ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2015
Reversing synapse loss in Alzheimer's disease: Rho-guanosine triphosphatases and insights from other brain disorders.
Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 17 citations in OpenAlex.
- Tailoring treatments: pharmacogenomics in the management of neurodegenerative diseases.Acta neurologica Belgica · 2026Review
- Unraveling the Genetic Landscape of Neurological Disorders: Insights into Pathogenesis, Techniques for Variant Identification, and Therapeutic Approaches.International journal of molecular sciences · 2024Review
- Pediococcus pentosaceus LAB6- and Lactiplantibacillus plantarum LAB12-Derived Cell Free Supernatant Inhibited RhoA Activation and Reduced Amyloid-Β In Vitro.Probiotics and antimicrobial proteins · 2024Article
- Associations of ARHGAP26 Polymorphisms with Alzheimer's Disease and Cardiovascular Disease.Journal of molecular neuroscience : MN · 2022Article
- From Menopause to Neurodegeneration-Molecular Basis and Potential Therapy.International journal of molecular sciences · 2021Review
- Small molecule modulation of the p75 neurotrophin receptor inhibits multiple amyloid beta-induced tau pathologies.Scientific reports · 2020Article
- Rate of brain aging andLife science alliance · 2019Article
- The emergence of Ephexin5 as a therapeutic target in Alzheimer's disease.Expert opinion on therapeutic targets · 2019Article
- Rho GTPases as therapeutic targets in Alzheimer's disease.Alzheimer's research & therapy · 2017Review
- Reducing expression of synapse-restricting protein Ephexin5 ameliorates Alzheimer's-like impairment in mice.The Journal of clinical investigation · 2017Article
- RHO to the DOCK for GDP disembarking: Structural insights into the DOCK GTPase nucleotide exchange factors.The Journal of biological chemistryReview
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a monumental public health crisis with no effective cure or treatment. To date, therapeutic strategies have focused almost exclusively on upstream signaling events in the disease, namely on β-amyloid and amyloid precursor protein processing, and have, unfortunately, yielded few, if any, promising results. An alternative approach may be to target signaling events downstream of β-amyloid and even tau. However, with so many pathways already linked to the disease, understanding which ones are "drivers" versus "passengers" in the pathogenesis of the disease remains a tremendous challenge. Given the critical roles of Rho-guanosine triphosphatases (GTPases) in regulating the actin cytoskeleton and spine dynamics, and the strong association between spine abnormalities and cognition, it is not surprising that mutations in a number of genes involved in Rho-GTPase signaling have been implicated in several brain disorders, including schizophrenia and autism. And now, there is mounting literature implicating Rho-GTPase signaling in AD pathogenesis as well. Here, I review this evidence, with a particular emphasis on the regulators of Rho-GTPase signaling, namely guanine nucleotide exchange factors and GTPase-activating proteins. Several of these have been linked to various aspects of AD, and each offers a novel potential therapeutic target for AD.
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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.