The role of inflammation in Alzheimer’s disease

Tuppo, Ehab E.; Arias, Hugo R.

doi:10.1016/j.biocel.2004.07.009

Cited by 734Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsNeurological Disease Mechanisms and Treatments

The role of inflammation in Alzheimer’s disease

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Tuppo, Ehab E., Arias, Hugo R.·2005·The International Journal of Biochemistry & Cell Biology

DOI 10.1016/j.biocel.2004.07.009

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Abstract

Considerable evidence gained over the past decade has supported the conclusion that neuroinflammation is associated with Alzheimer's disease (AD) pathology. Inflammatory components related to AD neuroinflammation include brain cells such as microglia and astrocytes, the classic and alternate pathways of the complement system, the pentraxin acute-phase proteins, neuronal-type nicotinic acetylcholine receptors (AChRs), peroxisomal proliferators-activated receptors (PPARs), as well as cytokines and chemokines. Both the microglia and astrocytes have been shown to generate beta-amyloid protein (Abeta), one of the main pathologic features of AD. Abeta itself has been shown to act as a pro-inflammatory agent causing the activation of many of the inflammatory components. Further substantiation for the role of neuroinflammation in AD has come from studies that demonstrate patients who took non-steroidal anti-inflammatory drugs had a lower risk of AD than those who did not. These same results have led to increased interest in pursuing anti-inflammatory therapy for AD but with poor results. On the other hand, increasing amount of data suggest that AChRs and PPARs are involved in AD-induced neuroinflammation and in this regard, future therapy may focus on their specific targeting in the AD brain.

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Increased activation of microglia and astrocytes could result in neuronal damage.
“However, increased activation of these systems could result in neuronal damage [21].”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [21]
Microglia and astrocytes release pro-inflammatory mediators such as cytokines, chemokines, reactive oxygen species, and complement proteins, promoting a neuroprotective function through cytotoxic and phagocytic activity.
“Both systems release pro-inflammatory mediators, such as cytokines, chemokines, reactive oxygen species (ROS), and complement proteins, thus promoting a neuroprotective function thanks to cytotoxic and phagocytic activity.”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [21]
Protein agglomerates characteristic of Alzheimer's disease are recognized as a threat to the immune system, triggering the inflammation process.
“Protein agglomerates (senile plaques and NFT), characteristic of the disease, are recognized as a threat to the immune system, which triggers the inflammation process.”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [21]

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Cann, S. A. H., Netten, J. P. V., & Netten, C. V. (2000) · Pure Amsterdam UMC · doi:10.1002/1531-8249(200003)47:3

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Inflammation as a central mechanism in Alzheimer's disease
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Authors: Tuppo, E. E., & Arias, H. R.
Affiliations: University of Medicine and Dentistry of New Jersey (US)
Western University of Health Sciences (US)
Corresponding author: Tuppo, Ehab E.
ORCID: Tuppo, Ehab E.
Arias, Hugo R.
Venue: The International Journal of Biochemistry & Cell Biology
Publisher: Elsevier BV
Published: 2005-02
Volume: 37
Issue: 2
Pages: 289-305
ISSN: 1357-2725 (ISSN-L)
DOI: 10.1016/j.biocel.2004.07.009
OpenAlex: W1974305753
Cited by: 734
References: 173
Citations by year: 2026: 8 · 2025: 22 · 2024: 24 · 2023: 23 · 2022: 34 · 2021: 31 · 2020: 31 · 2019: 44 · 2018: 37 · 2017: 37 · 2016: 40 · 2015: 46 · 2014: 39 · 2013: 66 · 2012: 47
FWCI: 2.44
Type: journal article
Language: en
Open access: green
hdl.handle.net
Licence: cc-by-nc-nd
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: The International Journal of Biochemistry & Cell Biology (publishedVersion)
PubMed (publishedVersion)
CONICET Digital (CONICET) (submittedVersion, cc-by-nc-nd)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords: Alzheimer's disease, neuroinflammation, microglia, astrocytes, complement system, pentraxins, acute phase proteins, nicotinic acetylcholine receptors, amyloid-beta, cytokines, chemokines, nonsteroidal anti-inflammatory drugs, anti-inflammatory therapy
MeSH terms: Acute-Phase Proteins, Alzheimer Disease, Animals, Anti-Inflammatory Agents, Non-Steroidal, Astrocytes, Brain, Humans, Inflammation, Receptors, Nicotinic, Drug Delivery Systems, Amyloid beta-Protein Precursor, Microglia, Peroxisome Proliferator-Activated Receptors

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The role of inflammation in Alzheimer’s disease

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