ArticleProtein & cell2019
Inhibition of Rac1-dependent forgetting alleviates memory deficits in animal models of Alzheimer's disease.
Article in Protein & cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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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
34 citing papers in PubMed, 62 citations in OpenAlex.
- Article
- Rac1 Constrains Memory Consolidation.eNeuro · 2026Article
- Differences in retroactive interference response reveal sex-specific memory resilience in pre-symptomatic triple transgenic Alzheimer's disease mice.Brain communications · 2026Article
- Peptide OM-LV20 demonstrates neuroprotective effects by attenuating mitochondria-mediated neuronal apoptosis and dysfunction in mice with traumatic brain injury.Zoological research · 2025Article
- A computational medicine framework integrating multi-omics, systems biology, and artificial neural networks for Alzheimer's disease therapeutic discovery.Acta pharmaceutica Sinica. B · 2025Article
- Mechanistic Role of Astrocytic Rac1 Protein in Alzheimer's Disease.Aging and disease · 2025Review
- Inhibition of the Integrated Stress Response Prevents Natural Forgetting and Corrects Accelerated Forgetting Associated with Epilepsy.Molecular neurobiology · 2025Article
- Resilience mechanisms underlying Alzheimer's disease.Metabolic brain disease · 2025Review
- Circulating RAC1 contributed to steroid-sensitive nephrotic syndrome: Mendelian randomization, single-cell RNA-sequencing, proteomic, and experimental evidence.Renal failure · 2024Article
- Article
- Active forgetting and neuropsychiatric diseases.Molecular psychiatry · 2024Review
- DCC, a potential target for controlling fear memory extinction and hippocampal LTP in male mice receiving single prolonged stress.Neurobiology of stress · 2024Article
- Small GTPases control macropinocytosis of amyloid precursor protein and cleavage to amyloid-β.Heliyon · 2024Article
- Roles of Rac1-Dependent Intrinsic Forgetting in Memory-Related Brain Disorders: Demon or Angel.International journal of molecular sciences · 2023Review
- Secreted endogenous macrosomes reduce Aβ burden and ameliorate Alzheimer's disease.Science advances · 2023Article
- Novel approaches to increase synaptic resilience as potential treatments for Alzheimer's disease.Seminars in cell & developmental biology · 2023Review
- Accelerated long-term forgetting: A sensitive paradigm for detecting subtle cognitive impairment and evaluating BACE1 inhibitor efficacy in preclinical Alzheimer's disease.Frontiers in dementia · 2023Review
- Diverse and Composite Roles of miRNA in Non-Neuronal Cells and Neuronal Synapses in Alzheimer's Disease.Biomolecules · 2022Review
- Social experiences switch states of memory engrams through regulating hippocampal Rac1 activity.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Forgetting as a form of adaptive engram cell plasticity.Nature reviews. Neuroscience · 2022Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accelerated forgetting has been identified as a feature of Alzheimer's disease (AD), but the therapeutic efficacy of the manipulation of biological mechanisms of forgetting has not been assessed in AD animal models. Ras-related C3 botulinum toxin substrate 1 (Rac1), a small GTPase, has been shown to regulate active forgetting in Drosophila and mice. Here, we showed that Rac1 activity is aberrantly elevated in the hippocampal tissues of AD patients and AD animal models. Moreover, amyloid-beta 42 could induce Rac1 activation in cultured cells. The elevation of Rac1 activity not only accelerated 6-hour spatial memory decay in 3-month-old APP/PS1 mice, but also significantly contributed to severe memory loss in aged APP/PS1 mice. A similar age-dependent Rac1 activity-based memory loss was also observed in an AD fly model. Moreover, inhibition of Rac1 activity could ameliorate cognitive defects and synaptic plasticity in AD animal models. Finally, two novel compounds, identified through behavioral screening of a randomly selected pool of brain permeable small molecules for their positive effect in rescuing memory loss in both fly and mouse models, were found to be capable of inhibiting Rac1 activity. Thus, multiple lines of evidence corroborate in supporting the idea that inhibition of Rac1 activity is effective for treating AD-related memory loss.
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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.