ArticleNature aging2024
GDF1 ameliorates cognitive impairment induced by hearing loss.
Article in Nature aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Exploring the Relationship Between Hearing Loss and Cognitive Dysfunction from the Perspective of Molecular Mechanisms.Biomolecules · 2026Review
- Development and Validation of a Predictive Model for Mild Cognitive Impairment in Older Adults with Multimorbidity.Clinical interventions in aging · 2026Article
- DNAH11 impairs memory via disrupted synaptic plasticity in noise-induced hidden hearing loss mice.Cell biology and toxicology · 2025Article
- Single-cell profiling identifies hair cell SLC35F1 deficiency as a signature of primate cochlear aging.Nature aging · 2025Article
- Rational Design of Inner Ear Drug Delivery Systems.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- METTL3 governs thymocyte development and thymic involution by regulating ferroptosis.Nature aging · 2024Article
- Comparative study on structural and functional brain differences in mild cognitive impairment patients with tinnitus.Frontiers in aging neuroscience · 2024Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
Abstract
Hearing loss is associated with an increased risk of Alzheimer disease (AD). However, the mechanisms of hearing loss promoting the onset of AD are poorly understood. Here we show that hearing loss aggravates cognitive impairment in both wild-type mice and mouse models of AD. Embryonic growth/differentiation factor 1 (GDF1) is downregulated in the hippocampus of deaf mice. Knockdown of GDF1 mimics the detrimental effect of hearing loss on cognition, while overexpression of GDF1 in the hippocampus attenuates the cognitive impairment induced by deafness. Strikingly, overexpression of GDF1 also attenuates cognitive impairment in APP/PS1 transgenic mice. GDF1 activates Akt, which phosphorylates asparagine endopeptidase and inhibits asparagine endopeptidase-induced synaptic degeneration and amyloid-β production. The expression of GDF1 is downregulated by the transcription factor CCAAT-enhancer binding protein-β. These findings indicate that hearing loss could promote AD pathological changes by inhibiting the GDF1 signaling pathway; thus, GDF1 may represent a therapeutic target for AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.