CSF concentrations of cAMP and cGMP are reduced in CJD.

<p>CSF concentrations of cAMP (A) and cGMP (B) in cases with Creutzfeldt-Jakob disease (CJD, n = 15) and control patients (CON, n = 11) measured by LC-MS/MS. Data are means ± SEM, **<i>p</i><0.01, Mann-Whitney test.</p

CSF concentrations of cAMP negatively correlate with tau protein in CJD.

<p>Correlation of tau protein with cAMP (A) or cGMP (B) concentrations in CSF of Creutzfeldt-Jakob disease (CJD) patients. Spearman's rank correlation coefficient (r) and the respective <i>p</i>-values are given.</p

Characteristics of potential CSF biomarkers for CJD in ROC analysis.

<p>AUC: area under the curve.</p>1<p>The cut-off was calculated using the Youden index <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0032664#pone.0032664-Baker1" target="_blank">[24]</a>.</p

Cyclic AMP and cGMP are stable in human CSF.

<p>Stability of cAMP and cGMP in human CSF after different handling and storage conditions. A CSF sample was splitted and subjected to the indicated procedures before being measured by LC-MS/MS in triplicate. Data were analysed by a one-way ANOVA followed by Dunnett's multiple comparison tests to compare the different groups against the control. Data are means ± SD, <i>p</i> = 0.58 (cAMP), <i>p</i> = 0.70 (cGMP).</p

CSF concentrations of cAMP and cGMP are not altered in PD and PDD.

<p>CSF concentrations of cAMP (A) and cGMP (B) in cases with Parkinson's disease (PD, n = 11), PD dementia (PDD, n = 8) and control patients (CON, n = 9) measured by LC-MS/MS. Data are means ± SEM, <i>p</i> = 0.50 (cAMP), <i>p</i> = 0.57 (cGMP), Kruskal-Wallis test.</p

CSF concentrations of cAMP and cGMP are not altered in ALS.

<p>CSF concentrations of cAMP (A) and cGMP (B) in cases with amyotrophic lateral sclerosis (ALS, n = 14) and control patients (CON, n = 14) measured by LC-MS/MS. Data are means ± SEM, <i>p</i> = 0.80 (cAMP), <i>p</i> = 0.48 (cGMP), Mann-Whitney test.</p

Characteristics of patients included in the study.

<p>Data are means ± SD, Data are missing for.</p>a<p>three,</p>b<p>six and.</p>c<p>one patients.</p><p>CON: control patients, m: male, f: female, S: spinal, B: bulbar, S+B: spinal and bulbar, PRNP: prion protein gene, M: methionine, V: valine.</p

Proteome analysis of CNTF knockout mice.

<p>2D-DIGE gel of spinal cord proteins from CNTF knock-out mice with EAE, labeled with Cy3 (shown in green) versus wild type mice with EAE labeled with Cy5 (shown in red). Selected proteins identified by Mass Spectrometry are indicated with roman indices (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0007624#pone-0007624-g005" target="_blank">Fig. 5</a>). Proteins were separated on 24 cm IPG Strip pH 3–10 non-linear.</p

Statistical evaluation of regulated proteins in CNTF −/− mice.

<p>2D DIGE analysis of the average spot volume increase ratio of proteins shown in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0007624#pone-0007624-g004" target="_blank">Fig. 4</a>. Using the DeCyder's Biological Variation Analysis module, a paired Student's t-test yielded a p-value within the 99th percentile confidence level. Mean value crosses are connected; IS  =  Internal Standard.</p

CNTF deficiency leads to destructive EAE lesions with enhanced apoptosis.

<p>EAE lesions in CTNF −/− mice (left) are destructive with vacuolar degeneration (asterisks) and multiple apoptotic cells with pycnotic nuclei (depicted by arrows). These changes are not present in EAE lesions from wild-type control mice (right side). Representative cervical spinal cord cross sections from a CNTF −/− knockout mouse and a wild-type CNTF +/+ control mouse on day 35 p.i. of MOG-EAE are shown. Bar  = 50 µm.</p