Abstract
The detection of α-synuclein (α-syn) in the cerebrospinal fluid (CSF) of patients with synucleinopathy has yielded promising but inconclusive results. The aim of the present study was to determine the diagnostic value of α-syn as a biological marker for Dementia with Lewy bodies (DLB) vs. normal subjects and patients with Alzheimer’s disease (AD), after strict control of several recognized confounders. Sixteen patients with DLB, 18 patients with AD and 22 age- and sex-matched normal controls (CTRL) were recruited. The levels of total α-syn in CSF were measured using a novel enzyme-linked immunosorbent assay. There was a significant increase of CSF α-syn levels in DLB patients as compared to the CTRL and AD groups (P= 0.049 and 0.01 respectively). ROC analysis revealed that increased α-syn was 81.8% specific for the discrimination of DLB vs. CTRL and 90% vs. AD. However, sensitivity was lower (56.2 % and 50% respectively). These findings provide evidence for a possible diagnostic role of α-syn as a surrogate biomarker for DLB.
Highlights
Diagnosis of dementing neurodegenerative disorders such as Alzheimer’s disease (AD) and Dementia with Lewy Bodies (DLB) is considered necessary for a number of reasons, including treatment initiation at the earliest stage [1]
Cerebrospinal fluid (CSF) biomarkers may offer a good tool for early diagnosis, since CSF directly interacts with the extracellular space of the brain, giving a clue of pathophysiological processes [2]
In AD, CSF biomarkers have been recognized to reflect the prevailing hypothesis for its pathogenesis and the typical biochemical profile is a decrease of Aβ42 levels, which is considered to reflect amyloidogenesis, as well as an increase of total tau (T-tau) and phosphorylated tau (P-tau), which reflect axonal degeneration and tangle formation [3,4]
Summary
Diagnosis of dementing neurodegenerative disorders such as Alzheimer’s disease (AD) and Dementia with Lewy Bodies (DLB) is considered necessary for a number of reasons, including treatment initiation at the earliest stage [1]. In AD, CSF biomarkers have been recognized to reflect the prevailing hypothesis for its pathogenesis and the typical biochemical profile is a decrease of Aβ42 levels, which is considered to reflect amyloidogenesis, as well as an increase of total tau (T-tau) and phosphorylated tau (P-tau), which reflect axonal degeneration and tangle formation [3,4]. It has been shown that α-Syn is present in detectable amounts in CSF of normal subjects and PD patients [7], with its origin to be mostly brain derived [8] and it has received much attention as a possible biomarker in synucleinopathies [9]. Studies measuring CSF α-Syn levels in DLB have yielded conflicting results showing either decreased levels [10,11,12,13,14,15], or no difference between patients and controls [16,17,18,19,20,21]
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