ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2018
Angiotensin Type 1 Receptor Antagonists Protect Against Alpha-Synuclein-Induced Neuroinflammation and Dopaminergic Neuron Death.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 87 citations in OpenAlex.
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- Brain-derived extracellular vesicle proteomics reveals neuroprotection induced by the ARB candesartan in Parkinson's disease patients.NPJ Parkinson's disease · 2025Article
- The application of telmisartan in central nervous system disorders.Pharmacological reports : PR · 2025Review
- Involvement of Neuroinflammation and Oxidative Stress in L-DOPA-Induced Dyskinesia in Parkinson's Disease: Role of Renin-Angiotensin System and ROCK Pathway.Antioxidants (Basel, Switzerland) · 2025Review
- Review
- Serum angiotensin type-1 receptor autoantibodies and neurofilament light chain as markers of neuroaxonal damage in post-COVID patients.Frontiers in immunology · 2025Article
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- Investigation in the cannabigerol derivative VCE-003.2 as a disease-modifying agent in a mouse model of experimental synucleinopathy.Behavioral and brain functions : BBF · 2024Article
- Mitochondrial Dysfunction in Parkinson's Disease: A Contribution to Cognitive Impairment?International journal of molecular sciences · 2024Review
- Non-HLA angiotensin-type-1 receptor autoantibodies mediate the long-term loss of grafted neurons in Parkinson's disease models.Stem cell research & therapy · 2024Article
- The role of the brain renin-angiotensin system in Parkinson´s disease.Translational neurodegeneration · 2024Review
- The role of angiotensin receptor blockers in treating epilepsy: a review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Review
- Angiotensin type 1 receptor activation promotes neuronal and glial alpha-synuclein aggregation and transmission.NPJ Parkinson's disease · 2024Article
- Research progress on ferroptosis in the pathogenesis and treatment of neurodegenerative diseases.Frontiers in cellular neuroscience · 2024Review
- Astrocytic insulin receptor controls circadian behavior via dopamine signaling in a sexually dimorphic manner.Nature communications · 2023Article
- Extracellular Vesicles and Their Renin-Angiotensin Cargo as a Link between Metabolic Syndrome and Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2023Article
- Interactions between Angiotensin Type-1 Antagonists, Statins, and ROCK Inhibitors in a Rat Model of L-DOPA-Induced Dyskinesia.Antioxidants (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The loss of dopaminergic neurons and α-synuclein accumulation are major hallmarks of Parkinson's disease (PD), and it has been suggested that a major mechanism of α-synuclein toxicity is microglial activation. The lack of animal models that properly reproduce PD, and particularly the underlying synucleinopathy, has hampered the clarification of PD mechanisms and the development of effective therapies. Here, we used neurospecific adeno-associated viral vectors serotype 9 coding for either the wild-type or mutated forms of human alpha-synuclein (WT and SynA53T, respectively) under the control of a synapsin promoter to further induce a marked dopaminergic neuron loss together with an important microglial neuroinflammatory response. Overexpression of neuronal alpha-synuclein led to increased expression of angiotensin type 1 receptors and NADPH oxidase activity, together with a marked increase in the number of OX-6-positive microglial cells and expression of markers of phagocytic activity (CD68) and classical pro-inflammatory/M1 microglial phenotype markers such as inducible nitric oxide synthase, tumor necrosis factor alpha, interleukin-1β, and IL-6. Moreover, a significant decrease in the expression of markers of immunoregulatory/M2 microglial phenotype such as the enzyme arginase-1 was constantly observed. Interestingly, alpha-synuclein-induced changes in microglial phenotype markers and dopaminergic neuron death were inhibited by simultaneous treatment with the angiotensin type 1 blockers candesartan or telmisartan. Our results suggest the repurposing of candesartan and telmisartan as a neuroprotective strategy for PD.
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