Decreased β-amyloid
            <sub>1-42</sub>
            in cerebrospinal fluid of patients with Creutzfeldt-Jakob disease

Otto, Markus; Esselmann, Hermann; Schulz‐Schaeffer, Walter; Neumann, Manuela; Schröter, Andreas; Ratzka, Peter; Cepek, Lukas; Zerr, Inga; Steinacker, Petra; Windl, Otto; Kornhuber, Johannes; Kretzschmar, Hans A.; Poser, S.; Wiltfang, Jens

doi:10.1212/wnl.54.5.1099

Cited by 166 publications

(103 citation statements)

References 42 publications

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“…A␤42 in disorders without ␤-amyloid plaques, such as CJD, 51 amyotrophic lateral sclerosis, 52 and multiple system atrophy. 53 These findings make a direct correlation questionable between low CSF A␤42 and deposition of A␤ in plaque.…”

Section: ␤-Amyloidmentioning

confidence: 99%

Cerebrospinal fluid protein biomarkers for Alzheimer’s disease

2004

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Summary:The introduction of acetylcholine esterase (AChE) inhibitors as a symptomatic treatment of Alzheimer's disease (AD) has made patients seek medical advice at an earlier stage of the disease. This has highlighted the importance of diagnostic markers for early AD. However, there is no clinical method to determine which of the patients with mild cognitive impairment (MCI) will progress to AD with dementia, and which have a benign form of MCI without progression. In this paper, the performance of cerebrospinal fluid (CSF) protein biomarkers for AD is reviewed. The diagnostic performance of the three biomarkers, total tau, phospho-tau, and the 42 amino acid form of ␤-amyloid have been evaluated in numerous studies and their ability to identify incipient AD in MCI cases has also been studied. Some candidate AD biomarkers including ubiquitin, neurofilament proteins, growth-associated protein 43 (neuromodulin), and neuronal thread protein (AD7c) show interesting results but have been less extensively studied. It is concluded that CSF biomarkers may have clinical utility in the differentiation between AD and several important differential diagnoses, including normal aging, depression, alcohol dementia, and Parkinson's disease, and also in the identification of Creutzfeldt-Jakob disease in cases with rapidly progressive dementia. Early diagnosis of AD is not only of importance to be able to initiate symptomatic treatment with AChE inhibitors, but will be the basis for initiation of treatment with drugs aimed at slowing down or arresting the degenerative process, such as ␥-secretase inhibitors, if these prove to affect AD pathology and to have a clinical effect.

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Section: ␤-Amyloidmentioning

confidence: 99%

Cerebrospinal fluid protein biomarkers for Alzheimer’s disease

2004

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“…However, low levels of Aβ in CSF have also been reported in disease without Aβ plaque pathology (i.e. CJD, multiple system atrophy and other dementias) [49][50][51] .…”

Section: Aβ1-42mentioning

confidence: 99%

Cerebrospinal fluid and blood biomarkers in Alzheimer’s disease

Humpel

Hochstrasser²

2011

WJP

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Due to an ever aging society and growing prevalence of Alzheimer's disease (AD), the challenge to meet social and health care system needs will become increasingly difficult. Unfortunately, a definite ante mortem diagnosis is not possible. Thus, an early diagnosis and identification of AD patients is critical for promising, early pharmacological interventions as well as addressing health care needs. The most advanced and most reliable markers are β-amyloid, total tau and phosphorylated tau in cerebrospinal fluid (CSF). In blood, no single biomarker has been identified despite an intense search over the last decade. The most promising approaches consist of a combination of several bloodbased markers increasing the reliability, sensitivity and specificity of the AD diagnosis. However, contradictory data make standardized testing methods in longitudinal and multi-center studies extremely difficult. In this review, we summarize a range of the most promising CSF and blood biomarkers for diagnosing AD.

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“…However there is a large overlap of tau-protein and β-amyloid levels in CSF of patients with different causes of dementia (36)(37)(38). Thus, in an individual case an etiological classification relying only on the tau-protein and β-amyloid level is not reliable.…”

Section: Analysis Of Brain Proteins In the Differential Diagnosis Ofmentioning

confidence: 99%

Reporting Cerebrospinal Fluid Data: Knowledge Base and Interpretation Software

Reiber¹,

Otto²,

Trendelenburg³

et al. 2001

Clinical Chemistry and Laboratory Medicine

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The compilation of cerebrospinal fluid (CSF) patient data together with a graphic display of immunoglobulin patterns in a single CSF report has two main advantages: analytical and clinical plausibility control of a complex set of data improves quality assessment and allows improved clinical specificity and sensitivity for recognition of disease-related "typical" data patterns. The widespread use of automated on-line evaluation programs can now be combined with knowledge-based programs for interpretation by clinical chemists and neurologists. These programs are based on knowledge of neuroimmunology, blood-CSF barrier function and dysfunction, influence of CSF flow on concentrations of blood-derived and brain-derived proteins in CSF, specific intrathecal antibody synthesis and relevance of brain proteins for differential diagnosis of degenerative diseases. The relevance of hyperbolic discrimination functions in quotient diagrams for the detection of intrathecal immunoglobulin synthesis is compared with earlier, still frequently used, linear interpretation functions. Differences found in commercially available interpretation software are discussed.

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Decreased β-amyloid _1-42 in cerebrospinal fluid of patients with Creutzfeldt-Jakob disease

Abstract: Low levels of Abeta1-42 in CSF do not exclude a diagnosis of CJD. Decreased levels of Abeta1-42 in CSF can occur without beta-amyloid plaque formation in the brain. However, the underlying mechanism of this phenomenon must be elucidated.

Cited by 166 publications

References 42 publications

Cerebrospinal fluid protein biomarkers for Alzheimer’s disease

Cerebrospinal fluid protein biomarkers for Alzheimer’s disease

Cerebrospinal fluid and blood biomarkers in Alzheimer’s disease

Reporting Cerebrospinal Fluid Data: Knowledge Base and Interpretation Software

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Decreased β-amyloid 1-42 in cerebrospinal fluid of patients with Creutzfeldt-Jakob disease

Abstract: Low levels of Abeta1-42 in CSF do not exclude a diagnosis of CJD. Decreased levels of Abeta1-42 in CSF can occur without beta-amyloid plaque formation in the brain. However, the underlying mechanism of this phenomenon must be elucidated.

Cited by 166 publications

References 42 publications

Cerebrospinal fluid protein biomarkers for Alzheimer’s disease

Cerebrospinal fluid protein biomarkers for Alzheimer’s disease

Cerebrospinal fluid and blood biomarkers in Alzheimer’s disease

Reporting Cerebrospinal Fluid Data: Knowledge Base and Interpretation Software

Contact Info

Product

Resources

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Decreased β-amyloid _1-42 in cerebrospinal fluid of patients with Creutzfeldt-Jakob disease