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Published on: December 26, 2016

Clinical aspects of inflammation in Alzheimer's disease

Paul B Rosenberg1

  • 1Division of Geriatric Psychiatry and Neuropsychiatry, John Hopkins University School of Medicine, Baltimore, MD 21205, USA. prosenb9@jhmi.edu

International Review of Psychiatry (Abingdon, England)
|January 13, 2006
PubMed

Insights

Central nervous system inflammation, involving microglia activation and cytokine release, is implicated in Alzheimer's disease (AD) neurotoxicity. Novel anti-inflammatory agents offer potential new treatments or adjuncts for AD.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Alzheimer's disease (AD) pathogenesis involves central nervous system (CNS) inflammation.
  • Microglial activation by amyloid-beta releases pro-inflammatory cytokines (e.g., IL-1beta, IL-6, TNF-alpha).
  • These cytokines contribute to neurotoxicity, impacting neuronal apoptosis, synaptic function, and neurogenesis.

Purpose of the Study:

  • To review the role of CNS inflammation in AD.
  • To discuss novel methods for measuring CNS inflammation.
  • To explore potential anti-inflammatory therapeutic strategies for AD.

Main Methods:

  • Review of existing literature on CNS inflammation in AD.
  • Discussion of emerging diagnostic markers for microglial activation and cytokine release.
  • Analysis of epidemiological and clinical trial data on NSAIDs and other anti-inflammatory agents.

Main Results:

  • CNS inflammation may precede AD hallmark pathologies and serve as an early prodromal marker.
  • Peripheral blood mononuclear cell cytokine release and PET imaging are new tools to assess CNS inflammation.
  • Epidemiological studies suggest serum IL-6 correlates with cognitive decline; NSAID trials have not shown AD prevention benefits.

Conclusions:

  • Targeting CNS inflammation presents a promising therapeutic avenue for AD.
  • Novel anti-inflammatory agents, including NSAIDs and opioid antagonists, are under development.
  • These agents may serve as alternatives or complements to anti-amyloid therapies in AD management.

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