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Katharina Stoeck, MD; Monika Bodemer; Barbara Ciesielczyk; Bettina Meissner, MD; Mario Bartl, MD; Uta Heinemann; Inga Zerr, MD

Arch Neurol. 2005;62:1591-1594.

Background  In neurodegenerative diseases, increasing attention has been focused on inflammatory mediators such as pro-inflammatory and anti-inflammatory cytokines and their potential influence in the process of neurodegeneration. In prion diseases, much data has been gained on the cell culture and animal disease models level, but only limited information is available on humans affected by Creutzfeldt-Jakob disease (CJD).

Objective  To obtain data on anti-inflammatory cytokines interleukin 4 and interleukin 10 in the cerebrospinal fluid of patients with CJD, patients with other dementia, and nondemented neurological patients and controls.

Design  Cerebrospinal fluid samples were collected from CJD patients and control subjects, and concentrations of the anti-inflammatory cytokines interleukin 4 and interleukin 10 were determined using an enzyme-linked immunosorbent assay.

Patients  Cerebrospinal fluid samples from 61 patients were analyzed. The group was composed of patients with CJD (n = 20), patients with other forms of dementia (n = 10), patients with motoneuron disease (n = 6), patients with normal pressure hydrocephalus (n = 5), and control subjects (n = 20).

Results  Interleukin 10 levels were significantly elevated in the cerebrospinal fluid of CJD patients (median, 9.8 pg/mL). The elevation was significant to other dementia (median, 7.9 pg/mL, P<.05), motoneuron disease (median, 7.9 pg/mL, P<.05), normal pressure hydrocephalus (median, 7.0 pg/mL, P<.05), and controls (median, 1.3 pg/mL, P<.001). Levels of interleukin 4 were significantly elevated in cerebrospinal fluid of patients with CJD (median, 26.4 pg/mL) compared with control subjects (median, 6.2 pg/mL, P<.001) and patients with a motoneuron disease (median, 10.5 pg/mL, P<.001)

Conclusions  Elevated levels of the anti-inflammatory cytokines interleukin 4 and interleukin 10 in cerebrospinal fluid of patients with CJD are new findings. The data of the present study provide a clue toward the possible role of cytokines as immunological modifiers in the neurodegenerative process of CJD.

Author Affiliations: Department of Neurology, University Hospital Göttingen, Göttingen, Germany.

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