Dendritic spine pathology: cause or consequence of neurological disorders?

By John C. Fiala, J. Špaček, Kristen M. Harris. Brain research. Brain research reviews, 2002

844 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/24eb6eeaa040a6531d432d7f0fa6727d9706f31f

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In Cellular and Molecular Neuroscience

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Citations in the corpus

Rare de novo variants associated with autism implicate a large functional network of genes involved in formation and function of synapses (2011, background): “On the other hand, an increase in spine size or density has been connected to Fragile X syndrome, a disorder frequently associated with autism (Fiala et al., 2002; Kaufmann Neuron 70, 898–907, June 9, 2011 ª2011 Elsevier Inc. 903 and Moser, 2000).”
Aβ Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease (2007, methodology): “The change in spine appearance caused by ADDLs is especially interesting because the elongated shape resembles that of immature spines or of diseased spines found in mental retardation and prionoses (Fiala et al., 2002).”
Mecp2 deficiency leads to delayed maturation and altered gene expression in hippocampal neurons. (2007, background): “Abnormalities in dendritic spines have been found in several developmental disorders [reviewed by Fiala et al., 2002].”
Fragile X Mental Retardation Protein Regulates Proliferation and Differentiation of Adult Neural Stem/Progenitor Cells (2010, result): “Consistent with the literature [69], we have observed that Fmr1 KO aNPCdifferentiated neurons had reduced dendritic complexity and length (data not shown), which could also contribute to behavioral deficits.”
Dendritic spine pathology in neuropsychiatric disorders (2011, background): “The brain may possess an innate ability to forestall Alzheimer's disease insults, as some studies note compensatory synaptic changes in Alzheimer's disease, such as increased size in remaining spine”
Neural remodeling in retinal degeneration. (2003, background): “…arrays evoke varied forms of negative remodeling, including atrophy (Globus, 1975; Pasic et al., 1994; Ginsberg and Martin, 2002), apoptosis (Ginsberg and Martin, 2002), axonal arbor restructuring (Kaas and Florence, 1997) and dendritic re-patterning (Anderton et al., 1998; Fiala et al., 2002).”
Structural plasticity associated with exposure to drugs of abuse. (2004, neutral): “, 2003), pathological states (Fiala et al., 2002), etc.”
A Computational Framework for Ultrastructural Mapping of Neural Circuitry (2009, background): “More importantly, from a biomedical perspective, remodeling and reprogramming of neural networks in disease strongly argues that network scrambling or re-weighting is a key pathology (Fiala et al. 2002; Sutula 2002; Cavazos and Cross 2006; Marc et al. 2007; He et al. 2008).”
Molecular mechanisms of dendritic spine morphogenesis. (2006, background): “As themolecular control of spinemorphogenesis becomes clearer, the challenge will be to use this knowledge to specifically manipulate dendritic spines in vivo and to address the question that is still outstanding: what is the functional significance of dendritic spines for cognitive functions such a”
Do thin spines learn to be mushroom spines that remember? (2007, background): “Developmental disorders such as Fragile X syndrome that are accompanied by varying degrees of mental retardation have been characterized by thinner more elongated spines that do not mature into large, mushroom spines [57,58]; these”
Synaptic Targeting by Alzheimer's-Related Amyloid β Oligomers (2004, background): “Changes in spine structure may rapidly alter synaptic signal processing and related information storage (Crick, 1982; Rao and Craig, 2000; Yuste and Bonhoeffer, 2001), and spine abnormalities are common to various brain dysfunctions (Fiala et al., 2002), including mental retardation, in which spines”
Repeated stress induces dendritic spine loss in the rat medial prefrontal cortex. (2006, background): “4C,D).”