a(MESH:"Dendritic Spines")
Dkk1 resulted in substantial loss of dendritic spines, which was blocked by 10µM fasudil treatment (Fig. 3e, f). PubMed:30232325
Dkk1 resulted in substantial loss of dendritic spines, which was blocked by 10µM fasudil treatment (Fig. 3e, f). PubMed:30232325
In addition to causing a significant reduction in the numbers of dendritic spines, Dkk1 treatment also resulted a substantial increase in levels of all three Aβ species (Fig. 3g). PubMed:30232325
As previously reported, Dkk1-treatment markedly reduced the number of dendritic spines on APP+/+ neurons (Fig. 3a, b). In contrast, APP-deficiency protected neurons against the synaptotoxic activity of Dkk1 (Fig. 3a, b). PubMed:30232325
The recovery curves indicated 3 pools of tau: a mobile, unbleached fraction comprising 9.72 1.03%, a dynamic fraction at 47.08 3.06%, and a stable, unrecoverable fraction at 42.75 2.78%. This stable fraction suggests that a large portion of tau is anchored in the spine. PubMed:24760868
The recovery curves indicated 3 pools of tau: a mobile, unbleached fraction comprising 9.72 1.03%, a dynamic fraction at 47.08 3.06%, and a stable, unrecoverable fraction at 42.75 2.78%. This stable fraction suggests that a large portion of tau is anchored in the spine. PubMed:24760868
The recovery curves indicated 3 pools of tau: a mobile, unbleached fraction comprising 9.72 1.03%, a dynamic fraction at 47.08 3.06%, and a stable, unrecoverable fraction at 42.75 2.78%. This stable fraction suggests that a large portion of tau is anchored in the spine. PubMed:24760868
Rac1 and RhoA are the best-studied members that regulate spine dynamics; their activation facilitates and prevents dendritic spine formation, respectively PubMed:27796283
In contrast, much less is known about how RhoA is regulated by excitatory glutamate receptors. The Rho-GEF Lfc (also known as GEF-H1) is one notable link between RhoA activity and glutamate receptors18. Lfc is inhibited by AMPA receptors; Lfc and RhoA inhibition is implicated in spine maintenance10. RhoA hyperactivity can lead to spine loss and impaired synaptic function. PubMed:27796283
In contrast, much less is known about how RhoA is regulated by excitatory glutamate receptors. The Rho-GEF Lfc (also known as GEF-H1) is one notable link between RhoA activity and glutamate receptors18. Lfc is inhibited by AMPA receptors; Lfc and RhoA inhibition is implicated in spine maintenance10. RhoA hyperactivity can lead to spine loss and impaired synaptic function. PubMed:27796283
MAPT-free dendrites in controls had a spine density of ~17 per 20-µm (17.2±0.5 per 20 µm) length, and there was a ~2- fold decrease in spine density in the MAPT-containing dendrites in neurons treated with wortmannin (7.4±1.0 per 20 µm) or epoxomicin (8.2±1.7 per 20 µm) (Fig. 6D). PubMed:30145931
MAPT-free dendrites in controls had a spine density of ~17 per 20-µm (17.2±0.5 per 20 µm) length, and there was a ~2- fold decrease in spine density in the MAPT-containing dendrites in neurons treated with wortmannin (7.4±1.0 per 20 µm) or epoxomicin (8.2±1.7 per 20 µm) (Fig. 6D). PubMed:30145931
Previous studies had shown that the missorting of MAPT into dendrites can cause loss of spines [6,7]. PubMed:30145931
The fibril-treated cells (cross-linked with GA or not) did not reduce the spine density significantly (Fig 4C, bars 8 and 9). PubMed:28528849
For comparison, in the case of Ab oligomers, only higher concentrations (w1 mM) cause an appreciable spine reduction of w30% (Fig. 4C, bar 3) (Zempel et al., 2010 [30]). PubMed:28528849
In this case, there was a dramatic loss (up to 50%) of spines in TauRDΔK oligomer-treated cells compared with monomer-treated cells (Fig. 4A and B, bar 3). PubMed:28528849
Drebrin, a neuronal actin-binding protein involved in spinogenesis and synaptogenesis, was decreased by up to 60% consistent with the reduced number of spines (Fig. 4D, bars 3, 6, and 9). PubMed:28528849
Endogenous tau protein retained its normal axonal localization and did not missort into the cell body and dendrites (Fig. 6A8), although there was a reduction in the spine density (Fig. 6B6) in the TauRDΔK oligomer-treated neurons. PubMed:28528849
The results revealed that both TauRDΔK and TauFLΔK oligomers reduce the density of spines up to 50% compared with the buffer-treated cells. PubMed:28528849
Some studies showed in cell toxicity assays that tau oligomers made from pro-aggregant recombinant tau were toxic to cultured cells; other studies in cultured neurons found that oligomers induced only local neurotoxicity that led to loss of spines PubMed:26631930
MAPT-free dendrites in controls had a spine density of ~17 per 20-µm (17.2±0.5 per 20 µm) length, and there was a ~2- fold decrease in spine density in the MAPT-containing dendrites in neurons treated with wortmannin (7.4±1.0 per 20 µm) or epoxomicin (8.2±1.7 per 20 µm) (Fig. 6D). PubMed:30145931
MAPT-free dendrites in controls had a spine density of ~17 per 20-µm (17.2±0.5 per 20 µm) length, and there was a ~2- fold decrease in spine density in the MAPT-containing dendrites in neurons treated with wortmannin (7.4±1.0 per 20 µm) or epoxomicin (8.2±1.7 per 20 µm) (Fig. 6D). PubMed:30145931
The recovery curves indicated 3 pools of tau: a mobile, unbleached fraction comprising 9.72 1.03%, a dynamic fraction at 47.08 3.06%, and a stable, unrecoverable fraction at 42.75 2.78%. This stable fraction suggests that a large portion of tau is anchored in the spine. PubMed:24760868
The recovery curves indicated 3 pools of tau: a mobile, unbleached fraction comprising 9.72 1.03%, a dynamic fraction at 47.08 3.06%, and a stable, unrecoverable fraction at 42.75 2.78%. This stable fraction suggests that a large portion of tau is anchored in the spine. PubMed:24760868
The recovery curves indicated 3 pools of tau: a mobile, unbleached fraction comprising 9.72 1.03%, a dynamic fraction at 47.08 3.06%, and a stable, unrecoverable fraction at 42.75 2.78%. This stable fraction suggests that a large portion of tau is anchored in the spine. PubMed:24760868
Rac1 and RhoA are the best-studied members that regulate spine dynamics; their activation facilitates and prevents dendritic spine formation, respectively PubMed:27796283
In contrast, much less is known about how RhoA is regulated by excitatory glutamate receptors. The Rho-GEF Lfc (also known as GEF-H1) is one notable link between RhoA activity and glutamate receptors18. Lfc is inhibited by AMPA receptors; Lfc and RhoA inhibition is implicated in spine maintenance10. RhoA hyperactivity can lead to spine loss and impaired synaptic function. PubMed:27796283
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.