China
Africa
Explore chapters and articles related to this topic
Therapeutic Strategies and Future Research
Published in Mark A. Mentzer, Mild Traumatic Brain Injury, 2020
Apolipoprotein (apo) E is a major genetic risk factor for Alzheimer’s disease (65%–80% of AD patients have one or more apoE4 allele). Perhaps as the allele plays a role in mTBI, the detrimental effects could be modulated by potential therapies (Mahley et al., 2012). The apoE receptor ligand reelin mediates signaling in several molecular pathways and could be an important factor in modulating amyloid and tau pathologies (Krstic et al., 2012). Reelin receptors apoER2 and VLDLR are part of normal synaptic plasticity, learning, and memory (Weeber, 2012). Therapies to slow the rate of decline from tau aggregation for both AD and mTBI are being pursued but none are currently available. Another potential therapy for mTBI and the secondary injury effects is the gamma-secretase inhibitors. Gamma-secretase blocking can reduce motor and cognitive deficits and reduce cell loss following TBI (Burns, 2012).
Organic Chemicals
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
NMDA receptor function is also strongly regulated by chemical reduction and oxidation, via the “redox modulatory site.”33 Through this site, reductants dramatically enhance NMDA channel activity, whereas oxidants either reverse the effects of reductants or depress native responses. It is generally believed that NMDA receptors are modulated by endogenous redox agents such as glutathione, lipoic acid, and the essential nutrient pyrroloquinoline quinone. Src kinase enhances NMDA receptor currents.34 Reelin modulates NMDA function through Src family kinases and DAB1,35 significantly enhancing LTP in the hippocampus. CDK5 regulates the amount of NR2B-containing NMDA receptors on the synaptic membrane, thus affecting synaptic plasticity.36,37
Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
SRC kinase enhances NMDA receptor currents.125 Reelin modulates NMDA function through Src family kinases and DAB1,126 significantly enhancing LTP in the hippocampus. CDK5 regulates the amount of NR2B-containing NMDA receptors on the synaptic membrane, thus affecting synaptic plasticity.127,128
Continuum modeling for neuronal lamination during cerebral morphogenesis considering cell migration and tissue growth
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2021
Hironori Takeda, Yoshitaka Kameo, Taiji Adachi
During neuronal lamination, it has been suggested that reelin secreted from neurons in the MZ plays an important role in regulating neuronal migration. Considering that reelin has been proposed to be a chemoattractive factor during neuronal migration (D'Arcangelo and Curran 1998; Caffrey et al. 2014), in this study, the effect of reelin was modeled as an additional migration velocity. As shown in Equation (5), this additional velocity corresponds to an increase in the maximum cell number density, which is dependent on cell–cell adhesion. Recent studies have shown that reelin regulates changes in the adhesiveness of neurons (Sekine et al. 2012; Matsunaga et al. 2017). Therefore, the simulation results shown in Figure 2 suggest that reelin enables the late-born neurons to migrate past the early-born neurons by enhancing the velocity of the neuronal migration or by inducing a decrease in the cell–cell adhesion, which results in an increase in the maximum cell number density. Additionally, reelin has been suggested to regulate formation of the MZ, in which cell bodies are sparsely distributed (Sekine et al. 2012; Matsunaga et al. 2017). Therefore, our simulation results suggest that reelin also contributes to the inside-out lamination by creating the space behind the accumulated early-born neurons by decreasing the cell density in the MZ.