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Fenugreek in Management of Neurological and Psychological Disorders
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Rohini Pujari, Prasad Thakurdesai
The beneficial effects of DG are also supported by the report on the Aβ-42 peptides and neurotoxicants-induced brain damage in transgenic 2576 (TG) mice injected with trimethyltin (TMT) (Koh et al. 2016). Treatment with DG significantly decreased the number of dead cells and Aβ-stained plaques in the dentate gyrus’s granule cells layer. Additionally, a significant suppression of apoptosis (suppressed apoptotic Bax/Bcl-2 expression) and acetylcholinesterase (AChE) activity indicated antiapoptotic and enhanced cholinergic activity of DG. The nerve growth factor (NGF) concentration was observed to be markedly enhanced with the recovery of decreased phosphorylation of downstream members in the TrkA high-affinity receptor signaling pathway. A similar pattern was exhibited in p75NTR expression and JNK phosphorylation in the NGF low-affinity receptor signaling pathway. These outcomes are suggested to be mediated by the enhancement of NGF biosynthesis and SOD activity of DG (Koh et al. 2016).
Angiogenesis and Roles of Adhesion Molecules in Psoriatic Disease
Published in Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi, Psoriasis and Psoriatic Arthritis, 2017
Asmita Hazra, Saptarshi Mandal
NGF receptors are tyrosine kinase A (TrkA), a receptor tyrosine kinase, and p75 neurotrophin receptor (p75NTR) (a neurotrophin receptor), a receptor that belongs to the TNF family. p75NTR is a common receptor for other neurotrophins, such as BDNF and NT3 and 4. TrkA and p75NTR together form the high-affinity receptor complex producing pro-survival and proliferative signaling. When p75NTR is expressed in the absence of TrkA, NGF can induce apoptosis through p75NTR-induced Rac GTPase-dependent activation of the c-Jun N-terminal kinase (JNK), including an injury-specific JNK3. The α9β1 integrin is a third receptor for NGF, which mimics TrkA in activity.
Suicide
Published in John R. Cutcliffe, José Carlos Santos, Paul S. Links, Juveria Zaheer, Henry G. Harder, Frank Campbell, Rod McCormick, Kari Harder, Yvonne Bergmans, Rahel Eynan, Routledge International Handbook of Clinical Suicide Research, 2013
With the development of neurosciences and genetics, more than three dozen candidate genes that may be involved in suicidality have been found until now. Among them, the most well-known and numerous are those of the serotonergic system (e.g., 5-HTT Gene, TPH1 Gene, TPH2 Gene, 5-HTR1A Gene, 5-HTRB Gene, 5-HTR2A Gene, 5-HTRC Gene, 5-HTR5A Gene). Other systems have been studied: noradrenergic, dopaminergic, gabaergic, glutamatergic, nitric oxid, neurotrophines. Among these, of particular interest is the deficit of BDNF (brain-derived neurotrophic factor) and the p75NTR Gene (p75 neurotrophine receptor). One is dealing with a fashionable research with surprising results every year which need to be replicated for a better consistency of the knowledge of the suicide genetics.
Urinary p75ECD levels in patients with amyotrophic lateral sclerosis: a meta-analysis
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2022
Guanzhong Shi, Shuai Shao, Jinxia Zhou, Kun Huang, Fang-Fang Bi
By interacting with different neurotrophic factors and other receptors, p75 NTR mediates cell survival and death (7,22). p75 NTR-induced apoptosis is thought to be a part of a constant program that removes damaged neurons and axons during injury and degeneration in adult nervous system. One drawback of this function is that p75NTR signaling can aggravate the damage after severe impairment and apparent neurodegenerative disease. Previous researches on ALS mouse model (SOD1G93A mouse) through p75 NTR showed significant effect in cellulo, but failed in vivo due to technical limits, marking it as a potential therapeutic target. Previous researches have made a series of attempts targeting p75NTR. Attempts to modulate p75NTR-mediated neuronal death in ALS models using antisense oligonucleotides have led to significant effect both in cellulo and in vivo (13). However, researches using pharmacological gene modulatory treatment, small molecule ligands of p75NTR or a cyclic peptide antagonist led to only effects in cellulo but modest or no protective effects in animal models due to the limit of blood–brain barrier or pharmacological toxicity (23–26).
The balance between cell survival and death in the placenta: Do neurotrophins have a role?
Published in Systems Biology in Reproductive Medicine, 2022
Prachi Pathare-Ingawale, Preeti Chavan-Gautam
The p75NTR receptor is a death domain-containing member of the TNF receptor superfamily involved in apoptosis (Bertrand et al. 2008). The apoptosis signaling by pro-NT/p75NTR interaction requires the presence of sortilin. Reports indicate that Sortilin functions as a co-receptor with p75NTR for binding and induction apoptosis by pro- NTs such as pro-BDNF (Teng et al. 2005) and pro-NGF (Nykjaer et al. 2004). Sortilin recognizes the pro-domain of pro-NT, thereby acting as a switch that enables p75NTR-expressing cells to undergo apoptosis rather than survival (Nykjaer et al. 2004; Teng et al. 2010). Such activation of p75NTR, followed by interactions with signaling molecules like NRAGE, TRAF, and NRIF, leads to apoptosis mainly through JNK dependant Bad phosphorylation (Freund-Michel and Frossard 2008). Other mechanisms such as the inhibition of Akt phosphorylation and upregulation of proapoptotic genes have also been suggested to contribute to apoptosis induced by proNT/p75NTR (Bhakar et al. 2003; Song et al. 2010). Thus, the proNT to mature NT ratio determines cell survival or apoptosis, depending on which form of the protein is secreted and which receptor is activated (Shen et al. 2013).
A narrative review of brain-derived neurotrophic factor (BDNF) on cognitive performance in Alzheimer’s disease
Published in Growth Factors, 2020
Noor Azila Ismail, Mohammad Farris Iman Leong Abdullah, Rohayu Hami, Hazwani Ahmad Yusof
BDNF binds with a specific affinity to the TrkB and p75NTR receptors. Specifically, it binds to the high-affinity TrkB receptor and low-affinity p75NTR receptor (Angoa-Perez, Anneken, and Kuhn 2017). When the p75NTR receptor is co-expressed with the TrkB receptor, it enhances neurotrophins binding affinity, thus accelerating ligand discrimination (Angoa-Perez, Anneken, and Kuhn 2017). A study by Bibel, Hoppe, and Barde (1999) demonstrated that an in-depth connection between the p75NTR and TrkB receptors indicated that the receptors could communicate with each other when they are triggered. This finding indicates that Pro-BDNF can be treated under the non-pathological condition as part of a regulatory mechanism of BDNF activity. The truncated form of the TrkB receptor may also be used by the internalisation and clearance of BDNF from the synapse as a dominant-negative inhibitor in BDNF signalling (Miranda et al. 2019).