Do you deny the fact that activating the sigma 1 receptor helps to fend off the neurodegeneration associated with Alzheimer's disease?
Do you deny the fact that coconut oil is has a very high concentration of myristic acid?
Do you deny the the following research relating myristic acid and the sigma 1 receptor for fending off neurodegeneration associated with Alzheimer's disease?
Myristic Acid Hitchhiking on Sigma-1 Receptor to Fend Off Neurodegeneration Jenna Ciesielski, Tsung-Ping Su, Shang-Yi Tsai
Abstract
Neurodegenerative diseases are linked to tauopathy as a result of cyclin dependent kinase 5 (cdk5) binding to its p25 activator instead of its p35 activator and becoming over-activated. The overactive complex stimulates the hyperphosphorylation of tau proteins, leading to neurofibrillary tangles (NFTs) and stunting axon growth and development. It is known that the Sigma-1 Receptor (Sig-1R), an endoplasmic reticulum chaperone, can be involved in axon growth by promoting neurite sprouting through nerve growth factor (NGF) and tropomyosin receptor kinase B (TrkB) [1, 2]. It has also been previously demonstrated that a Sig-1R deficiency impairs the process of neurogenesis by causing a down-regulation of N-methyl-D-aspartate receptors (NMDArs) [3]. The recent study by Tsai et al. sought to understand the relationship between Sig-1R and tauopathy. It was found that the Sig-1R helps maintain proper tau phosphorylation and axon development by facilitating p35 myristoylation and promoting p35 turnover. Neurons that had the Sig-1R knocked down exhibited shortened axons and higher levels of phosphorylated tau proteins compared to control neurons. Here we discuss these recent findings on the role of Sig-1R in tauopathy and highlight the newly presented physiological consequences of the Sig-1R-lipid interaction, helping to understand the close relationship between lipids and neurodegeneration.
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