Skip to main content

Advertisement

Log in

Increased intrathecal TGF-β1, but not IL-12, IFN-γ and IL-10 levels in Alzheimer’s disease patients

  • ORIGINAL
  • Published:
Neurological Sciences Aims and scope Submit manuscript

Abstract

An inflammatory response has been hypothesised to be involved in the pathogenesis of primary dementias, above all Alzheimer’s disease (AD). This study was aimed at evaluating interleukin (IL)-12 and a panel of related cytokine levels in paired CSF and sera of demented patients. IL-12 (p70 heterodimer and total IL-12 p40 chain), interferon (IFN)-γ, IL-10 and transforming growth factor (TGF)-β1 levels were measured in 30 patients with probable Alzheimer’s disease (PrAD), 57 patients with other dementing disorders, including probable vascular dementia (PrVD), Parkinson’s disease (PD) and normal pressure hydrocephalus (NPH), and 25 cognitively normal control subjects. In the presence of unchanged concentrations of IL-12, IFN-γ and IL-10, the mean CSF level of TGF-β1 and the correspondent TGF-β1 index, but not the serum level, were significantly increased in PrAD compared to controls and PrVD, whereas no difference was found vs. NPH and PD. Our results support the pathophysiological role of TGF-β1 system in AD.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to E. Rota.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Rota, E., Bellone, G., Rocca, P. et al. Increased intrathecal TGF-β1, but not IL-12, IFN-γ and IL-10 levels in Alzheimer’s disease patients. Neurol Sci 27, 33–39 (2006). https://doi.org/10.1007/s10072-006-0562-6

Download citation

  • Received:

  • Accepted:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s10072-006-0562-6

Key words

Navigation