ReviewJournal of Alzheimer's disease : JAD2016
Collapsin Response Mediator Protein-2 (CRMP2) is a Plausible Etiological Factor and Potential Therapeutic Target in Alzheimer's Disease: Comparison and Contrast with Microtubule-Associated Protein Tau.
Review in Journal of Alzheimer's disease : JAD, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 72 citations in OpenAlex.
- A distinct tau oligomer strain defines the molecular and proteomic landscape of rapidly progressive Alzheimer's disease.Acta neuropathologica · 2026Article
- Article
- Lanthionine Ketimine Ethyl Ester Induces Proliferation and Maturation and Regulates Calcium Flux in Primary Mouse Oligodendrocyte Progenitor Cells.Journal of neuroscience research · 2025Article
- Article
- Development of quantitative detection methods for four Alzheimer's disease specific biomarker panels using electrochemical immunosensors based on enzyme immunoassay.Analytical sciences : the international journal of the Japan Society for Analytical Chemistry · 2024Article
- Protein Oxidation in Aging and Alzheimer's Disease Brain.Antioxidants (Basel, Switzerland) · 2024Review
- Overlap in synaptic neurological condition susceptibility pathways and the neural pannexin 1 interactome revealed by bioinformatics analyses.Channels (Austin, Tex.) · 2023Article
- Effect of lidocaine on cognitively impaired rats: Anti-inflammatory and antioxidant mechanisms in combination with CRMP2 antiphosphorylation.Immunity, inflammation and disease · 2023Article
- Proteomic Profiling of Cerebrum Mitochondria, Myelin Sheath, and Synaptosome Revealed Mitochondrial Damage and Synaptic Impairments in Association with 3 × Tg-AD Mice Model.Cellular and molecular neurobiology · 2022Article
- High Resolution Magic Angle Spinning Proton NMR Study of Alzheimer's Disease with Mouse Models.Metabolites · 2022Article
- Comparative Analysis of Aducanumab, Zagotenemab and Pioglitazone as Targeted Treatment Strategies for Alzheimer's Disease.Aging and disease · 2021Review
- Phosphorylated tau targeted small-molecule PROTACs for the treatment of Alzheimer's disease and tauopathies.Biochimica et biophysica acta. Molecular basis of disease · 2021Review
- Proteomic Analysis Unveils Expressional Changes in Cytoskeleton- and Synaptic Plasticity-Associated Proteins in Rat Brain Six Months after Withdrawal from Morphine.Life (Basel, Switzerland) · 2021Article
- Beyond Neuronal Microtubule Stabilization: MAP6 and CRMPS, Two Converging Stories.Frontiers in molecular neuroscience · 2021Article
- Downregulation of hippocampal SIRT6 activates AKT/CRMP2 signaling and ameliorates chronic stress-induced depression-like behavior in mice.Acta pharmacologica Sinica · 2020Article
- Article
- Mitochondrial Dysfunction: a Potential Therapeutic Target to Treat Alzheimer's Disease.Molecular neurobiology · 2020Review
- Natural Medicines and Their Underlying Mechanisms of Prevention and Recovery from Amyloid Β-Induced Axonal Degeneration in Alzheimer's Disease.International journal of molecular sciences · 2020Review
- Multiple Herpes Simplex Virus-1 (HSV-1) Reactivations Induce Protein Oxidative Damage in Mouse Brain: Novel Mechanisms for Alzheimer's Disease Progression.Microorganisms · 2020Article
- Ketamine Regulates Phosphorylation of CRMP2 To Mediate Dendritic Spine Plasticity.Journal of molecular neuroscience : MN · 2020Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) has long been viewed as a pathology that must be caused either by aberrant amyloid-β protein precursor (AβPP) processing, dysfunctional tau protein processing, or a combination of these two factors. This is a reasonable assumption because amyloid-β peptide (Aβ) accumulation and tau hyperphosphorylation are the defining histological features in AD, and because AβPP and tau mutations can cause AD in humans or AD-like features in animal models. Nonetheless, other protein players are emerging that one can argue are significant etiological players in subsets of AD and potentially novel, druggable targets. In particular, the microtubule-associated protein CRMP2 (collapsin response mediator protein-2) bears striking analogies to tau and is similarly relevant to AD. Like tau, CRMP2 dynamically regulates microtubule stability; it is acted upon by the same kinases; collects similarly in neurofibrillary tangles (NFTs); and when sequestered in NFTs, complexes with critical synapse-stabilizing factors. Additionally, CRMP2 is becoming recognized as an important adaptor protein involved in vesicle trafficking, amyloidogenesis and autophagy, in ways that tau is not. This review systematically compares the biology of CRMP2 to that of tau in the context of AD and explores the hypothesis that CRMP2 is an etiologically significant protein in AD and participates in pathways that can be rationally engaged for therapeutic benefit.
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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.