Neuroinflammation and regeneration in the early stages of Alzheimer's disease pathology.

Hoozemans JJ; Veerhuis R; Rozemuller JM; Eikelenboom P

doi:10.1016/j.ijdevneu.2005.11.001

Neuroinflammation and regeneration in the early stages of Alzheimer's disease pathology.

Affiliations

1. Department of Neuropathology, Academic Medical Center, University of Amsterdam, P.O. Box 22700, 110DE Amsterdam, The Netherlands.
Authors
Hoozemans JJ¹
(1 author)

ORCIDs linked to this article

Hoozemans JJ | 0000-0002-2888-8967

International Journal of Developmental Neuroscience : the Official Journal of the International Society for Developmental Neuroscience, 27 Dec 2005, 24(2-3):157-165
https://doi.org/10.1016/j.ijdevneu.2005.11.001 PMID: 16384684

Review

Abstract

The initial stages of Alzheimer's disease pathology in the neocortex show upregulation of cell cycle proteins, adhesion and inflammation related factors, indicating the early involvement of inflammatory and regenerating pathways in Alzheimer's disease pathogenesis. These brain changes precede the neurofibrillary pathology and the extensive process of neurodestruction and (astro)gliosis. Amyloid beta deposition, inflammation and regenerative mechanisms are also early pathogenic events in transgenic mouse models harbouring the pathological Alzheimer's disease mutations, while neurodegenerative characteristics are not seen in these models. This review will discuss the relationship between neuroinflammation and neuroregeneration in the early stages of Alzheimer's disease pathogenesis.

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Funding

Funders who supported this work.

Internationale Stichting Alzheimer Onderzoek (2)

Grant ID: 03509
1 publication
Grant ID: 04503
1 publication

Search life-sciences literature (45,105,671 articles, preprints and more)

Neuroinflammation and regeneration in the early stages of Alzheimer's disease pathology.

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Authors

ORCIDs linked to this article

Abstract

Full text links

References

Inflammation and Alzheimer's disease.

Beta-amyloid-induced glial expression of both pro- and anti-inflammatory cytokines in cerebral cortex of aged transgenic Tg2576 mice with Alzheimer plaque pathology.

Microglia, amyloid and dementia in alzheimer disease. A correlative study.

Alzheimer's disease as a disorder of mechanisms underlying structural brain self-organization.

Synaptic plasticity and cell cycle activation in neurons are alternative effector pathways: the 'Dr. Jekyll and Mr. Hyde concept' of Alzheimer's disease or the yin and yang of neuroplasticity.

Expression of the cyclin-dependent kinase inhibitor p16 in Alzheimer's disease.

Imaging of amyloid-beta deposits in brains of living mice permits direct observation of clearance of plaques with immunotherapy.

Lack of apolipoprotein E dramatically reduces amyloid beta-peptide deposition.

Peripherally administered antibodies against amyloid beta-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease.

Evidence for glial-mediated inflammation in aged APP(SW) transgenic mice.

Citations & impact

Impact metrics

Citations of article over time

Alternative metrics

Smart citations by scite.ai
Explore citation contexts and check if this article has been supported or disputed.
https://scite.ai/reports/10.1016/j.ijdevneu.2005.11.001

Article citations

Prediction of Alzheimer's disease stages based on ResNet-Self-attention architecture with Bayesian optimization and best features selection.

The Inflammation-Induced Dysregulation of Reelin Homeostasis Hypothesis of Alzheimer's Disease.

Associations of serum DNA methylation levels of chemokine signaling pathway genes with mild cognitive impairment (MCI) and Alzheimer's disease (AD).

Hippocampus of the APP^NL-G-F mouse model of Alzheimer's disease exhibits region-specific tissue softening concomitant with elevated astrogliosis.

An update on stem cell and stem cell-derived extracellular vesicle-based therapy in the management of Alzheimer's disease.

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Neuroinflammation and regeneration in the early stages of Alzheimer's disease pathology.

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