Which aging-associated molecular pathways are causally linked to neurodegeneration versus correlative?

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50%

Description

The incomplete analysis highlights the unresolved challenge of distinguishing protective aging responses from pathological precursors. Without this distinction, therapeutic targets remain unclear.

Source: Debate session sess_SDA-2026-04-02-gap-aging-mouse-brain-v3-20260402 (Analysis: SDA-2026-04-02-gap-aging-mouse-brain-v3-20260402)

Resolution criteria

Resolution requires: (1) genetic fate-mapping in mouse models ( inducible CreERT2 crossed with aging reporter lines) tracing whether aging-responsive gene expression changes in neurons are protective adaptations or drivers of neurodegeneration; (2) longitudinal single-cell multiome (ATAC+RNA) of neurons from aged (>=18 months) vs young mice tracking chromatin state transitions toward either protective or pathological endpoints; (3) intervention study modulating candidate aging pathway (e.g., mTOR, AMPK, sirtuins) demonstrating causal separation of protective vs pathogenic outcomes with >=30% difference in behavioral readouts. Correlation without causal intervention does not resolve the protective/pathogenic distinction.

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