Do the 432 differentially expressed proteins represent cause or consequence of AD pathology?

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Composite

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Novelty

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Mechanistic

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Druggability

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Priority

85%

Importance

90%

Tractability

70%

Market price

50%

Description

The study identifies extensive proteomic changes but cannot distinguish primary pathogenic drivers from secondary responses to neurodegeneration. This fundamental question is critical for identifying viable therapeutic targets versus downstream biomarkers.

Gap type: open_question Source paper: Quantitative proteomic analysis of the frontal cortex in Alzheimer’s disease. (2021, Journal of neurochemistry, PMID:32614981)

Resolution criteria

Resolved when the 432 AD frontal-cortex protein changes are separated into upstream drivers versus downstream consequences. Required evidence: integration of human proteomics with Braak/amyloid stage, cell-type deconvolution or spatial proteomics, genetic or longitudinal biomarker instruments, and perturbation tests for prioritized proteins in iPSC-neuron/organoid or mouse models. Closure requires a ranked driver/consequence classification with at least several candidates validated by perturbation that alters AD-relevant pathology.

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