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Cardiac Alpha-Synuclein Is Present in Alpha-Synucleinopathies
Author(s) -
Keivan Javanshiri,
Tove Drakenberg,
Mattias Haglund,
Elisabet Englund
Publication year - 2022
Publication title -
journal of parkinson's disease/journal of parkinson's disease (online)
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.747
H-Index - 45
eISSN - 1877-718X
pISSN - 1877-7171
DOI - 10.3233/jpd-223161
Subject(s) - synucleinopathies , medicine , alpha synuclein , pathology , dementia with lewy bodies , atrophy , dementia , autopsy , neuropathology , parkinson's disease , disease
Background: Alpha-synucleinopathies (AS) are characterized by pathologic aggregations of alpha-synuclein (α-syn) in the central nervous system, and comprise dementia with Lewy bodies, Parkinson’s disease, and multiple system atrophy. Previous studies on AS have reported findings of α-syn pathology in the peripheral nervous system of multiple organs, including the heart. Objective: The aim of this study was to further investigate and confirm the presence of cardiac α-syn in AS compared to other major neurocognitive disorders in a neuropathologically confirmed cohort. Methods: All deceased patients with performed autopsy and with neuropathologically confirmed AS at the Clinical Department of Pathology in Lund 2010–May 2021 were evaluated for inclusion. Cases with insufficiently sampled cardiac tissue or only limited neuropathological investigation were excluded. An age-matched group of individuals with other neurodegenerative diseases, having no α-syn in the CNS, served as controls. In total, 68 AS and 32 control cases were included in the study. Immunohistochemistry for detection of cardiac α-syn aggregates was performed. Results: The AS group had a significantly higher prevalence of cardiac α-syn pathology (p≤0.001) than the control group, 82% and 0%, respectively. Conclusion: This study confirms the association between AS and the presence of cardiac α-syn in a neuropathologically confirmed cohort. This motivates further research on potential pathophysiological effects on cardiac function in AS patients.

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