Background: We examined the utility of quantification of α-synuclein (SNCA) in the cerebrospinal fluid (CSF) to differentiate patients with Alzheimer disease (AD), dementia with Lewy bodies (DLB), Parkinson disease (PD), and multiple system atrophy (MSA).
Methods: Thirty-seven patients were divided into 4 age-matched and sex-matched clinical groups: AD (n = 9), DLB (n = 6), PD (n = 11), and MSA (n = 11). Eleven subjects served as neurological disease controls. The total of 48 subjects included 27 men and 21 women, aged 66.5 ± 11.4 years. We performed a solid-phase sandwich enzyme-linked immunosorbent assay, which enables the sensitive quantification of CSF SNCA.
Results: In comparison with controls, CSF SNCA levels in AD were significantly higher (P < 0.05). CSF SNCA levels in PD (P < 0.001), DLB (P < 0.01), and MSA (P < 0.05) were all significantly lower than those in AD. However, CSF SNCA levels did not differ significantly among the 3 synucleinopathies.
Conclusions: The results of the present study suggest that quantification of CSF SNCA helps in the differentiation of synucleinopathies (PD, DLB, and MSA) from AD. However, CSF SNCA levels did not differ significantly among the 3 synucleinopathies.
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http://dx.doi.org/10.1097/WAD.0b013e31823899cc | DOI Listing |
Acta Neuropathol Commun
January 2025
Department of Neurology, University Hospital Carl Gustav Carus, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Parkinson's disease (PD) is a heterogeneous neurodegenerative disorder with a wide range of clinical phenotypes. Pathologically, it is characterized by neuronal inclusions containing misfolded, fibrillar alpha-synuclein (aSyn). Prion-like properties of aSyn contribute to the spread of aSyn pathology throughout the nervous system as the disease progresses.
View Article and Find Full Text PDFClin Transl Sci
December 2024
Department of Neurology, Affiliated Hospital of Qingdao University, Qingdao, China.
Glial fibrillary acidic protein (GFAP) is an intermediate filament protein expressed mainly in astrocytes of the central nervous system (CNS), a potential biomarker of cognitive decline in Parkinson's disease (PD). The central motor subtypes of PD include tremor-dominant (TD), postural instability and gait disorder (PIGD), and indeterminate subtypes, whose different course of disease requires the development of biomarkers that can predict progression based on motor subtypes. In this study, we aimed to assess the predictive value of cerebrospinal fluid (CSF) GFAP for PD motor subtypes in PD.
View Article and Find Full Text PDFAnn Med
December 2024
Department of Neurology, Liaocheng People's Hospital, Shandong University, Jinan, P.R. China.
Objectives: This study aimed to identify key genes related to copper metabolism in Parkinson's disease (PD), providing insight into their roles in disease progression.
Methods: Using bioinformatic analyses, the study identified hub genes related to copper metabolism in PD patients. Differentially expressed genes (DEGs) were identified using the limma package, and copper-metabolism-related genes (CMRGs) were sourced from the Genecard database.
Front Neurosci
September 2024
Scantox Neuro GmbH, Grambach, Austria.
Background: Parkinson's disease (PD) is a debilitating neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons and the accumulation of α-synuclein (α-syn) aggregates. The A53T missense point mutation occurs in autosomal dominant familial PD and has been found to promote the aggregation of α-syn. To investigate the role of the A53T mutation in PD, researchers have developed various mouse models with this mutation.
View Article and Find Full Text PDFNeurology
September 2024
From the Tanz Centre for Research in Neurodegenerative Diseases (C.A., I.M.-V., A.V., S.T., M.H., F.T., C. Sato, D.M., C.J.A., K.M., A.E.L., E.R., G.G.K., M.C.T.); Krembil Brain Institute (I.M.-V., A.M.-R., B.C., D.F.T.-W., A.E.L., S.H.F., G.G.K., M.C.T.); The Edmond J. Safra Program in Parkinson's Disease and Morton and Gloria Shulman Movement Disorders Clinic (I.M.-V., A.M.-R., B.C., A.E.L., S.H.F., G.G.K., M.C.T.); Rossy Progressive Supranuclear Palsy Centre (I.M.-V., A.M.-R., A.E.L., G.G.K., M.C.T.), University Health Network and the University of Toronto; and University Health Network Memory Clinic (D.M.-F., C. Salvo, D.F.T.-W.), Toronto, Ontario, Canada.
Background And Objectives: There is no disease-modifying treatment of corticobasal syndrome (CBS) and progressive supranuclear palsy (PSP), 2 disorders characterized by their striking phenotypic, and, in CBS, pathologic heterogeneity. Seed amplification assays (SAAs) could enable the detection of neuropathologic processes, such as α-synuclein (αSyn) copathology, that affect the success of future disease-modifying treatment strategies. The primary objective was to assess possible αSyn copathology in CBS and PSP, as detected in CSF using an αSyn SAA (αSyn-SAA).
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