Alzheimer Disease: Rösler N

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A digest of articles written 1999 and later, on the topic "Alzheimer Disease," originating from Planet Earth —» Rösler N.  Display:  All Citations ·  All Abstracts
1 Article Immunoreactivities of amyloid beta peptide((1-42)) and total tau protein in lumbar cerebrospinal fluid of patients with normal pressure hydrocephalus. 2004

Lins H, Wichart I, Bancher C, Wallesch CW, Jellinger KA, Rösler N. · Department of Neurology, Otto-von-Guericke-University, Magdeburg, Germany. · J Neural Transm. · Pubmed #14991454 No free full text.

Abstract: Immunoreactivities of amyloid beta peptide((1-42)) (Abeta42-IR) and total tau protein (TTIR) were measured in lumbar cerebrospinal fluid of 48 patients (12 patients in each group) with normal pressure hydrocephalus (NPH), vascular dementia (VD), Alzheimer's disease (AD), Parkinson's disease without dementia (PD) and 24 controls (CON) using sensitive and specific enzyme immunoassays. TTIR in NPH was not significantly changed compared with VD, PD and CON, while NPH-Abeta42-IR was significantly decreased compared with PD and CON. In AD, significant increases of TTIR and significant decreases of Abeta42-IR were found. Using a TTIR by Abeta42 plot, all NPH, PD, and CON samples were within the non-AD plot region. 92% of AD and VD samples were within the AD and non-AD area, respectively. We conclude that combined measurement of Abeta42-IR and TTIR contributes to the differential diagnosis of NPH vs. AD and of AD vs. VD, respectively.

2 Article Clinical significance of neurobiochemical profiles in the lumbar cerebrospinal fluid of Alzheimer's disease patients. 2001

Rösler N, Wichart I, Jellinger KA. · Ludwig Boltzmann Institute of Clinical Neurobiology, Vienna, Austria. · J Neural Transm. · Pubmed #11314776 No free full text.

Abstract: Immunoreactivities of total apolipoprotein E (ApoE-IR), amyloid beta peptide(1-42) (Abeta42-IR), interleukin-6 (IL-6-IR), substance P (SPIR) and total tau protein (TTIR) were measured in lumbar cerebrospinal fluid samples of patients with Alzheimer's disease (AD), non-Alzheimer's dementias (NAD), neurological disorders without cognitive impairment (OND) and controls without central nervous system disease using sensitive and specific enzyme immunoassay methods. TTIR was highly significantly increased (P < 0,001) and Abeta42-IR was significantly decreased (P < 0,001 vs. OND/CO, P < 0,03 vs. NAD) in the AD cohort compared with the other diagnostic groups. Significant increases in AD were also found for ApoE-IR (P < 0,001) and IL-6 (P < 0,03), but there was a considerable overlap between groups. In the total AD cohort, SPIR was not significantly changed, but AD patients with late disease onset (>65 years) showed significantly higher values than both early onset patients (<65 years) and controls (P < 0,05). Discriminant function analysis showed that Abeta42-IR (cut-off value 375pg/ml) and TTIR (cut-off value 440 pg/ml) levels contributed most to the group classification of patients. At 85% sensitivity for AD and 100% specificity for controls, the combined evaluation of Abeta42-IR and TTIR in this cross-sectional study resulted in a graph separating AD from non-AD patients with increased specificity of 91% and 75% for AD versus OND and NAD, respectively.

3 Article Intra vitam lumbar and post mortem ventricular cerebrospinal fluid immunoreactive interleukin-6 in Alzheimer's disease patients. 2001

Rösler N, Wichart I, Jellinger KA. · Ludwig Boltzmann Institute of Clinical Neurobiology, Vienna, Austria. · Acta Neurol Scand. · Pubmed #11227132 No free full text.

Abstract: OBJECTIVES: In view of contradictory findings in previous studies, to examine the diagnostic value of interleukin-6 measurements in cerebrospinal fluid (CSF) of Alzheimer's disease patients. MATERIAL AND METHODS: Interleukin-6-immunoreactivity (IL-6-IR) was measured in 169 intra vitam lumbar and 21 post mortem ventricular CSF samples of patients with probable and neuropathologically confirmed Alzheimer's disease (AD), non-AD dementias (NAD), neurological disorders without cognitive impairment (OND) and controls (CON) using a specific sandwich enzyme immunoassay. RESULTS: Intra vitam lumbar samples had significantly elevated (P < 0.03) IL-6-IR not only in the AD, but also in the NAD and OND group compared with controls. AD patients with late onset (> 65 years) had slightly (P > 0.05) higher values than patients with early onset (< 65 years). In post mortem ventricular fluid, differences among groups did not reach significance (P > 0.05). CONCLUSION: We conclude that elevations of CSF IL-6-IR can not serve as a diagnostic marker of the disease, but, hypothetically, could reflect presence or activity of IL-6 mediated immunological phenomena in single AD patients.

4 Article Ex vivo lumbar and post mortem ventricular cerebrospinal fluid substance P-immunoreactivity in Alzheimer's disease patients. 2001

Rösler N, Wichart I, Jellinger KA. · Ludwig Boltzmann Institute of Clinical Neurobiology, PKH/B Building, Baumgartner Höhe 1, A-1140 Vienna, Austria. · Neurosci Lett. · Pubmed #11166952 No free full text.

Abstract: The concentration of substance P-immunoreactivity (SPIR) in ex vivo lumbar cerebrospinal fluid (CSF) of patients with probable Alzheimer's disease (AD), non-Alzheimer dementias, neurological patients without dementia and control subjects was determined using a sensitive and specific competitive enzyme-immunoassay. There were no significant differences between AD patients and the other groups, but patients with late onset AD (>65 years) showed significantly higher levels of SPIR than patients with early onset (<65 years) and controls. In post mortem ventricular fluid, SPIR levels of all groups were lower compared with the lumbar compartment, but without significant group differences. It is concluded that CSF SPIR may not serve as a diagnostic marker for AD, but possibly could reflect immunological or neuroprotective processes modulated by substance P in late onset AD patients.

5 Minor Elevated CNS concentrations of NFL in idiopathic normal pressure hydrocephalus (INPH) and subcortical arteriosclerotic encephalopathy (SAE). 2008

Jellinger KA, Rösler N. · No affiliation provided · Acta Neurol Scand. · Pubmed #18307570 No free full text.

This publication has no abstract.

6 Minor Cerebrospinal fluid interleukin-6 levels: a possible marker of disease activity. 2001

Jellinger KA, Rösler N, Wichart I. · No affiliation provided · Ann Neurol. · Pubmed #11761489 No free full text.

This publication has no abstract.