months of age, respectively. The proportion of engulfed dystrophic neurites was low, around 7% of total dystrophies around plaques at both ages. This fact, along with the accumulation of dystrophic neurites during disease course, suggests that the efficiency of the astrocyte phagocytic process might be limited or impaired. Reactive astrocytes surrounding and engulfing dystrophic neurites were also detected in the hippocampus of Alzheimer's patients by confocal and ultrastructural analysis. We posit that the phagocytic activity of reactive astrocytes might contribute to clear dysfunctional synapses or synaptic debris, thereby restoring impaired neural circuits and reducing the inflammatory impact of damaged neuronal parts and/or limiting the amyloid pathology. Therefore, potentiation of the phagocytic properties of reactive astrocytes may represent a potential therapy in Alzheimer's disease.
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Aβ accumulation in the brain is one of the hallmarks of Alzheimer's disease and plays a key role in initiating and propagating Alzheimer's disease pathogenesis.
“Accumulation of β-amyloid (Aβ) in the brain is one of the hallmarks of Alzheimer's disease (AD) and plays a key role in initiating and propagating AD pathogenesis (Querfurth and LaFerla, 2010;Gomez-Arboledas et al., 2018).”
From Cell Adhesion Molecule Protocadherin-γC5 Ameliorates Aβ Plaque Pathogenesis by Modulating Astrocyte Function in Alzheimer's Disease (2025) · cites this paper as Gomez-Arboledas et al., 2018
The Introduction (page unavailable) identifies amyloid plaques as one of the two signature pathological lesions of Alzheimer’s disease, supporting the hallmark portion of the claim. The Discussion (page unavailable) discusses possible exacerbation of amyloid pathology, but does not establish that Aβ accumulation initiates and propagates Alzheimer’s disease pathogenesis. (LLM, conf=0.86)
Experimental — accuracy not yet measuredFunctions lost or altered in reactive astrocytes include neurotransmitter and ion buffering in mouse HD models, communication via gap junctions in the sclerotic hippocampus of patients with epilepsy, phagocytic clearance of dystrophic neurites, and metabolic coupling by glycolysis-derived d-serine and lactate in mouse AD models.
“Functions lost or altered in reactive astrocytes include neurotransmitter and ion buffering in mouse HD models58, communication via gap junctions in the sclerotic hippocampus of patients with epilepsy59, phagocytic clearance of dystrophic neurites60, and metabolic coupling by glycolysis-derived d-serine61 and lactate62 in mouse AD models.”
From Reactive astrocyte nomenclature, definitions, and future directions (2021) · cites this paper as [60]
Aberrant tau in astrocytes may come from the phagocytosis of neuronal debris and dystrophic synapses containing tau aggregates.
“The aberrant tau in astrocytes may also come from the phagocytosis of neuronal debris and dystrophic synapses containing tau aggregates [198, 199].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [199]
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- Authors
- Gomez‐Arboledas, A., Davila, J. C., Sanchez‐Mejias, E., Navarro, V., Nuñez‐Diaz, C., Sanchez‐Varo, R., Sanchez‐Mico, M. V., Trujillo‐Estrada, L., Fernandez‐Valenzuela, J. J., Vizuete, M., Comella, J. X., Galea, E., Vitorica, J., & Gutierrez, A.
- Affiliations
- Dpto. Biologia Celular, Genetica y Fisiologia. Facultad de Ciencias Instituto de Biomedicina de Malaga (IBIMA), Universidad de Malaga Spain
- Biomedical Research Networking Center on Neurodegenerative Diseases (ES)
- Dpto. Bioquimica y Biologia Molecular, Facultad de Farmacia Universidad de Sevilla Spain
- Universitat Autònoma de Barcelona (ES)
- Institució Catalana de Recerca i Estudis Avançats (ES)
- ORCID
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2017-11-27
- Volume
- 66
- Issue
- 3
- Pages
- 637-653
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- PMC
- PMC5814816
- OpenAlex
- W2769484728
- Cited by
- 220
- References
- 48
- Citations by year
- 2026: 15 · 2025: 25 · 2024: 30 · 2023: 35 · 2022: 29 · 2021: 22 · 2020: 30 · 2019: 25 · 2018: 8
- FWCI
- 12.74
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Glia (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Dipòsit Digital de Documents de la UAB (Universitat Autònoma de Barcelona) (submittedVersion, cc-by-nc-nd)
- RISalud Institutional Health Repository of Andalucía (submittedVersion, cc-by-nc-nd)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by-nc-nd)
- Deposito de Investigacion Universidad de Sevilla (University of Seville) (submittedVersion, cc-by-nc-nd)
- Repositorio Institucional de la Universidad de Málaga (University of Málaga) (submittedVersion, cc-by-nc-nd)
- Funders
- Fondo de Investigación Sanitaria (FIS) Instituto de Salud Carlos III (ISCiii) of Spain-
- FEDER funds from European Union (PI15/00796, PI15/00957)
- Junta de Andalucia - Proyecto de Excelencia (CTS-2035)
- La Marató-TV3 Foundation (20141432, 20141431, 20141433, 20141430)
- CIBERNED (PI2015-2/02)
- Topics
- Health Sciences › Medicine › Physiology › 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
- reactive astrocytes, dystrophic neurites, Alzheimer's disease, amyloid plaques, APP/PS1 mice, hippocampus, microglia, astrocyte activation, neuroinflammation
- MeSH terms
- Alzheimer Disease, Animals, Astrocytes, Disease Models, Animal, Hippocampus, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Phagocytosis, Synapses, Amyloid beta-Protein Precursor, Microglia, Presenilin-1, Plaque, Amyloid
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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