scholarly journals Revisiting nicotine’s role in the ageing brain and cognitive impairment

2017 ◽  
Vol 28 (7) ◽  
pp. 767-781 ◽  
Author(s):  
Alireza Majdi ◽  
Farzin Kamari ◽  
Manouchehr Seyedi Vafaee ◽  
Saeed Sadigh-Eteghad
Keyword(s):  
Cognitive Impairment ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Therapeutic Potential ◽  
Amyloid Β ◽  
Therapeutic Effects ◽  
Molecular Pathways ◽  
Pharmacological Chaperone ◽  
Age Related ◽  
Brain Ageing

AbstractBrain ageing is a complex process which in its pathologic form is associated with learning and memory dysfunction or cognitive impairment. During ageing, changes in cholinergic innervations and reduced acetylcholinergic tonus may trigger a series of molecular pathways participating in oxidative stress, excitotoxicity, amyloid-β toxicity, apoptosis, neuroinflammation, and perturb neurotrophic factors in the brain. Nicotine is an exogenous agonist of nicotinic acetylcholine receptors (nAChRs) and acts as a pharmacological chaperone in the regulation of nAChR expression, potentially intervening in age-related changes in diverse molecular pathways leading to pathology. Although nicotine has therapeutic potential, paradoxical effects have been reported, possibly due to its inverted U-shape dose-response effects or pharmacokinetic factors. Additionally, nicotine administration should result in optimum therapeutic effects without imparting abuse potential or toxicity. Overall, this review aims to compile the previous and most recent data on nicotine and its effects on cognition-related mechanisms and age-related cognitive impairment.

scholarly journals Peptide Blockers of the Inhibition of Neuronal Nicotinic Acetylcholine Receptors by Amyloid β

2005 ◽  
Vol 280 (35) ◽  
pp. 31085-31090 ◽  
Author(s):  
Margaret H. Magdesian ◽  
Arthur A. Nery ◽  
A. Henrique B. Martins ◽  
Maria Aparecida Juliano ◽  
Luiz Juliano ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Amyloid Β ◽  
Neuronal Nicotinic Acetylcholine Receptors ◽  
Nicotinic Acetylcholine

scholarly journals Galantamine-induced Amyloid-β Clearance Mediated via Stimulation of Microglial Nicotinic Acetylcholine Receptors

2010 ◽  
Vol 285 (51) ◽  
pp. 40180-40191 ◽  
Author(s):  
Kazuyuki Takata ◽  
Yoshihisa Kitamura ◽  
Mana Saeki ◽  
Maki Terada ◽  
Sachiko Kagitani ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Amyloid Β ◽  
Nicotinic Acetylcholine ◽  
Stimulation Of

scholarly journals Pharmacological effects of saffron and its constituents in ocular disorders from in vitro studies to clinical trials; a systematic review

2020 ◽  
Vol 18 ◽  
Author(s):  
Samaneh Sepahi ◽  
Adel Ghorani-Azam ◽  
Seyedeh Maryam Hossieni ◽  
Seyed Ahmad Mohajeri ◽  
Elham Khodavrdi
Keyword(s):  
Clinical Trials ◽  
Clinical Studies ◽  
Therapeutic Potential ◽  
In Vitro Studies ◽  
Therapeutic Effects ◽  
Potential Candidate ◽  
Retinal Cells ◽  
Age Related ◽  
Eye Disorders

Introduction: Some medicinal plants have shown promising therapeutic potential for management of the diseases. We aimed to systematically review the literature wherein the therapeutic effects of saffron have been studied on eye disorders. Methods: A systematic literature search was performed in PubMed, Scopus, Web of Science, Google scholar and other databases using eye disorders, and saffron as key terms. No strict inclusion criteria were defined, and almost all clinical studies, as well as in vivo and in vitro studies were included. The reported data in each study were extracted and then qualitatively described. Results: Finally, 78 articles were found but only 29 relevant articles were included. Nine articles are clinical trials and 20 articles were done on cellular and molecular aspects of saffron on eye disorders. According to the included studies, crocin prevented the pro-inflammatory response in retinal cells and decreased glucose level in diabetic mice. Also, crocetin prevented retinal degeneration and saffron protected photoreceptors from light-induced damage in retinal cells. Saffron also improved visual function in age-related macular edema and decreased intraocular pressure in patients with glaucoma. In addition, it was shown that crocin can improve best corrected visual acuity and decreased central macular thickness in patients with diabetic maculopathy. Conclusion: The results of this review indicated that saffron and its main ingredients such as crocin could be a potential candidate for the treatment of ocular disease especially eye inflammation; however, further clinical studies are needed to confirm such efficiency.

scholarly journals Cholinergic anti-inflammatory pathway ameliorates murine experimental Th2-type colitis by suppressing the migration of plasmacytoid dendritic cells

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Yuya Kanauchi ◽  
Takeshi Yamamoto ◽  
Minako Yoshida ◽  
Yue Zhang ◽  
Jaemin Lee ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Therapeutic Potential ◽  
Plasmacytoid Dendritic Cells ◽  
Nerve Fibers ◽  
Chronic Inflammatory Bowel Disease ◽  
Jak2 Inhibitor ◽  
Cholinergic Pathway ◽  
Anti Inflammatory

AbstractUlcerative colitis (UC) is a chronic inflammatory bowel disease. Several studies have demonstrated that α7 nicotinic acetylcholine receptors (α7nAChRs) exert anti-inflammatory effects on immune cells and nicotine suppress UC onset and relapse. Plasmacytoid dendritic cells (pDCs) reportedly accumulate in the colon of UC patients. Therefore, we investigated the pathophysiological roles of α7nAChRs on pDCs in the pathology of UC using oxazolone (OXZ)-induced Th2-type colitis with BALB/c mice. 2-deoxy-D-glucose, a central vagal stimulant suppressed OXZ colitis, and nicotine also ameliorated OXZ colitis with suppressing Th2 cytokines, which was reversed by α7nAChR antagonist methyllycaconitine. Additionally, α7nAChRs were expressed on pDCs, which were located very close to cholinergic nerve fibers in the colon of OXZ mice. Furthermore, nicotine suppressed CCL21-induced bone marrow-derived pDC migration due to Rac 1 inactivation, which was reversed by methyllycaconitine, a JAK2 inhibitor AG490 or caspase-3 inhibitor AZ-10417808. CCL21 was mainly expressed in the isolated lymphoid follicles (ILFs) of the colon during OXZ colitis. The therapeutic effect of cholinergic pathway on OXZ colitis probably through α7nAChRs on pDCs were attributed to the suppression of pDC migration toward the ILFs. Therefore, the activation of α7nAChRs has innovative therapeutic potential for the treatment of UC.

scholarly journals Amyloid Beta Peptide (Aβ1-42) Reverses the Cholinergic Control of Monocytic IL-1β Release

2020 ◽  
Vol 9 (9) ◽  
pp. 2887
Author(s):  
Katrin Richter ◽  
Raymond Ogiemwonyi-Schaefer ◽  
Sigrid Wilker ◽  
Anna I. Chaveiro ◽  
Alisa Agné ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Amyloid Β ◽  
Inhibitory Effect ◽  
Mononuclear Leukocytes ◽  
Amyloid Β Peptide ◽  
Monocytic Cells ◽  
Cholinergic Mechanism ◽  
Beta Peptide ◽  
Α7 Nicotinic Acetylcholine Receptors

Amyloid-β peptide (Aβ1-42), the cleavage product of the evolutionary highly conserved amyloid precursor protein, presumably plays a pathogenic role in Alzheimer’s disease. Aβ1-42 can induce the secretion of the pro-inflammatory cytokine intereukin-1β (IL-1β) in immune cells within and out of the nervous system. Known interaction partners of Aβ1-42 are α7 nicotinic acetylcholine receptors (nAChRs). The physiological functions of Aβ1-42 are, however, not fully understood. Recently, we identified a cholinergic mechanism that controls monocytic release of IL-1β by canonical and non-canonical agonists of nAChRs containing subunits α7, α9, and/or α10. Here, we tested the hypothesis that Aβ1-42 modulates this inhibitory cholinergic mechanism. Lipopolysaccharide-primed monocytic U937 cells and human mononuclear leukocytes were stimulated with the P2X7 receptor agonist 2′(3′)-O-(4-benzoylbenzoyl)adenosine-5′-triphosphate triethylammonium salt (BzATP) in the presence or absence of nAChR agonists and Aβ1-42. IL-1β concentrations were measured in the supernatant. Aβ1-42 dose-dependently (IC50 = 2.54 µM) reversed the inhibitory effect of canonical and non-canonical nicotinic agonists on BzATP-mediated IL-1β-release by monocytic cells, whereas reverse Aβ42-1 was ineffective. In conclusion, we discovered a novel pro-inflammatory Aβ1-42 function that enables monocytic IL-1β release in the presence of nAChR agonists. These findings provide evidence for a novel physiological function of Aβ1-42 in the context of sterile systemic inflammation.

scholarly journals RgIA4 Accelerates Recovery from Paclitaxel-Induced Neuropathic Pain in Rats

Marine Drugs ◽  
2019 ◽  
Vol 18 (1) ◽  
pp. 12 ◽  
Author(s):  
Peter N. Huynh ◽  
Denise Giuvelis ◽  
Sean Christensen ◽  
Kerry L. Tucker ◽  
J. Michael McIntosh
Keyword(s):  
Neuropathic Pain ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Therapeutic Effects ◽  
Chemotherapeutic Drugs ◽  
Chemotherapeutic Drug ◽  
Sprague Dawley ◽  
Once Daily ◽  
Sprague Dawley Rats ◽  
Rescue Mechanism

Chemotherapeutic drugs are widely utilized in the treatment of human cancers. Painful chemotherapy-induced neuropathy is a common, debilitating, and dose-limiting side effect for which there is currently no effective treatment. Previous studies have demonstrated the potential utility of peptides from the marine snail from the genus Conus for the treatment of neuropathic pain. α-Conotoxin RgIA and a potent analog, RgIA4, have previously been shown to prevent the development of neuropathy resulting from the administration of oxaliplatin, a platinum-based antineoplastic drug. Here, we have examined its efficacy against paclitaxel, a chemotherapeutic drug that works by a mechanism of action distinct from that of oxaliplatin. Paclitaxel was administered at 2 mg/kg (intraperitoneally (IP)) every other day for a total of 8 mg/kg. Sprague Dawley rats that were co-administered RgIA4 at 80 µg/kg (subcutaneously (SC)) once daily, five times per week, for three weeks showed significant recovery from mechanical allodynia by day 31. Notably, the therapeutic effects reached significance 12 days after the last administration of RgIA4, which is suggestive of a rescue mechanism. These findings support the effects of RgIA4 in multiple chemotherapeutic models and the investigation of α9α10 nicotinic acetylcholine receptors (nAChRs) as a non-opioid target in the treatment of chronic pain.

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