<p dir="ltr">Alpha-synuclein is a synaptic protein important for cell communication and protein degradation processes. Abnormal increases in alpha-synuclein protein and changes in its structure are detected in neurodegenerative diseases such as Parkinson's disease. In a prior publication, we showed that an adeno-associated virus (AAV) driving expression of the human alpha-synuclein gene (hSNCA) in a dedicated vocal brain region (basal ganglia Area X) in the adult male zebra finch results in increased alpha-synuclein protein levels and Parkinsonian-like song changes. (Vocal changes in a zebra finch model of Parkinson’s disease characterized by alpha-synuclein overexpression in the song-dedicated anterior forebrain pathway, <a href="https://doi.org/10.1371/journal.pone.0265604" rel="noreferrer" target="_blank">https://doi.org/10.1371/journal.pone.0265604</a>; University of Arizona ReData link: <a href="https://doi.org/10.25422/azu.data.16619782" rel="noreferrer" target="_blank">https://doi.org/10.25422/azu.data.16619782</a>).</p>We extend upon this work in the present study by characterizing the cellular distribution and protein pathology of alpha-synuclein in finch vocal control brain regions Area X and lMAN that underlie the Parkinsonian-like song changes.<br><br><br><br><hr><i>For inquiries regarding the contents of this dataset, please contact the Corresponding Author listed in the README.txt file. Administrative inquiries (e.g., removal requests, trouble downloading, etc.) can be directed to data-management@arizona.edu</i><p></p>
Funding
Alpha-synuclein driven cellular changes and vocal dysfunction in Parkinson's Disease
National Institute of Neurological Disorders and Stroke
Research reported in this publication was supported by the National Institute on Neurological Diseases and Stroke of the National Institutes of Health under Award Number R21 NS123512 to J.E. Miller. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Microscopy work was supported by a Core Facilities Pilot Program grant award to J.E. Miller through the University of Arizona Imaging Cores - Optical Core Facility (RRID:SCR_023355). R. Bjork was supported by the University of Arizona Graduate and Professional Students Council research award. F. Patel and M. Daly were also supported by research grants through the University of Arizona Honors College, and F. Patel, from the Department of Neuroscience.