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Open AccessJournal ArticleDOI

Molecular mechanisms of dendrite stability

Anthony J. Koleske
- 01 Aug 2013 - 
- Vol. 14, Iss: 8, pp 536-550
TLDR
New evidence reveals that dendritic spine and dendrite arbor stability have crucial roles in the correct functioning of the adult brain and that loss of stability is associated with psychiatric disorders and neurodegenerative diseases.
Abstract
In the developing brain, dendrite branches and dendritic spines form and turn over dynamically. By contrast, most dendrite arbors and dendritic spines in the adult brain are stable for months, years and possibly even decades. Emerging evidence reveals that dendritic spine and dendrite arbor stability have crucial roles in the correct functioning of the adult brain and that loss of stability is associated with psychiatric disorders and neurodegenerative diseases. Recent findings have provided insights into the molecular mechanisms that underlie long-term dendrite stabilization, how these mechanisms differ from those used to mediate structural plasticity and how they are disrupted in disease.

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Gene discovery and polygenic prediction from a genome-wide association study of educational attainment in 1.1 million individuals

James J. Lee, +94 more
- 23 Jul 2018 - 
TL;DR: A joint (multi-phenotype) analysis of educational attainment and three related cognitive phenotypes generates polygenic scores that explain 11–13% of the variance ineducational attainment and 7–10% ofthe variance in cognitive performance, which substantially increases the utility ofpolygenic scores as tools in research.
Journal ArticleDOI

Dendritic Spines: The Locus of Structural and Functional Plasticity

Carlo Sala, +1 more
TL;DR: Issues with respect to spine formation and plasticity are addressed and the complexity of molecular pathways involved in regulation of spine structure and function is highlighted, which contributes to the understanding of central synaptic interactions in health and disease.
Journal ArticleDOI

Common mechanisms of excitatory and inhibitory imbalance in schizophrenia and autism spectrum disorders.

TL;DR: Key genetic, physiological, neuropathological, functional, and pathway studies that suggest alterations to excitatory/inhibitory circuits are keys to ASD and SCZ pathogenesis are reviewed.
Journal ArticleDOI

Dendritic Structural Plasticity and Neuropsychiatric Disease

TL;DR: The importance of recent genetic findings on the different mechanisms of structural plasticity are discussed and it is proposed that these converge on shared pathways that can be targeted with novel therapeutics.
Journal ArticleDOI

Dendritic Spines in Depression: What We Learned from Animal Models

TL;DR: Current understanding of the chronic stress-induced remodeling of dendritic spines in the hippocampus, prefrontal cortex, orbitofrontal cortex, amygdala, and nucleus accumbens is summarized and the putative underlying mechanisms are discussed.
References
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Journal ArticleDOI

Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid beta-peptide.

TL;DR: Findings in other neurodegenerative diseases indicate that a broadly similar process of neuronal dysfunction is induced by diffusible oligomers of misfolded proteins.
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Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment.

TL;DR: Both linear regressions and multivariate analyses correlating three global neuropsychological tests with a number of structural and neurochemical measurements performed on a prospective series of patients with Alzheimer's disease and 9 neuropathologically normal subjects reveal very powerful correlations with all three psychological assays.
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Cellular Motility Driven by Assembly and Disassembly of Actin Filaments

TL;DR: A core set of proteins including actin, Arp2/3 complex, profilin, capping protein, and ADF/cofilin can reconstitute the process in vitro, and mathematical models of the constituent reactions predict the rate of motion.
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LTP and LTD: an embarrassment of riches.

TL;DR: This work reviews those forms of LTP and LTD for which mechanisms have been most firmly established and examples are provided that show how these mechanisms can contribute to experience-dependent modifications of brain function.
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Subgenual prefrontal cortex abnormalities in mood disorders

TL;DR: Using positron emission tomographic images of cerebral blood flow and rate of glucose metabolism to measure brain activity, an area of abnormally decreased activity is localized in the pre-frontal cortex ventral to the genu of the corpus callosum in both familial bipolar depressives and familial unipolar depressives.
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