Identification of neurodegenerative factors using translatome–regulatory network analysis
Open accessAbstract
For degenerative disorders of the CNS, the main obstacle to therapeutic advancement has been the challenge of identifying the key molecular mechanisms underlying neuronal loss. We developed a combinatorial approach including translational profiling and brain regulatory network analysis to search for key determinants of neuronal survival or death. Following the generation of transgenic mice for cell type-specific profiling of midbrain dopaminergic neurons, we established and compared translatome libraries reflecting the molecular signature of these cells at baseline or under degenerative stress. Analysis of these libraries by interrogating a context-specific brain regulatory network led to the identification of a repertoire of intrinsic upstream regulators that drive the dopaminergic stress response. The altered activity of these regulators was not associated with changes in their expression levels. This strategy can be generalized for the identification of molecular determinants involved in the degeneration of other classes of neurons.
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The substantia nigra of individuals with Parkinson disease has reduced SATB1 and increased CDKN2A, MMP3, IL-6, IL-1α, and CXCL8 compared with healthy brains, suggesting increased senescence burden.
“Compared with brains of healthy individuals, the substantia nigra of individuals with Parkinson disease has reduced levels of SATB1 (a CDKN1A repressor) and increased levels of CDKN2A, MMP3, IL-6, IL-1α and CXCL8, suggesting an increased burden of senescence106,116.”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [116]
The Results section ('Validation of novel determinants of DA neurodegeneration'; page unavailable) reports significantly decreased SATB1 transcriptional activity in substantia nigra samples from people with incipient Parkinson disease versus controls. It explicitly says SATB1 expression levels did not change, contrary to the claimed reduction in levels. Our copy does not report increases in CDKN2A, MMP3, IL-6, IL-1α or CXCL8, or an increased senescence burden. (LLM, conf=0.87)
Experimental — accuracy not yet measuredBulk profiling experiments comparing substantia nigra pars compacta and ventral tegmental area neurons yielded gene expression differences but could not distinguish heterogeneous populations within each anatomical cluster.
“Bulk profiling experiments comparing SNc and VTA neurons did indeed yield some interesting gene expression differences [6–9], but suffered from the caveat that they could not distinguish heterogeneous populations within each anatomical cluster.”
From Classification of midbrain dopamine neurons using single-cell gene expression profiling approaches (2020) · cites this paper as [9]
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“Compared with brains of healthy individuals, the substantia nigra of individuals with Parkinson disease has reduced levels of SATB1 (a CDKN1A repressor) and increased levels of CDKN2A, MMP3, IL-6, IL-1α and CXCL8, suggesting an increased burden of senescence 106,116 .”
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Self-citation
- Authors
- Brichta, L., Shin, W., Jackson-Lewis, V., Blesa, J., Yap, E.-L., Walker, Z., Zhang, J., Roussarie, J.-P., Alvarez, M. J., Califano, A., Przedborski, S., & Greengard, P.
- Affiliations
- Rockefeller University (US)
- Columbia University (US)
- Corresponding author
- Brichta, Lars
- Greengard, Paul
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2015-07-27
- Volume
- 18
- Issue
- 9
- Pages
- 1325-1333
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC4763340
- OpenAlex
- W2200183975
- Cited by
- 118
- References
- 60
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 10 · 2023: 11 · 2022: 12 · 2021: 8 · 2020: 15 · 2019: 17 · 2018: 11 · 2017: 16 · 2016: 6 · 2015: 2
- FWCI
- 8.23
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Depósito Digital e-UCJC (submittedVersion)
- Funders
- National Institute of General Medical Sciences (T32GM008798)
- National Institute of Neurological Disorders and Stroke (NS088009, R01NS072428, R21NS078614, NS078614, NS072428, R21NS088009)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bioinformatics and Genomic Networks
- Keywords
- Parkinson's disease, neurodegeneration, dopaminergic neurons, translatome, translational profiling, regulatory network analysis, upstream regulators, neuronal survival, midbrain, transgenic mice
- MeSH terms
- Animals, Male, Mesencephalon, Mice, Inbred C57BL, Mice, Transgenic, Nerve Net, Substantia Nigra, Protein Biosynthesis, Neurodegenerative Diseases, Mice, Dopaminergic Neurons
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