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Chunk #35 — Discussion

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Integrated single-cell multiomic profiling of caudate nucleus suggests key mechanisms in alcohol use disorder.
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Another limitation is that in post-mortem brain samples, both pre-existing differences that increase risk for AUD and differences associated with the extended, excessive alcohol consumption characteristic of AUD are present. Some AUD-associated differences we observed (e.g., changes in inflammatory and myelinating processes) are likely to be associated with the consequences of AUD. Therefore, future studies should further leverage genetic information to tease apart cause and consequence. Future directions should also include experimental validation of the upstream genes identified in the above gene regulatory network and cell-cell communication computational analyses.