ALERT: Beta-amyloid Protein Levels in CSF May Serve as Novel Marker for Diagnosing Alzheimer Disease
October 3, 2009
Currently, there lacks a single test for accurately diagnosing Alzheimer disease (AD), with autopsy being the only definitive diagnostic tool. Gothenburg researchers have reported that AD patients have increased levels of beta-amyloid protein (Aβ1-16) in the cerebrospinal fluid (CSF) compared to healthy people. The identification of the novel marker in the CSF could help in diagnosing the condition, as well as determining the most effective medications for the disease.
Since the disease pathogenesis involves the accumulation of beta-amyloid peptides in specific regions of the brain, several studies are proposing the use of Aβ, found in CSF, as a core biomarker for diagnosing the mild cognitive impairment stage of AD. Extensive research has been conducted on Aβ to identify markers that can show the disrupted balance between the peptide production and clearance, and also to investigate whether the Aβ peptide aids in AD diagnosis.
Erik Portelius, a biochemist at the University of Gothenburg, Sweden, and coworkers, conducted the study on 18 AD patients and 18 healthy controls, to determine the effectiveness of Aβ peptides in diagnosing the condition using immunoprecipitation (IP) and mass spectrometry (MS). On multivariate analysis of the CSF samples, the results demonstrated that the 4 peptides, Aβ1-16, Aβ1-33, Aβ1-39 and Aβ1-42, helped in distinguishing AD from controls. Further, the combined model identified the diseased from normal individuals with 86% accuracy, 89% sensitivity, and 83% specificity. Also, the researchers found that Aβ1-16 played a key role in identifying AD from non-demented controls.
The same group of researchers confirmed the efficacy of the biomarker by conducting another independent study on 18 sporadic AD (SAD) patients, 6 depression patients, 7 carriers of familial AD (FAD) associated mutation, and 17 healthy subjects. The results of the study are listed below:
• Variation in the CSF Aβ isoform pattern of SAD patients compared to the controls and depression group
• Aβ1-16 in the CSF serves as a positive biomarker for AD
The investigators also found in their studies the prevalence of Aβ1-42 in the amyloid plaque. The formation of both Aβ1-42 and Aβ1-16 are from the same precursor, but the latter peptide is not found to be harmful. The new drugs that are currently being developed for AD decrease the Aβ1-42 production and raise the Aβ1-16 levels. Based on the findings, it was suggested that Aβ1-16 has the potential to diagnose and verify the efficacy of the drugs against the neurological disorder.
Alzheimer disease (AD), an irreversible progressive brain disorder, is the most common etiological factor of dementia in aged individuals. According to 2009 statistics of the Alzheimer’s Association, around 5.3 million people in the US are estimated to have AD, with a new case developing every 70 seconds. AD is primarily diagnosed by the exclusion of other dementias, and is based on medical history, clinical, neurological, and psychiatric evaluation. Since prompt and early identification facilitates immediate treatment initiation and prepares the families for a further course of action, the current discovery may serve as a breakthrough in the diagnosis and management of Alzheimer disease.
References
1. New marker for Alzheimer’s discovered. News Release. University of Gothenburg. Last accessed September 19, 2009.
2. Portelius E. Targeted Aβ proteomics – a tool to study the pathogenesis of Alzheimer’s disease [thesis]. Sweden: University of Gothenburg;2009.
3. 2009 Alzheimer’s Disease Facts and Figures. Alzheimer’s Association. Last accessed September 19, 2009.
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