One of the hallmarks of MND is the accumulation of aggregated proteins in the affected motor neurons. These proteins can interfere with normal cellular processes, leading to neuronal dysfunction and death. Therefore, addressing protein aggregation is an important therapeutic strategy .
Preventing further protein synthesis can be a useful approach to reduce the production of misfolded proteins. However, it may not be sufficient to fully restore function in MND. This is because the existing aggregated proteins can persist and continue to interfere with cellular processes, even if new protein synthesis is blocked.
Therefore, a more comprehensive approach that targets both protein synthesis and protein aggregation may be necessary to restore motor neuron function.Several approaches are being developed to address protein aggregation.
These include the use of chaperones, which can help refold misfolded proteins, and the use of proteasome inhibitors, which can prevent the breakdown of misfolded proteins.
Additionally, some researchers are exploring the use of gene therapy to increase the expression of proteins that can clear misfolded proteins from cells.In summary, preventing further protein synthesis can be a useful strategy in MND, but it may not be sufficient to fully restore function. Addressing protein aggregation through a combination of approaches may be necessary to achieve better outcomes in the treatment of MND.
In the Pharmaust research article "Induction of endoplasmic reticulum stress is associated with the anti-tumour activity of Monepantel across cancer types," the authors investigated the anti-tumor effects of monepantel (MPL) and its potential mechanism of action. MPL is an anthelmintic drug that has shown promising anti-cancer activity in preclinical studies.
The role of the mTOR signaling pathway in MPL's effects is not a primary focus of the study, and the information provided in the article is limited. The authors did not directly investigate the involvement of the mTOR pathway in MPL's anti-tumor effects. However, they did mention that MPL-induced endoplasmic reticulum (ER) stress can lead to the downregulation of the PI3K/AKT/mTOR signaling pathway, which is known to play a critical role in cancer cell growth and survival.
The authors also noted that MPL-induced ER stress can activate the unfolded protein response (UPR) pathway, which is a cellular stress response that helps to restore ER homeostasis. The UPR pathway can either promote cell survival or trigger cell death, depending on the severity of ER stress and the cellular context. The authors suggested that MPL-induced ER stress may contribute to its anti-tumor effects by promoting UPR-mediated cell death in cancer cells.
In summary, while the role of the mTOR signaling pathway in MPL's effects is not clear based on the information provided in the article, the study suggests that Monepantel-induced ER stress and UPR activation may contribute to its anti-tumor activity across different cancer types.
Further research is needed to fully elucidate the mechanism of MPL's anti-cancer effects and its potential interaction with the mTOR pathway.Monepantel may also have the potential to prevent the development of drug tolerance in certain cancers.One of the mechanisms by which cancer cells develop drug tolerance is through the activation of drug efflux pumps, which can pump out chemotherapy drugs and reduce their effectiveness.
Monepantel has been shown to inhibit drug efflux pumps and enhance the efficacy of chemotherapy drugs in cancer cells, suggesting that it may help prevent the development of drug tolerance.
Havelots, to answer your most difficult question/s, I did have to delve into Medical AI for assistance. I normally would reference a study or three but couldn't find anything at the moment that would suit.
Your questions were excellent and I hope my attempt at an answer or two will suffice.
Kpax
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