Actin and Diseases of the Nervous System

Bernstein, Ben C.; Maloney, Michael T.; Bamburg, James R.

doi:10.1007/978-1-4419-7368-9_11

Cited by 12 publications

(7 citation statements)

References 223 publications

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“…Cofilin-actin enriched inclusions are a common pathological feature observed in a broad spectrum of neurodegenerative diseases (reviewed in Maloney et al, 2007; Bernstein et al, 2009). These often take the form of rod shaped bundles of filaments (cofilin-actin rods), as irregular aggregates (probably aggresomes), or as cytoplasmic paracrystalline lattices (Hirano bodies).…”

Section: Cytoskeletal Pathologiesmentioning

confidence: 99%

Cytoskeletal pathologies of Alzheimer disease

Bamburg

Bloom

2009

Cell Motil. Cytoskeleton

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145

111

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The histopathological hallmarks of Alzheimer disease are the extracellular amyloid plaques, composed principally of the amyloid beta peptide, and the intracellular neurofibrillary tangles, composed of paired helical filaments of the microtubuleassociated protein, tau. Other histopathological structures involving actin and the actin-binding protein, cofilin, have more recently been recognized. Here we review new findings about these cytoskeletal pathologies, and, emphasize how plaques, tangles, the actin-containing inclusions and their respective building blocks may contribute to Alzheimer pathogenesis and the primary behavioral symptoms of the disease. Cell Motil. Cytoskeleton 66: 635-649, 2009. '

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Section: Cytoskeletal Pathologiesmentioning

confidence: 99%

Cytoskeletal pathologies of Alzheimer disease

Bamburg

Bloom

2009

Cell Motil. Cytoskeleton

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145

111

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“…Instead, this suggests that normal F-actin dynamics are essential for proper SV exocytosis (Rust and Maritzen, 2015 ), which could be, at least partially, mediated by the activity-dependent F-actin assembly function of the AZ protein Piccolo (Waites et al, 2011 ; Wagh et al, 2015 ). Defects in actin function or dysregulation of synaptic actin are also implicated in several mental disorders (Bernstein et al, 2011 ). Moreover, altered synapse development and morphology has been observed in a mouse model for Fragile X syndrome.…”

Section: Introductionmentioning

confidence: 99%

The axonal cytoskeleton: from organization to function

Kevenaar

Hoogenraad

2015

Front. Mol. Neurosci.

142

122

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The axon is the single long fiber that extends from the neuron and transmits electrical signals away from the cell body. The neuronal cytoskeleton, composed of microtubules (MTs), actin filaments and neurofilaments, is not only required for axon formation and axonal transport but also provides the structural basis for several specialized axonal structures, such as the axon initial segment (AIS) and presynaptic boutons. Emerging evidence suggest that the unique cytoskeleton organization in the axon is essential for its structure and integrity. In addition, the increasing number of neurodevelopmental and neurodegenerative diseases linked to defect in actin- and microtubule-dependent processes emphasizes the importance of a properly regulated cytoskeleton for normal axonal functioning. Here, we provide an overview of the current understanding of actin and microtubule organization within the axon and discuss models for the functional role of the cytoskeleton at specialized axonal structures.

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“…Neuronal structural plasticity, such as morphogenesis of dendrites and dendritic spines, is primarily regulated by the actin cytoskeleton (43, 44). Disruption of normal actin organization has been associated with numerous neurological and psychiatric diseases (45). It has been demonstrated that S1P/S1PRs modulate significant cytoskeletal rearrangements in various cellular systems through actin regulatory proteins such as Rho GTPases, including Rac1 and Cdc42 (28, 46).…”

Section: Resultsmentioning

confidence: 99%

Dysfunctional S1P/S1PR1 signaling in the dentate gyrus drives vulnerability of chronic pain-related memory impairment

Cui,

Pan,

Fan

et al. 2024

Preprint

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Memory impairment in chronic pain patients is substantial and common, and few therapeutic strategies are available. Chronic pain-related memory impairment has susceptible and unsusceptible features. Therefore, exploring the underlying mechanisms of its vulnerability is essential for developing effective treatments. Here, combining two spatial memory tests (Y-maze test and Morris water maze), we segregated chronic pain mice into memory impairment-susceptible and -unsusceptible subpopulations in a chronic neuropathic pain model induced by chronic constrictive injury of the sciatic nerve. RNA-seq analysis and gain/loss-of-function study revealed that S1P/S1PR1 signaling is a determinant for vulnerability to chronic pain-related memory impairment. Knockdown of the S1PR1 in the DG promoted a susceptible phenotype and led to structural plasticity changes of reduced excitatory synapse formation and abnormal spine morphology as observed in susceptible mice, while overexpression of the S1PR1 and pharmacological administration of S1PR1 agonist in the DG promoted an unsusceptible phenotype and prevented the occurrence of memory impairment, and rescued the morphological abnormality. Finally, GO enrichment analysis and biochemical evidence indicated that down-regulation of S1PR1 in susceptible mice may impair DG structural plasticity via interaction with actin cytoskeleton rearrangement-related signaling pathways including Itga2 and its downstream Rac1/Cdc42 signaling and Arp2/3 cascade. These results reveal a novel mechanism and provide a promising preventive and therapeutic molecular target for vulnerability to chronic pain-related memory impairment.

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Actin and Diseases of the Nervous System

Cited by 12 publications

References 223 publications

Cytoskeletal pathologies of Alzheimer disease

Cytoskeletal pathologies of Alzheimer disease

The axonal cytoskeleton: from organization to function

Dysfunctional S1P/S1PR1 signaling in the dentate gyrus drives vulnerability of chronic pain-related memory impairment

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