The DOI matches its Crossref record; 103 of the 103 references it cites were found in a registry or an index.
Progress towards therapies for disease modification in Parkinson's disease
Open accessAbstract
The development of interventions to slow or halt the progression of Parkinson's disease remains a priority for patients and researchers alike. To date, no agents have been shown to have unequivocal evidence of disease-modifying effects in Parkinson's disease. The absence of disease-modifying treatments might relate not only to inadequate approaches for the selection of therapeutic candidates but also to insufficient attention to detail in clinical trial design. Better understanding of Parkinson's disease pathogenesis associated with advances in laboratory models, the use of objective biomarkers of disease progression and target engagement, and a focus on agents known to be safe for human use, alongside the use of precision medicine approaches, should together greatly increase the likelihood for successful identification of disease-modifying treatments for Parkinson's disease.
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Self-citationMulticenter Analysis of Glucocerebrosidase Mutations in Parkinson's Disease
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Self-citationTrial of Lixisenatide in Early Parkinson’s Disease
Meissner, W. G., Remy, P., Giordana, C., Maltête, D., Derkinderen, P., Houéto, J.-L., Anheim, M., Benatru, I., Boraud, T., Brefel-Courbon, C., et al. (2024) · New England Journal of Medicine · doi:10.1056/nejmoa2312323 · Cited by 369
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Recent advances in the study of Na+/K+-ATPase in neurodegenerative diseases
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Metadata
- Authors
- Vijiaratnam, N., Simuni, T., Bandmann, O., Morris, H. R., & Foltynie, T.
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2021-07
- Volume
- 20
- Issue
- 7
- Pages
- 559-572
- ISSN
- 1474-4422 (ISSN-L)
- OpenAlex
- W3172058623
- Cited by
- 419
- References
- 103
- FWCI
- 21.64
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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