Amyloid and tau display distinct patterns across Alzheimer's in anterior caudate.

In the anterior caudate of 41 Alzheimer's donors, diffuse amyloid beta plaques in gray matter and phosphorylated tau threads in white matter co-occur with tau-linked microglial and interneuron gene changes.

• Why it matters: Subcortical regions like the anterior caudate are less characterized than cortex, leaving a gap in cellular-resolution maps of how Alzheimer’s pathology relates to specific cell populations.
• What they did: The study combined digital pathology with single-nucleus and spatial gene expression analyses to test whether neuronal cell-type abundance changes with pathology and to identify cell-type–specific gene shifts.
• The result: No significant neuronal cell-type abundance loss or gain was detected with increasing pathology, but FLT1+/IL1B+ microglia increased with tau burden, and fast-spiking PTHLH-PVALB interneurons showed gene changes tied to ion channels, cellular trafficking, and phosphorylation.

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