Cited by 27Alzheimer's disease research and treatmentsCellular transport and secretionNeuroinflammation and Neurodegeneration Mechanisms

Clathrin mediated endocytosis in Alzheimer’s disease: cell type specific involvement in amyloid beta pathology

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Jaye, Sierra, Sandau, Ursula S., Saugstad, Julie A.·2024·Frontiers in Aging Neuroscience

Abstract

This review provides a comprehensive examination of the role of clathrin-mediated endocytosis (CME) in Alzheimer’s disease (AD) pathogenesis, emphasizing its impact across various cellular contexts beyond neuronal dysfunction. In neurons, dysregulated CME contributes to synaptic dysfunction, amyloid beta (Aβ) processing, and Tau pathology, highlighting its involvement in early AD pathogenesis. Furthermore, CME alterations extend to non-neuronal cell types, including astrocytes and microglia, which play crucial roles in Aβ clearance and neuroinflammation. Dysregulated CME in these cells underscores its broader implications in AD pathophysiology. Despite significant progress, further research is needed to elucidate the precise mechanisms underlying CME dysregulation in AD and its therapeutic implications. Overall, understanding the complex interplay between CME and AD across diverse cell types holds promise for identifying novel therapeutic targets and interventions.

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Crossref · 10.3389/fnagi.2024.1378576

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  • These mechanisms (autophagy, phagocytosis, endocytosis) have been shown to be impaired in AD brains.

    “These mechanisms has been shown to be impaired in AD brains [45, 55].”

    From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [45]

    The Introduction identifies impaired autophagy in AD, and “AD and endolysosomal function” describes defects in that pathway. The Astrocytes section reports impaired phagocytosis of diseased synapses when astrocytes are overburdened with Aβ. But the paper does not establish that all three mechanisms are impaired in AD brains: it says how endocytosis itself is altered remains to be considered, and the phagocytosis passage does not establish a brain-wide finding. (LLM, conf=0.84)

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Authors
Jaye, S., Sandau, U. S., & Saugstad, J. A.
Affiliations
Oregon Health & Science University (US)
Corresponding author
Saugstad, Julie A.
Venue
Frontiers in Aging Neuroscience
Published
2024-04-17
Volume
16
Pages
1378576-1378576
ISSN
1663-4365 (ISSN-L)
OpenAlex
W4394904573
Cited by
26
References
178
Citations by year
2026: 13 · 2025: 8 · 2024: 5
FWCI
1.48
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Aging Neuroscience (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
  • National Institutes of Health
  • National Institute on Aging (RF1AG059392, T32AG055378)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
clathrin-mediated endocytosis, Alzheimer's disease, amyloid-beta, synaptic dysfunction, tau pathology, astrocytes, microglia, neuroinflammation, amyloid-beta clearance

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