A Dynamic Relationship between Intracellular and Extracellular Pools of Aβ

Oddo, Salvatore; Caccamo, Antonella; Smith, Ian F.; Green, Kim N.; LaFerla, Frank M.

doi:10.2353/ajpath.2006.050593

Cited by 261Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

A Dynamic Relationship between Intracellular and Extracellular Pools of Aβ

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Oddo, Salvatore, Caccamo, Antonella, Smith, Ian F., Green, Kim N., LaFerla, Frank M.·2006·The American Journal of Pathology

DOI 10.2353/ajpath.2006.050593PMC PMC1592652

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Abstract

The accumulation of the amyloid-beta peptide (Abeta) in the brain is considered to have a primary role in Alzheimer's disease (AD). In addition to the extracellular accumulation of Abeta in the parenchyma and cerebrovasculature, emerging evidence indicates that intraneuronal Abeta also plays a pathophysiological role in AD. It is unclear, however, if the intracellular and extracellular pools of Abeta are unrelated or connected. In these studies, we sought to establish a relationship between these two pools of Abeta. We identified an inverse relationship between intracellular and extracellular Abeta in the 3xTg-AD transgenic model of AD. Using an immunotherapy approach, we further found that extracellular Abeta was cleared before intracellular Abeta. After the antibody dissipated, however, the reappearance of extracellular plaques was preceded by the accumulation of intraneuronal Abeta. Taken together, these results provide strong experimental evidence that intraneuronal Abeta may serve as a source for some of the extracellular amyloid deposits.

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An inverse dynamic relationship between intracellular and extracellular pools of Aβ appears to influence deposit formation in 3XTg-AD mouse brain.
“Interestingly, a recent study has indicated an inverse dynamic relationship between intracellular and extracellular pools of A 𝛃 that appears to influence deposit formation in 3XTg-AD mouse brain (Oddo et al., 2006).”
From Intraneuronal β-Amyloid Aggregates, Neurodegeneration, and Neuron Loss in Transgenic Mice with Five Familial Alzheimer's Disease Mutations: Potential Factors in Amyloid Plaque Formation (2006) · cites this paper as Oddo et al., 2006
Intracellular Aβ accumulation in neurons that are particularly vulnerable in AD precedes plaque formation but decreases later on with the progression of Aβ deposition in both mice and humans.
“Indeed, intracellular Aβ accumulation in neurons that are particularly vulnerable in AD precedes plaque formation but decreases later on with the progression of Aβ deposition in both mice [89, 117] and humans [41, 81].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [89]
There is a dynamic correlation between extra- and intracellular pools of Aβ, the latter being the source for some of the extracellular Aβ plaques.
“Indeed, there is a dynamic correlation between extra- and intracellular pools of Aβ, the latter being the source for some of the extracellular Aβ plaques [89].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [89]
There is an apparent decline in intraneuronal Aβ42 labeling with advancing plaque pathology.
“this and subsequent studies noted an apparent decline in intraneuronal Aβ42 labeling with advancing plaque pathology [95, 139].”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [139]

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Authors: Oddo, S., Caccamo, A., Smith, I. F., Green, K. N., & LaFerla, F. M.
Affiliations: University of California, Irvine (US)
Corresponding author: LaFerla, Frank M.
ORCID: Oddo, Salvatore
Caccamo, Antonella
Smith, Ian F.
Green, Kim N.
LaFerla, Frank M.
Venue: The American Journal of Pathology
Publisher: Elsevier BV
Published: 2006-01
Volume: 168
Issue: 1
Pages: 184-194
ISSN: 0002-9440 (ISSN-L)
DOI: 10.2353/ajpath.2006.050593
PMC: PMC1592652
OpenAlex: W2110998913
Cited by: 261
References: 45
Citations by year: 2026: 4 · 2025: 11 · 2024: 21 · 2023: 12 · 2022: 8 · 2021: 5 · 2020: 9 · 2019: 14 · 2018: 15 · 2017: 8 · 2016: 3 · 2015: 10 · 2014: 8 · 2013: 11 · 2012: 11
FWCI: 16.13
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: American Journal Of Pathology (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Alzheimer's Association
National Institute on Aging (AG0212982)
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: amyloid-beta, intraneuronal amyloid-beta, Alzheimer's disease, immunotherapy, amyloid plaques, amyloid clearance
MeSH terms: Age Factors, Alzheimer Disease, Animals, Brain Chemistry, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Immunohistochemistry, Intracellular Fluid, Mice, Transgenic, Neurons, Blotting, Western, Amyloid beta-Peptides, Extracellular Fluid, Mice

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A Dynamic Relationship between Intracellular and Extracellular Pools of Aβ

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