We are analyzing https://link.springer.com/article/10.1007/s10072-006-0562-6.

Title:
Increased intrathecal TGF-β1, but not IL-12, IFN-γ and IL-10 levels in Alzheimer’s disease patients | Neurological Sciences
Description:
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.
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Keywords {🔍}

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Topics {✒️}

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