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Plaques, Tangles and Amyloid:
Published in Robert E. Becker, Ezio Giacobini, Alzheimer Disease, 2020
Robert G. Struble, H. Brent Clark
An initial stage of AD-type cortical SP formation has been suggested to be represented by circular disruption of the neuropil, without evidence of β-amyloid or abnormal neurites (Probst et al, 1987). Stereologic estimates also suggested that each of these “early” SP had a microglia at its core. The distribution and amorphous nature of this type of plaque led those authors to suggest that it might presage the formation of a classic SP containing both neurites and β-amyloid. The predominance of “early” SP, in the absence of the classic SP, in specific cortical areas was explained by proposing that the evolution of the SP was arrested. If this neuropil abnormality does indeed represent a primitive plaque, and that continuation to a classic SP can be arrested, it suggests that SP formation is regulated by local factors, and that the type of SP formed (or whether they are formed at all) is largely determined by the cortical neuropil. This hypothesis is comparable to that suggested for the transmitter- specificity of neurites in plaques, i.e., it is largely related to the local characteristics of the neuropil. Finally, antisera raised against the A4 protein have detected clusters of immuno- staining not visualized with thioflavin, Congo red or routine silver stains. These reports suggest that an early stage of senile plaque formation (Tagliavini et al, 1988; Braak et al, 1989) might be characterized by deposits of β-amyloidogenic peptide not yet in a β-pleated sheet.
Nerve Growth Factor Synthesis and Biological Activity in Malignant Cells
Published in Velibor Krsmanović, James F. Whitfield, Malignant Cell Secretion, 2019
Philippe Brachet, Eleni Dicou, Rémi Houlgatte, Didier Wion
The response of some tumor cells to NGF was the object of extensive studies. Some human neuroblastoma cells extend neurites in the presence of the factor, a morphological differentiating action which is mimicked by retinoic acid.93,95 NGF was found to stimulate either differentiation or division in different clones of murine neuroblastoma.96 Pheochrom-ocytomas, which are tumors of adrenal medullary cells, are also responsive to NGF. Tumor explants from humans or rats97,98 also respond to the factor by extending neurites. The system which is presently the most widely studied was derived by Greene and Tischler99 from a rat pheochromocytoma. It consists of a clonal cell line, referred to as PC 12. Cells of this line grow in vitro in the absence of NGF and differentiate into sympathetic-like neurons in its presence. The factor exerts short-term and long-term effects involving numerous biochemical, physiological, or morphological changes which lead eventually to a prolonged outgrowth of neurites.100 Several other NGF-responsive clonal cell lines were isolated from the same rat pheochromocytoma.101 They differ from PC 12 in that the factor does not cause them to extend neurites, but, like PC 12, they are interesting model systems for the study of the mode of action of NGF.
Nervous System
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Mark T. Butt, Alys Bradley, Robert Sills
The large motor neurons of the ventral gray column in the spinal column are the classic bipolar neuron, with multiple dendrites, a dendritic zone close to the cell body, and a long terminal axon that courses through the ventral spinal nerve roots to a muscle (the effector site). The sensory neurons of the dorsal root ganglion, for example, have their dendritic-like zone in the periphery (e.g., skin), communicating via the axon to the cell body in the ganglion. These neurons are unipolar, meaning that there is a single neurite (a neurite is a projection from the cell body of a neuron), the axon, which passes through the dorsal root ganglion and then into the spinal cord.
A perspective on C. elegans neurodevelopment: from early visionaries to a booming neuroscience research
Published in Journal of Neurogenetics, 2020
Concurrently to or after migration, neurons grow neurites to reach their partners. The specification of neurites to become axons or dendrites and dendrite development, in particular, were not subject of early research. However, later work uncovered that axon-dendrite sorting is polarized by ankyrin and kinesin, while guidance cues and neuronal asymmetry define the site of axon formation (Adler, Fetter, & Bargmann, 2006; Maniar et al., 2011). Glial-like mesodermal cells also specify certain axons through calcium signaling (Meng, Zhang, Jin, & Yan, 2016). Recent work reveals that the morphogenesis of dendrites and axons differ. Sensory dendrites form by retrograde extension upon extracellular attachment during neuronal migration (Heiman & Shaham, 2009). Some mechanosensory dendrites grow extensive arborization, driven by hypodermal cues, extracellular matrix, adhesion, and actin effectors (Dong, Liu, Howell, & Shen, 2013; Liu & Shen, 2012; Oren-Suissa, Hall, Treinin, Shemer, & Podbilewicz, 2010; Salzberg et al., 2013; W. Zou et al., 2018). Dendrites are also shaped by self-avoidance and axon-dendrite fasciculation (Chen, Hsu, Chang, & Pan, 2019; Smith, Watson, Vanhoven, Colón-Ramos, & Miller, 2012).
Downregulation of Thbs4 caused by neurogenic niche changes promotes neuronal regeneration after traumatic brain injury
Published in Neurological Research, 2020
Tong Zhao, Zhifu Wang, Tongming Zhu, Rong Xie, Jianhong Zhu
Following brain injury, regenerated neurites sprout and attempt to extend to the injured area during the process of neuronal repair. However, the inhibitory environment at the injured area prevents neurite regrowth [18,19]. We performed further experiments to assess neuronal regeneration after treatment with the glial pump. Using immunofluorescence, we studied expression of microtubule-associated protein 2 (MAP2), a cell body and neuronal dendrite marker, and neurofilament (NF), an axonal marker, to assess neurite regrowth after injury. We found that almost no neurites were present in the glial scar core of the control and matrix groups (n = 6; Figure 4(b-d)). In contrast, in the glial pump group, we observed MAP2+ cell bodies, dendrites, and neurofilaments beyond the boundaries of the glial scar and normal tissue, distributed within the perilesional area. Additionally, statistical analysis revealed a significant difference in the number of neurites between the glial pump group and the other two groups (Figure 4(d)). After staining with NeuN, we found NeuN+ neurons in the glial scar on the glial pump group (Figure 4(e)). No NeuN+ neurons were present in the control and matrix groups. In addition, the perilesional area around the glial scar core was decreased in the glial pump group (n = 6; Figure 4(e)). These results strongly suggest that the altered pathological niche contributes to the NeuN+ neuronal cell bodies and neurites penetrating the glial scar area and to the reduction in the size of the perilesional area.
Developing therapeutic strategies to promote myelin repair in multiple sclerosis
Published in Expert Review of Neurotherapeutics, 2019
Laura E. Baldassari, Jenny Feng, Benjamin L.L. Clayton, Se-Hong Oh, Ken Sakaie, Paul J. Tesar, Yanming Wang, Jeffrey A. Cohen
Neurite orientation dispersion and density imaging (NODDI) is a diffusion imaging technique developed to characterize the complex microstructural arrangement in tissue. Neurites correspond to axons or dendrites. NODDI provides three parameters, the neurite density index, which quantifies the density of neurites, the orientation dispersion index, which quantifies the variability in the orientation of the neurites, and the isotropic volume fraction, which quantifies the amount of free water. NODDI differentiates the density of neurites from their spatial orientations. Therefore, it is a more specific microstructural measure of tissue compared to standard DTI. It is unaffected by crossing fiber tracts and variations in fiber density. It has been shown that neurite density correlated strongly with myelin stain intensity in rat models [117], suggestive of its potential in myelin monitoring.