Explore chapters and articles related to this topic
Carriers for Brain Targeting
Published in Raj K. Keservani, Anil K. Sharma, Rajesh K. Kesharwani, Nanocarriers for Brain Targeting, 2019
Md. Sahab Uddin, Mst. Marium Begum
Neurodegenerative diseases indicate similar pathological features such as abnormal protein aggregation, mitochondrial dysfunction, and disease-specific neuronal degeneration (Maday et al., 2014; Millecamps and Julien, 2013). There are several pathogenic proteins, such as tau, a-synuclein, parkin, leucine-rich repeat kinase 2, and Huntingtin, related to neurodegenerative diseases which have been indicated to directly bind tubulin or modulate microtubule stability. Recently, increase of lines of evidence suggests that MTAs can ameliorate the pathogenic symptoms in animal models of neurodegenerative diseases (Maday et al., 2014; Millecamps and Julien, 2013). Additionally, for the administration of drugs that directly stabilize microtubules, strategies for tackling microtubule-based transport system are also under development, as impairment in the axonal transport has recently come up as an usual factor in several neurodegenerative diseases such as Alzheimer disease and Parkinson disease (Maday et al., 2014; Millecamps and Julien, 2013).
Occupational toxicology of the nervous system
Published in Chris Winder, Neill Stacey, Occupational Toxicology, 2004
The axon is often a very long cell process, in some cells being 5000–10,000 times as long as the cell body is wide. This presents some difficulties in resource management for the cell, since the genetic material and the bulk of the synthetic material is located in or close to the nucleus. Nerve cells have evolved a specialised axonal transport process to facilitate the physical movement of cell products to the terminal (anterograde transport). Similarly the terminal may absorb substances which are important as metabolic precursors or as regulators of cell processes which are transported back to the cell body (retrograde transport).
Why slow axonal transport is bidirectional – can axonal transport of tau protein rely only on motor-driven anterograde transport?
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2023
Ivan A. Kuznetsov, Andrey V. Kuznetsov
Due to the great length of axons, neurons must rely on a complicated “railway” system composed of microtubules (MTs). Various cargos are transported along MTs while pulled by molecular motors. Typically, newly synthesized cargos are transported in the anterograde direction (from the soma to the axon terminal) by molecular motors that belong to the kinesin superfamily. Cargos that need to be recycled in the somatic lysosomes are transported in the retrograde direction by molecular motors that belong to the dynein superfamily. Axonal transport is classified into fast anterograde axonal transport, which is driven by kinesin motors (representative velocity 1 μm s−1), fast retrograde axonal transport, which is driven by dynein motors (representative velocity is also 1 μm s−1), and slow axonal transport (SAT) (Morfini et al. 2012; Brown 2016; Roy 2020; Sleigh et al. 2019; Guedes-Dias and Holzbaur 2019).
Identifying stage of Alzheimer disease using multiclass particle swarm optimisation technique
Published in Journal of Experimental & Theoretical Artificial Intelligence, 2018
In early AD, intra-neuronal filamentous deposits, or neuro fibrillary tangles (NFTs), accumulate within neurons. These deposits are composed of hyper phosphorylated tau-protein (Shiino et al., 2006). This cellular pathology disrupts axonal transport and induces widespread metabolic decline. The resulting neuronal loss is observable as gross atrophy with MRI. Temporoparietal association cortices and the medial temporal lobe are severely atrophied in AD (DeCarli, 2000), with the entorhinal cortex and hippocampus the earliest and most severely affected (Janke et al., 2001; Thompson et al., 2001). Profound atrophy is also observed in the posterior cingulate gyrus and adjacent precuneus. Specific atrophic patterns differentiate AD from frontotemporal, semantic, and Lewy body dementias (Paling et al., 2001; Studholme et al., 2001). Patients with AD show minimal primary visual, sensorimotor, and frontal atrophy until late in the disease. Before symptom onset in AD, and also in those at genetic risk, grey matter loss is detectable in the anterior hippocampal/amygdala region (Lehtovirta, Laakso, Frisoni, & Soininen, 2000; Reiman et al., 2001). Atrophying grey matter (Lˇders., Steinmetz1, & Jncke, 2002) is a sign of the progression of Alzheimer’s disease and other forms of dementia. Atrophy in the grey matter is shown as the amount of grey matter shrinks in the imaging tests (Douaud et al., 2013).