ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2026
Integrative genomic and functional analyses reveal NINL as a modulator of tau aggregation.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionProteostasis dysfunction is a hallmark of frontotemporal dementia (FTD) and Alzheimer's disease (AD), yet the genetic and molecular pathways that disrupt protein homeostasis remain poorly understood.
methodsWe integrated human genetics, transcriptomics, and functional studies to identify proteostasis network components involved in tauopathy.
resultsWe identified 18 proteostasis network genes harboring 75 rare, damaging variants enriched in FTD and/or AD. These genes, spanning multiple proteostasis pathways, were differentially expressed in microtubule associated protein tau (MAPT) mutant neurons and dysregulated in FTD and AD brains. NINL, which encodes Nlp, emerged as the only gene consistently upregulated across all datasets. NINL overexpression reduced tau seeding and enhanced lysosomal proteolytic activity, whereas two FTD-enriched NINL frame shift variants impaired Nlp expression and abolished these protective effects. DISCUSSION: We identified a set of proteostasis genes with genetic and transcriptional links to neurodegeneration and revealed NINL as a novel regulator of tau aggregation.
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