The role of inflammation in Alzheimer's disease

Ehab E. Tuppo, Hugo R. Arias

Research output: Contribution to journalReview article

502 Citations (Scopus)

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 (Aβ), one of the main pathologic features of AD. Aβ 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.

Original languageEnglish
Pages (from-to)289-305
Number of pages17
JournalInternational Journal of Biochemistry and Cell Biology
Volume37
Issue number2
DOIs
StatePublished - 1 Feb 2005
Externally publishedYes

Fingerprint

Alzheimer Disease
Inflammation
Microglia
Astrocytes
Brain
Anti-Inflammatory Agents
Cytokine Receptors
Acute-Phase Proteins
Chemokine Receptors
Amyloid beta-Peptides
Staphylococcal Protein A
Nicotinic Receptors
Cholinergic Receptors
Pathology
Chemokines
Chemical activation
Cytokines
Therapeutics
Pharmaceutical Preparations

Keywords

  • Alzheimer's disease
  • Beta-amyloid protein
  • Chemokines
  • Complement system
  • Cyclooxygenase
  • Cytokines
  • Glial cells
  • Interleukin
  • Neuroinflammation
  • Nicotinic acetylcholine receptors
  • NSAIDS
  • Pentraxins
  • Senile plaques
  • Steroids
  • Tumor necrosis factor

Cite this

@article{951b117ff4c54f19bfa41e05d5cdea0e,
title = "The role of inflammation in Alzheimer's disease",
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 (Aβ), one of the main pathologic features of AD. Aβ 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.",
keywords = "Alzheimer's disease, Beta-amyloid protein, Chemokines, Complement system, Cyclooxygenase, Cytokines, Glial cells, Interleukin, Neuroinflammation, Nicotinic acetylcholine receptors, NSAIDS, Pentraxins, Senile plaques, Steroids, Tumor necrosis factor",
author = "Tuppo, {Ehab E.} and Arias, {Hugo R.}",
year = "2005",
month = "2",
day = "1",
doi = "10.1016/j.biocel.2004.07.009",
language = "English",
volume = "37",
pages = "289--305",
journal = "International Journal of Biochemistry and Cell Biology",
issn = "1357-2725",
number = "2",

}

The role of inflammation in Alzheimer's disease. / Tuppo, Ehab E.; Arias, Hugo R.

In: International Journal of Biochemistry and Cell Biology, Vol. 37, No. 2, 01.02.2005, p. 289-305.

Research output: Contribution to journalReview article

TY - JOUR

T1 - The role of inflammation in Alzheimer's disease

AU - Tuppo, Ehab E.

AU - Arias, Hugo R.

PY - 2005/2/1

Y1 - 2005/2/1

N2 - 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 (Aβ), one of the main pathologic features of AD. Aβ 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.

AB - 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 (Aβ), one of the main pathologic features of AD. Aβ 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.

KW - Alzheimer's disease

KW - Beta-amyloid protein

KW - Chemokines

KW - Complement system

KW - Cyclooxygenase

KW - Cytokines

KW - Glial cells

KW - Interleukin

KW - Neuroinflammation

KW - Nicotinic acetylcholine receptors

KW - NSAIDS

KW - Pentraxins

KW - Senile plaques

KW - Steroids

KW - Tumor necrosis factor

UR - http://www.scopus.com/inward/record.url?scp=4944258716&partnerID=8YFLogxK

U2 - 10.1016/j.biocel.2004.07.009

DO - 10.1016/j.biocel.2004.07.009

M3 - Review article

C2 - 15474976

AN - SCOPUS:4944258716

VL - 37

SP - 289

EP - 305

JO - International Journal of Biochemistry and Cell Biology

JF - International Journal of Biochemistry and Cell Biology

SN - 1357-2725

IS - 2

ER -