ArticleCerebral cortex (New York, N.Y. : 1991)2018
Cholinergic Grb2-Associated-Binding Protein 1 Regulates Cognitive Function.
Article in Cerebral cortex (New York, N.Y. : 1991), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed.
- Ursolic acid reduces Aβ-driven aggression via Gab1-mediated autophagy and dorsal hippocampal circuit modulation in Alzheimer's disease.Journal of advanced research · 2026Article
- Exploration of the shared gene signatures and molecular mechanisms between Alzheimer's disease and intracranial aneurysm.Scientific reports · 2024Article
- Gene therapy for polygenic or complex diseases.Biomarker research · 2024Review
- The Chronic Effects of a Single Low-Intensity Blast Exposure on Phosphoproteome Networks and Cognitive Function Influenced by Mutant Tau Overexpression.International journal of molecular sciences · 2024Article
- Striatal CDK5 Regulates Cholinergic Neuron Activation and Dyskinesia-like Behaviors through BK Channels.Research (Washington, D.C.) · 2023Article
- Effect of low-dose Levamlodipine Besylate in the treatment of vascular dementia.Scientific reports · 2019Article
- Functional coupling of Tmem74 and HCN1 channels regulates anxiety-like behavior in BLA neurons.Molecular psychiatry · 2019Article
- State-of-the-art: functional fluorescent probes for bioimaging and pharmacological research.Acta pharmacologica Sinica · 2019Review
- Myt1l induced direct reprogramming of pericytes into cholinergic neurons.CNS neuroscience & therapeutics · 2018Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Grb2-associated-binding protein 1 (Gab1) is a docking/scaffolding molecule known to play an important role in cell growth and survival. Here, we report that Gab1 is decreased in cholinergic neurons in Alzheimer's disease (AD) patients and in a mouse model of AD. In mice, selective ablation of Gab1 in cholinergic neurons in the medial septum impaired learning and memory and hippocampal long-term potentiation. Gab1 ablation also inhibited SK channels, leading to an increase in firing in septal cholinergic neurons. Gab1 overexpression, on the other hand, improved cognitive function and restored hippocampal CaMKII autorphosphorylation in AD mice. These results suggest that Gab1 plays an important role in the pathophysiology of AD and may represent a novel therapeutic target for diseases involving cholinergic dysfunction.
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Registered trials
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