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Detection of Disease-associated α-synuclein by Enhanced ELISA in the Brain of Transgenic Mice Overexpressing Human A53T Mutated α-synuclein
Published on: May 30, 2015
α-Synuclein seed amplification assay positivity beyond synucleinopathies
Ivan Martinez-Valbuena1, Sarah Fullam2, Sean O'Dowd2
1Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Canada; Krembil Brain Institute, University Health Network, Toronto, Ontario, M5T 0S8, Canada; Rossy Centre for PSP, Toronto Western Hospital, Toronto, Ontario, M5T 2S8, Canada.
Abstract:
Neurodegenerative diseases are increasingly recognized as complex disorders involving multiple protein pathologies, with α-synuclein frequently observed beyond classical synucleinopathies such as Parkinson's disease and multiple system atrophy. Recent advances in seed amplification assays (SAAs) have enabled the highly sensitive and specific detection of misfolded α-synuclein in vivo, particularly in cerebrospinal fluid (CSF). This review focuses on CSF-based α-synuclein SAAs and their application in detecting co-pathology across non-synucleinopathies, including Alzheimer's disease, progressive supranuclear palsy, corticobasal syndrome, idiopathic normal pressure hydrocephalus, and traumatic brain injury. Evidence indicates a role for α-synuclein in clinical heterogeneity and disease progression. Emerging diagnostic frameworks increasingly support integrating co-pathologies into classification and therapeutic strategies. Addressing key knowledge gaps, such as α-synuclein interactions with other protein pathologies, and current limitations of α-syn SAA, such as the lack of quantification of misfolded α-synuclein seeds, will refine precision medicine and improve outcomes for patients with neurodegenerative diseases.

