Cited by 701Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

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The role of microglia in amyloid clearance from the AD brain

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Lee, C. Y. Daniel, Landreth, Gary E.·2010·Journal of Neural Transmission

DOI 10.1007/s00702-010-0433-4PMC PMC3653296

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Abstract

Alzheimer's disease (AD), the most prominent cause of senile dementia, is clinically characterized by the extracellular deposition of beta-amyloid (Abeta) and the intracellular neurofibrillary tangles. It has been well accepted that AD pathogenesis arises from perturbation in the homeostasis of Abeta in the brain. Abeta is normally produced at high levels in the brain and cleared in an equivalent rate. Thus, even a moderate decrease in the clearance leads to the accumulation of Abeta and subsequent amyloid deposition. Microglia are the tissue macrophages in the central nervous system (CNS) and have been shown to play major roles in internalization and degradation of Abeta. Abeta exists in the brain both in soluble and in fibrillar forms. Microglia interact with these two forms of Abeta in different ways. They take up soluble forms of Abeta through macropinocytosis and LDL receptor-related proteins (LRPs) mediated pathway. Fibrillar forms of Abeta interact with the cell surface innate immune receptor complex, initiating intracellular signaling cascades that stimulate phagocytosis. Inflammatory responses influence the activation status of microglia and subsequently regulate their ability to take up and degrade Abeta. ApoE and its receptors have been shown to play critical roles in these processes. In this review, we will explore the mechanisms that microglia utilize to clear Abeta and the effectors that modulate the processes.

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Ultrastructure of the microglia that phagocytose amyloid and the microglia that produce ?-amyloid fibrils
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Authors: Lee, C. Y. D., & Landreth, G. E.
Affiliations: Case Western Reserve University (US)
Corresponding author: Landreth, Gary E.
ORCID: Landreth, Gary E.
Venue: Journal of Neural Transmission
Publisher: Springer Science and Business Media LLC
Published: 2010-06-15
Volume: 117
Issue: 8
Pages: 949-960
ISSN: 0300-9564 (ISSN-L)
1435-1463
DOI: 10.1007/s00702-010-0433-4
PMC: PMC3653296
OpenAlex: W2038594716
Cited by: 701
References: 161
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FWCI: 3.02
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Journal of Neural Transmission (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute on Aging (R01AG020202, R01AG030482, R01AG016740)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: microglia, amyloid-beta clearance, Alzheimer's disease, amyloid deposition, macropinocytosis, LDL receptor-related protein, phagocytosis, innate immune receptors, inflammation, microglial activation, apolipoprotein E, amyloid clearance
MeSH terms: Alzheimer Disease, Amyloid, Apolipoproteins E, Brain, Humans, Inflammation, Microglia

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The role of microglia in amyloid clearance from the AD brain

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