Migration of blood cells to β-amyloid plaques in Alzheimer's disease
Open accessAbstract
Alzheimer's disease (AD) is a neurodegenerative disease that leads to the progressive deterioration of cognitive and memory functions. The deposition of extracellular beta-amyloid (Aβ) senile plaques and intracellular tau neurofibrillary tangles are considered the cardinal pathological hallmarks of AD, however, accumulating evidence indicates that immune cells may also play an important role in disease pathogenesis. Among these immune cells, blood-derived cells and their infiltration into the CNS towards Aβ plaques have been implicated in therapeutic strategies against AD. Here, we review the current literature on blood cell migration into the AD brain and the important players involved in this selective migration towards Aβ plaques.
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The primary mechanism of action of 10D5 mAb is based on its direct binding to deposited Aβ and stimulating Fc receptor-mediated Aβ plaque removal by activated microglia and possibly blood derived macrophages.
“The primary mechanism of action of 10D5 mAb is based on its direct binding to deposited Aβ and stimulating Fc receptor-mediated Aβ plaque removal by activated microglia and possibly blood derived macrophages [9, 34].”
From APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice (2017) · cites this paper as [34]
Section 3.5 (page unavailable) reports that blood-derived monocytes or macrophages can reach Aβ plaques and eliminate deposits by phagocytosis. It does not identify 10D5 mAb, describe its binding to deposited Aβ, or establish Fc receptor-mediated removal as its primary mechanism. (LLM, conf=0.82)
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“The primary mechanism of action of 10D5 mAb is based on its direct binding to deposited Aβ and stimulating Fc receptor-mediated Aβ plaque removal by activated microglia and possibly blood derived macrophages [9, 34].”
Background
- Authors
- Hohsfield, L. A., & Humpel, C.
- Affiliations
- Innsbruck Medical University (AT)
- Corresponding author
- Humpel, Christian
- Venue
- Experimental Gerontology
- Publisher
- Elsevier BV
- Published
- 2015-05
- Volume
- 65
- Pages
- 8-15
- ISSN
- 0531-5565 (ISSN-L)
- PMC
- PMC4526125
- OpenAlex
- W1989038107
- Cited by
- 79
- References
- 21
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 5 · 2023: 5 · 2022: 10 · 2021: 11 · 2020: 5 · 2019: 7 · 2018: 11 · 2017: 9 · 2016: 8 · 2015: 3 · 2013: 1
- FWCI
- 1.27
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Experimental Gerontology (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion, cc-by-nc-nd)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Keywords
- Alzheimer's disease, amyloid plaques, leukocyte infiltration, blood-brain barrier, neuroinflammation, immune cells, neurofibrillary tangles, pathogenesis
- MeSH terms
- Alzheimer Disease, Blood Cells, Brain, Cell Movement, Humans, Amyloid beta-Protein Precursor, Neurofibrillary Tangles, 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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