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Basic Science and Pathogenesis.

Sunny Kumar1,2,3, Ibai Diez1,4, Ana Claudia Amaral1,2,5

  • 1Harvard Medical School, Boston, MA, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 25, 2025
PubMed
Summary
This summary is machine-generated.

Individuals with Alzheimer disease neuropathologic changes (ADNC) but no cognitive decline show reduced neuroinflammation and downregulated TNF and NF-κB pathways. This suggests glial cell pro-inflammatory reactions influence cognitive outcomes in ADNC.

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Area of Science:

  • Neuroscience
  • Genomics
  • Pathology

Background:

  • Some individuals with Alzheimer disease neuropathologic changes (ADNC) remain cognitively normal, indicating resilience mechanisms.
  • Understanding resilience to ADNC is crucial for identifying new biomarkers and therapeutic targets for Alzheimer disease (AD).

Purpose of the Study:

  • To compare brain changes and gene expression profiles in resilient individuals (cognitively normal with ADNC) and demented AD patients with equivalent ADNC loads.
  • To identify molecular mechanisms underlying cognitive resilience in the presence of AD neuropathology.

Main Methods:

  • Compared neuropathological assessments and RNA-seq data from dorsolateral prefrontal cortex of resilient, demented AD, and control individuals (ROSMAP cohort).
  • Utilized DESeq2 for differential gene expression analysis, accounting for age, gender, batch, and post-mortem interval.
  • Employed a Wald test to identify differentially expressed genes (DEGs) between demented AD and resilient groups.

Main Results:

  • Resilient brains had equivalent amyloid plaques and tangles but lower tau neuropil threads and pTau levels compared to demented AD brains.
  • Resilient brains showed reduced burdens of activated astrocytes and microglia, with decreased apoptotic, neuroinflammatory, and protein phosphorylation processes.
  • Pathway analysis revealed downregulation of TNF, JAK-STAT, and NF-κB signaling in resilient brains, including shared downregulation of CXCL1 and CXCL2.

Conclusions:

  • Aberrant pathological tau species in neurites and synapses may trigger glial pro-inflammatory responses involving TNF and NF-κB pathways.
  • These inflammatory pathways appear critical in determining cognitive fate (dementia vs. preserved cognition) in individuals with ADNC.