Dysregulation of AMPA receptor subunit expression in sporadic ALS post‐mortem brain Article Swipe
Jenna M. Gregory
,
Matthew R. Livesey
,
Karina McDade
,
Bhuvaneish T. Selvaraj
,
Samantha K. Barton
,
Siddharthan Chandran
,
Colin Smith
·
YOU?
·
· 2019
· Open Access
·
· DOI: https://doi.org/10.1002/path.5351
YOU?
·
· 2019
· Open Access
·
· DOI: https://doi.org/10.1002/path.5351
Amyotrophic lateral sclerosis (ALS) is characterised by progressive motor neuron degeneration. Although there are over 40 genes associated with causal monogenetic mutations, the majority of ALS patients are not genetically determined. Causal ALS mutations are being increasingly mechanistically studied, though how these mechanisms converge and diverge between the multiple known familial causes of ALS (fALS) and sporadic forms of ALS (sALS) and furthermore between different neuron types, is poorly understood. One common pathway that is implicated in selective motor neuron death is enhanced α‐amino‐3‐hydroxyl‐5‐methyl‐4‐isoxazole‐propionate (AMPAR)‐mediated excitoxicity. Specifically, human in vitro and pathological evidence has linked the C9orf72 repeat expansion mutation to a relative increase in the Ca 2+ ‐permeable AMPAR population due to AMPAR subunit dysregulation. Here, we provide the first comparative quantitative assessment of the expression profile of AMPAR subunit transcripts, using BaseScope, in post‐mortem lower motor neurons (spinal cord, anterior horn), upper motor neurons (motor cortex) and neurons of the pre‐frontal cortex in sALS and fALS due to mutations in SOD1 and C9orf72 . Our data indicated that AMPAR dysregulation is prominent in lower motor neurons in all ALS cases. However, sALS and mutant C9orf72 cases exhibited GluA1 upregulation whereas mutant SOD1 cases displayed GluA2 down regulation. We also showed that sALS cases exhibited widespread AMPAR dysregulation in the motor and pre‐frontal cortex, though the exact identity of the AMPAR subunit being dysregulated was dependent on brain region. In contrast, AMPAR dysregulation in mutant SOD1 and C9orf72 cases was restricted to lower motor neurons only. Our data highlight the complex dysregulation of AMPAR subunit expression that reflects both converging and diverging mechanisms at play between different brain regions and between ALS cohorts. © 2019 Authors. Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.
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- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1002/path.5351
- https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/path.5351
- OA Status
- hybrid
- Cited By
- 48
- References
- 27
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W2978024463
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W2978024463Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1002/path.5351Digital Object Identifier
- Title
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Dysregulation of AMPA receptor subunit expression in sporadic ALS post‐mortem brainWork title
- Type
-
articleOpenAlex work type
- Language
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enPrimary language
- Publication year
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2019Year of publication
- Publication date
-
2019-10-03Full publication date if available
- Authors
-
Jenna M. Gregory, Matthew R. Livesey, Karina McDade, Bhuvaneish T. Selvaraj, Samantha K. Barton, Siddharthan Chandran, Colin SmithList of authors in order
- Landing page
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https://doi.org/10.1002/path.5351Publisher landing page
- PDF URL
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https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/path.5351Direct link to full text PDF
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YesWhether a free full text is available
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hybridOpen access status per OpenAlex
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https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/path.5351Direct OA link when available
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AMPA receptor, Protein subunit, Neuroscience, Receptor, Expression (computer science), Biology, Glutamate receptor, Genetics, Gene, Computer science, Programming languageTop concepts (fields/topics) attached by OpenAlex
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48Total citation count in OpenAlex
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2025: 8, 2024: 5, 2023: 9, 2022: 11, 2021: 8Per-year citation counts (last 5 years)
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27Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.One | 71 |
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| abstract_inverted_index.GluA1 | 190 |
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| abstract_inverted_index.Wiley | 284 |
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| abstract_inverted_index.upper | 144 |
| abstract_inverted_index.using | 133 |
| abstract_inverted_index.vitro | 90 |
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| abstract_inverted_index.(motor | 147 |
| abstract_inverted_index.(sALS) | 61 |
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| abstract_inverted_index.profile | 128 |
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| abstract_inverted_index.region. | 230 |
| abstract_inverted_index.regions | 270 |
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| abstract_inverted_index.evidence | 93 |
| abstract_inverted_index.familial | 51 |
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| abstract_inverted_index.highlight | 250 |
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| abstract_inverted_index.prominent | 174 |
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| abstract_inverted_index.population | 111 |
| abstract_inverted_index.restricted | 242 |
| abstract_inverted_index.widespread | 207 |
| abstract_inverted_index.Amyotrophic | 1 |
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| abstract_inverted_index.furthermore | 63 |
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| abstract_inverted_index.upregulation | 191 |
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| corresponding_author_ids | https://openalex.org/A5069145955, https://openalex.org/A5062181327 |
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| institutions_distinct_count | 7 |
| corresponding_institution_ids | https://openalex.org/I1283521677, https://openalex.org/I98677209 |
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