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Cyclin D1 and cyclin E are co-localized with cyclo-oxygenase 2 (COX-2) in pyramidal neurons in Alzheimer disease

Jeroen J M Hoozemans1, Martina K Brückner, Annemieke J M Rozemuller

  • 1Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Vrije Universiteit, Department of Pathology, VU University Medical Center, The Netherlands.

Journal of Neuropathology and Experimental Neurology
|August 3, 2002
PubMed

Insights

Non-steroidal anti-inflammatory drugs (NSAIDs) target cyclo-oxygenase-2 (COX-2), an enzyme linked to cell cycle regulators. This study found COX-2 and cell cycle markers co-expressed in Alzheimer

Area of Science:

  • Neuroscience
  • Oncology
  • Pharmacology

Background:

  • Non-steroidal anti-inflammatory drugs (NSAIDs) show potential in reducing the progression of diseases like Alzheimer's disease (AD).
  • NSAIDs primarily target cyclo-oxygenase (COX) enzymes, with COX-2 being implicated in various cellular processes.
  • Previous research indicates NSAIDs modulate cell cycle progression, particularly in the G0/G1 phase.

Purpose of the Study:

  • To investigate the expression of COX-2, cyclin D1, and cyclin E in the temporal cortex of AD and non-demented control brains.
  • To explore the relationship between COX-2 expression and cell cycle markers in neurons.
  • To examine the correlation between neuronal COX-2/cell cycle marker expression and Alzheimer's disease pathology severity (Braak score).

Main Methods:

  • Immunohistochemistry was used to detect the expression of COX-2, cyclin D1, and cyclin E in neuronal cells.
  • Sequential tissue sections and double immunofluorescence labeling were employed to confirm co-expression.
  • Correlation analyses were performed between marker expression and Braak scores.

Main Results:

  • COX-2, cyclin D1, and cyclin E were detected in pyramidal neurons in both AD and control brains.
  • A positive correlation was observed between the number of COX-2-immunoreactive neurons and the number of cyclin D1- and cyclin E-immunoreactive neurons.
  • Co-expression of COX-2 with cyclin D1 and E was confirmed in neuronal cells.
  • An inverse correlation was found between neuronal COX-2/cyclin E expression and the Braak score for amyloid beta deposits.

Conclusions:

  • Neuronal expression of COX-2 is related to the expression of cell cycle markers (cyclin D1 and E) in the brain.
  • This relationship suggests a potential role for COX-2 and cell cycle modulation in the early stages of Alzheimer's disease pathology.
  • Findings support the investigation of NSAIDs for their potential therapeutic effects in AD.

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