2011
DOI: 10.3233/jad-2011-110617
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Abstract: Collapsin response mediator protein 2 (CRMP2) is an abundant brain-enriched protein that regulates neurite outgrowth. It is phosphorylated by Cdk5 and GSK3, and these modifications are abnormally high in the brains of Alzheimer's disease (AD) patients. Increased phosphorylation of CRMP2 is also apparent in mouse models of AD that express mutated AβPP and PSEN1, but not AβPP or tau alone, where it is detectable before the appearance of amyloid plaques and neurofibrillary tangles, suggesting it is an early event… Show more

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Cited by 53 publications
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References 30 publications
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“…100 Although the relationship between pathophysiological mechanisms and AD symptoms remains to be clarified, these findings position phosphorylated CRMP2 as a potential biomarker for early AD, especially since it seems specific to this type of dementia. 101 In an animal model of AD, suppression of CRMP2 phosphorylation is associated with amelioration of β-amyloid-induced cognitive dysfunction and hippocampal axon degeneration. 102 • Human prion diseases, which include sporadic/familial Creutzfeld-Jacob disease, are disorders of protein conformation in which PrP c , the normal cellular conformer, is converted to the abnormal protease-resistant PrP Sc .…”
Section: Human Nervous System Diseases: Insights From Crmp-altered Lementioning
confidence: 99%
“…100 Although the relationship between pathophysiological mechanisms and AD symptoms remains to be clarified, these findings position phosphorylated CRMP2 as a potential biomarker for early AD, especially since it seems specific to this type of dementia. 101 In an animal model of AD, suppression of CRMP2 phosphorylation is associated with amelioration of β-amyloid-induced cognitive dysfunction and hippocampal axon degeneration. 102 • Human prion diseases, which include sporadic/familial Creutzfeld-Jacob disease, are disorders of protein conformation in which PrP c , the normal cellular conformer, is converted to the abnormal protease-resistant PrP Sc .…”
Section: Human Nervous System Diseases: Insights From Crmp-altered Lementioning
confidence: 99%
“…As phosphorylation of CRMP2 is important in mediating CRMP2's negative effects on the cytoskeleton and is facilitated by SEMA3A binding (Deo et al, 2004; Uchida et al, 2005; Hensley et al, 2011; Khanna et al, 2012), overexpression of CRMP2 alone, especially in an uninjured system where SEMA3A is not present, may not result in adequate phosphorylation of CRMP2 to allow for cytoskeletal abnormalities and subsequent motor neuron degeneration as mediated by CRMP4a overexpression (Duplan et al, 2010). In addition, abnormal phosphorylation of CRMP2 has been identified as a characteristic feature of Alzheimer's disease (Williamson et al, 2011) and further work is focusing on its role in other neurodegenerative disorders in terms of cytoskeletal alterations (Hensley et al, 2011). In its unphosphorylated state, CRMP2 can actively stimulate neurite outgrowth (Yoshimura et al, 2005) thus by inhibiting SEMA3A signaling one could promote the accumulation of unphosphorylated CRMP2 in an effort to create an environment at the NMJ that is more permissible to maintaining the synapse in a healthy state.…”
Section: Molecular Mechanisms That Govern Distal Axon and Nmj Stabilimentioning
confidence: 99%
“…Like Aβ oligomers, intermediate aggregates of abnormal τ molecules are cytotoxic [38] and impair cognition [39]. NFTs also contain significant percentage of hyperphosphorylated neurofilaments (NF) [4041] and collapsin response mediator protein 2 (CRMP2) [42]. Neurofilaments promote an increase in axonal diameter in myelinated fibers, thereby increasing nerve conduction velocity.…”
Section: Pathomolecular-clinical Correlationsmentioning
confidence: 99%