Cited by 356Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsDementia and Cognitive Impairment Research

Review: Systemic inflammation and A lzheimer's disease

Holmes, C.·2013·Neuropathology and Applied Neurobiology

Abstract

There is a great deal of evidence suggesting an important role for systemic inflammation in the pathogenesis of A lzheimer's disease. The role of systemic inflammation, and indeed inflammation in general, is still largely considered to be as a contributor to the disease process rather than of aetiological importance although there is emerging evidence to suggest that its role may predate the deposition of amyloid. Therapies aimed at reducing inflammation in individuals with mild cognitive impairment and A lzheimer's disease have been disappointing and have largely focused on the need to ameliorate central inflammation with little attention to the importance of dampening down systemic inflammation. Novel approaches in this area require a greater understanding of the effects of systemic inflammation on the development and progression of A lzheimer's disease and of the communicating pathways between the systemic and central innate immune systems.

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Crossref · 10.1111/j.1365-2990.2012.01307.x

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  • Numerous findings support the involvement in AD pathogenesis of other mechanisms such as inflammation, imbalance among production and removal of ROS, mitochondrial dysfunction, in addition to the β-amyloid cascade and the deficiency of central cholinergic neurotransmitters.

    “Although the genetic susceptibility, numerous findings support the involvement in AD pathogenesis of other mechanisms such as inflammation [95], imbalance among production and removal of ROS [96], mitochondrial dysfunction [82], in addition to the β-amyloid cascade [97] and the deficiency of central cholinergic neurotransmitters [98] on which are based most of anti-AD drugs so far approved.”
  • Crosstalk between systemic and central innate immune systems by release of inflammatory mediators is observed in AD.

    “Crosstalk between systemic and central innate immune systems by the release of inflammatory mediators is observed in AD (Holmes, 2013).”

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Authors
Holmes, C.
Affiliations
Moorgreen Hospital (GB)
Corresponding author
Holmes, C.
Venue
Neuropathology and Applied Neurobiology
Publisher
Wiley
Published
2013-01-22
Volume
39
Issue
1
Pages
51-68
ISSN
  • 0305-1846 (ISSN-L)
  • 1365-2990
OpenAlex
W1916976076
Cited by
356
References
208
Citations by year
2026: 17 · 2025: 12 · 2024: 29 · 2023: 52 · 2022: 48 · 2021: 33 · 2020: 38 · 2019: 32 · 2018: 23 · 2017: 24 · 2016: 15 · 2015: 16 · 2014: 11 · 2013: 4 · 2012: 1
FWCI
0.95
Type
journal article
Language
en
Open access
closed
Locations
  • Neuropathology and Applied Neurobiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Alzheimer Society
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
systemic inflammation, Alzheimer's disease, pathogenesis, amyloid deposition, mild cognitive impairment, anti-inflammatory therapy, innate immune system, neuroinflammation
MeSH terms
Alzheimer Disease, Animals, Humans, Inflammation

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