The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
Targeted Overexpression of Human α-Synuclein Triggers Microglial Activation and an Adaptive Immune Response in a Mouse Model of Parkinson Disease
Open accessAbstract
Microglial activation and adaptive immunity have been implicated in the neurodegenerative processes in Parkinson disease. It has been proposed that these responses may be triggered by modified forms of alpha-synuclein (alpha-SYN), particularly nitrated species, which are released as a consequence of dopaminergic neurodegeneration. To examine the relationship between alpha-SYN, microglial activation, and adaptive immunity, we used a mouse model of Parkinson disease in which human alpha-SYN is overexpressed by a recombinant adeno-associated virus vector, serotype 2 (AAV2-SYN); this overexpression leads to slow degeneration of dopaminergic neurons. Microglial activation and components of the adaptive immune response were assessed using immunohistochemistry; quantitative polymerase chain reaction was used to examine cytokine expression. Four weeks after injection, there was a marked increase in CD68-positive microglia and greater infiltration of B and T lymphocytes in the substantia nigra pars compacta of the AAV2-SYN group than in controls. At 12 weeks, CD68 staining declined, but B- and T-cell infiltration persisted. Expression of proinflammatory cytokines was enhanced, whereas markers of alternative activation (i.e. arginase I and interleukins 4 and 13) were not altered. Increased immunoreactivity for mouse immunoglobulin was detected at all time points in the AAV2-SYN animals. These data show that overexpression of alpha-SYN alone, in the absence of overt neurodegeneration, is sufficient to trigger neuroinflammation with both microglial activation and stimulation of adaptive immunity.
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“Early activation of microglia is also present in a transgenic mouse model of PD in which wild-type human >-SYN is expressed under a tyrosine hydroxylase promoter (31).”
Cited by
Differential Roles of M1 and M2 Microglia in Neurodegenerative Diseases
Tang, Y., & Le, W. (2016) · Molecular Neurobiology · doi:10.1007/s12035-014-9070-5 · Cited by 2,190
The Role of Oxidative Stress in Parkinson's Disease
Dias, V., Junn, E., & Mouradian, M. M. (2013) · Journal of Parkinson’s Disease · doi:10.3233/jpd-130230 · Cited by 1,845
Innate immune activation in neurodegenerative disease
Heneka, M. T., Kummer, M. P., & Latz, E. (2014) · Nature Reviews Immunology · doi:10.1038/nri3705 · Cited by 1,437
Inflammation in neurodegenerative diseases
Amor, S., Puentes, F., Baker, D., & Van Der Valk, P. (2010) · Immunology · doi:10.1111/j.1365-2567.2009.03225.x · Cited by 1,355
Tansey, M. G., & Goldberg, M. S. (2010) · Neurobiology of Disease · doi:10.1016/j.nbd.2009.11.004 · Cited by 1,045
Metadata
- Authors
- Theodore, S., Cao, S., McLean, P. J., & Standaert, D. G.
- Venue
- Journal of Neuropathology & Experimental Neurology
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-12
- Volume
- 67
- Issue
- 12
- Pages
- 1149-1158
- ISSN
- 0022-3069 (ISSN-L)
- 1554-6578
- OpenAlex
- W1965624208
- Cited by
- 367
- References
- 17
- FWCI
- 5.99
- Type
- journal article
- Language
- en
- Open access
- green
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- Theodore, S., Cao, S., McLean, P. J., & Standaert, D. G. (2008). Targeted Overexpression of Human α-Synuclein Triggers Microglial Activation and an Adaptive Immune Response in a Mouse Model of Parkinson Disease. Journal of Neuropathology & Experimental Neurology. https://doi.org/10.1097/nen.0b013e31818e5e99
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