Tau Pathology

Sergeant, Nicolas; Buée, Luc

doi:10.1007/978-1-4419-6787-9_4

Cited by 2 publications

(3 citation statements)

References 320 publications

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“…MTs and their MAPs (MAP1B, MAP2, etc.) participate in the promotion of neurite extension, the induction of distinctive morphologies between axons and dendrites, axonal transport, neuronal plasticity, and neuronal degeneration ( 85 ). Lastly, MFs are constituted by actin filaments, and their polymerization dynamic is closely associated with the activity of actin-binding proteins (ABPs) like drebrin and ADF/cofilin.…”

Section: The Cytoskeleton In Neuronal Plasticitymentioning

confidence: 99%

“…Neuronal MAPs are differentially expressed during brain development: MAP1B is expressed in early stages of newly forming axons, MAP1A is expressed in mature axons, and both MAP2 and Tau isoforms are expressed during development and adulthood, predominantly in dendrites and axons, respectively ( 117 , 118 ). In particular, Tau isoforms are of clinical relevance, given that they are the major component of paired helical filaments found in Alzheimer’s disease (AD) and other brain diseases ( 85 , 119 ).…”

Section: E2 and P4 Effects On Microtubule-associated Protein 2 And Tamentioning

confidence: 99%

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Sex Hormones Regulate Cytoskeletal Proteins Involved in Brain Plasticity

2015

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In the brain of female mammals, including humans, a number of physiological and behavioral changes occur as a result of sex hormone exposure. Estradiol and progesterone regulate several brain functions, including learning and memory. Sex hormones contribute to shape the central nervous system by modulating the formation and turnover of the interconnections between neurons as well as controlling the function of glial cells. The dynamics of neuron and glial cells morphology depends on the cytoskeleton and its associated proteins. Cytoskeletal proteins are necessary to form neuronal dendrites and dendritic spines, as well as to regulate the diverse functions in astrocytes. The expression pattern of proteins, such as actin, microtubule-associated protein 2, Tau, and glial fibrillary acidic protein, changes in a tissue-specific manner in the brain, particularly when variations in sex hormone levels occur during the estrous or menstrual cycles or pregnancy. Here, we review the changes in structure and organization of neurons and glial cells that require the participation of cytoskeletal proteins whose expression and activity are regulated by estradiol and progesterone.

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Section: The Cytoskeleton In Neuronal Plasticitymentioning

confidence: 99%

Section: E2 and P4 Effects On Microtubule-associated Protein 2 And Tamentioning

confidence: 99%

Sex Hormones Regulate Cytoskeletal Proteins Involved in Brain Plasticity

2015

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“…Tau levels in brain homogenates from Alzheimer’s disease may be elevated Khatoon, 1992 #7}, but this is still controversial [7]. Although there are no known mutations of tau in AD, tau mutations cause FTDP-17 and are associated with development of corticobasal degeneration, progressive supranuclear palsy and Pick’s disease [1, 8]. These observations unequivocally establish a pathogenic role of tau in neurodegenerative diseases.…”

Section: Introductionmentioning

confidence: 99%

Global Axonal Transport Rates are Unaltered in Htau Mice in vivo

Yuan

Kumar

Sasaki

et al. 2013

JAD

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Microtubule-based axonal transport is believed to become globally disrupted in Alzheimer’s disease in part due to alterations of tau expression or phosphorylation. We previously showed that axonal transport rates along retinal ganglion axons are unaffected by deletion of normal mouse tau or by overexpression of wild-type human tau. Here, we report that htau mice expressing 3-fold higher levels of human tau in the absence of mouse tau also display normal fast and slow transport kinetics despite the presence of abnormally hyperphosphorylated tau in some neurons. In addition, markers of slow transport (neurofilament light subunit) and fast transport (snap25) exhibit normal distributions along optic axons of these mice. These studies demonstrate that human tau overexpression, even when associated with a limited degree of tau pathology, does not necessarily impair general axonal transport function in vivo. This investigation is contributed for the issue of Journal of Alzheimer’s Disease dedicated to the memory of Inge Grunke-Iqbal and to the celebration of her contributions to Alzheimer’s disease research.

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Tau Pathology

Cited by 2 publications

References 320 publications

Sex Hormones Regulate Cytoskeletal Proteins Involved in Brain Plasticity

Sex Hormones Regulate Cytoskeletal Proteins Involved in Brain Plasticity

Global Axonal Transport Rates are Unaltered in Htau Mice in vivo

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