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Inside Alzheimer's Disease Diagnosis
Published in Parimelazhagan Thangaraj, Lucindo José Quintans Júnior, Nagamony Ponpandian, Nanophytomedicine, 2023
Gomathi Rajkumar, Murugan Rajan, Mairim Russo Serafini, Narendra Narain, Adriano A.S. Araujo, Lucindo José Quintans Júnior, Lijing Ke
During the past two decades, the cholinergic hypothesis, i.e. a dysfunction of acetylcholine-containing neurons in the brain, was associated with cognitive decline in Alzheimer's disease (Hansen et al., 2008). Acetylcholinesterase inhibitors, which inhibit the breakdown of acetylcholine into choline and acetate in the central nervous system (CNS), used to be the key focus in developing anti-AD drugs. However, the acetylcholinesterase inhibitors (i.e. donepezil) that once dominated the market are now declining, owing to their short effective period and limited efficiency (Hansen et al., 2008). In the past decade, several other hypotheses have emerged on the pathogenesis of AD. The major hallmark has been attributed to amyloid β (Aβ) deposition, neurofibrillary tangles induced by hyperphosphorylated tau proteins and neuronal death.
Sleep Promoting Improvement of Declarative Memory
Published in Bahman Zohuri, Patrick J. McDaniel, Electrical Brain Stimulation for the Treatment of Neurological Disorders, 2019
Bahman Zohuri, Patrick J. McDaniel
The effects of ACh on memory have to be regarded separately for the acquisition, consolidation, and recall phase and for different memory systems. A number of studies did this by using either cholinergic receptor antagonists (e.g., scopolamine) or cholinesterase inhibitors (e.g., physostigmine). The latter increases the availability of ACh by preventing its breakdown in the synaptic cleft. The main outcome of these studies was a reduced acquisition of new memories under conditions of cholinergic deficiency, perhaps via an influence on attentional processes.72,73
List of Chemical Substances
Published in T.S.S. Dikshith, and Safety, 2016
Fenitrothion is toxic to animals and humans. After prolonged periods of exposures to high concentrations of fenitrothion, occupational workers show poisoning. The symptoms include, but are not limited to, general malaise, fatigue, headache, loss of memory and ability to concentrate, anorexia, nausea, thirst, loss of weight, cramps, muscular weakness, and tremors, and at sufficiently high dosage produce typical cholinergic poisoning. The formulation product, sumithion 50EC, causes delayed neurotoxicity in adult rats, as well as humans.
Characterization of the antioxidant activity, total phenolic content, enzyme inhibition, and anticancer properties of Achillea millefolium L. (yarrow)
Published in Instrumentation Science & Technology, 2022
Nagihan Karaaslan Ayhan, Merve Goksin Karaaslan Tunc, Samir Abbas Ali Noma, Ali Kurucay, Burhan Ates
Acetylcholinesterase (AChE, E.C.3.1.1.7) is a key cholinesterase that plays an important role in cholinergic transmission. Enzymes are expressed in all tissue cells but have less activity. Acetylcholinesterase enzyme is primarily in muscles, brain, and cholinergic neurons and is responsible for the rapid hydrolysis of acetylcholine (ACh) at synapses.[24] Indeed, in the late phase of Alzheimer’s disease (AD), AChE levels increase significantly. Cholinesterase inhibitors or anti-cholinesterase prevent the breakdown of the neurotransmitter butyrylcholine or acetylcholine. The cholinergic system, which plays a significant role in the regulation of cognition, learning, and memory processes, has been extensively studied for the design of Alzheimer’s disease drugs.[25]
Neuromotor activity inhibition in zebrafish early-life stages after exposure to environmental relevant concentrations of caffeine
Published in Journal of Environmental Science and Health, Part A, 2021
Natália Oliveira de Farias, Thayres de Sousa Andrade, Viviani Lara Santos, Pedro Galvino, Paula Suares-Rocha, Inês Domingues, Cesar Koppe Grisolia, Rhaul Oliveira
The neurotransmitter acetylcholine has a key role in central and neuromuscular synapses of the cholinergic system. Following its release into the synaptic cleft, it is rapidly degraded by the enzyme AChE.[48] Our results showed inhibition of AChE activity of approximately 20% in concentrations ≥ 0.0088 mg/L, after 168 h. The inhibition of AChE by CAF has been previously reported for vertebrates.[49] This inhibition may trigger behavioral disturbances with ecological effects, since a decrease in cholinesterase activity may cause progressive myopathy of skeletal muscles and, consequently, loss of motility.[50] The molecular mechanism of CAF action on AChE is not fully known. The reversible antagonism on adenosine receptor has been considered as the most evident molecular effect of CAF.[51] Adenosine receptors are found in glutaminergic, dopaminergic and GABAergic neurons. Thus, by blocking these neurons, CAF may also induce an indirect effect on cholinergic pathways.[52,53] In addition, a structural feature common to CAF and other xanthine compounds is the N-methyl determinant of the pyrrolidine ring, which may be important in binding to the AChE, provoking its inhibition.[54]
Green synthesis of silver nanoparticles using Ilex paraguariensis extracts: antimicrobial activity and acetilcolinesterase modulation in rat brain tissue
Published in Green Chemistry Letters and Reviews, 2022
Mirela Vanin dos Santos Lima, Grasieli Beloni de Melo, Liandra Gracher Teixeira, Cristiane Grella Miranda, Pedro Henrique Hermes de Araújo, Claudia Sayer, Rafael Porto Ineu, Fernanda Vitória Leimann, Odinei Hess Gonçalves
Figure 7 presents AChE activity assay results. It is possible to observe in Figure 7 that the extract group does not differ from Control group indicating a non per se effect of extract. Both experiment E2 and experiment E4 were able to inhibit the enzyme (150 and 200 µL, respectively). Results also demonstrated that at 200 µL, E2 (p < 0.01) has a potency enzymés inhibition higher than E4 (p < 0.05). These results could be explained by the spherical shape of E2 facilitating an enzyme–substrate interaction. Santos et al. (49) demonstrated a significant increment in the ex vivo AChE activity in the hippocampus of animals when treated chronically with 300 mg kg−1 of Ilex paraguariensis, a result contrary to that obtained in this work for AgNPs obtained with Ilex paraguariensis extract as silver reducing and capping agent. Therefore, the results showed that AgNPs were able to inhibit the enzyme activity even were capped/stabilized with Ilex paraguariensis extract. Since levels of the neurotransmitter acetylcholine (ACh) can modulate stress and anxiety-like behavior (50) it is important to verify the involvement of AgNPs in the modulation of the cholinergic system by evaluating AChE enzyme activity. According to the cholinergic hypothesis, neurodegenerative diseases, such as Alzheimer’s disease, are caused by loss of ACh neurotransmitters or by an increase in AChE activity in the brain. As a result, contact time between neurotransmitters and post-synaptic membrane receptors is reduced, hindering information transmission through neurons and leading to memory loss. Therefore, usual drugs in neurodegenerative diseases treatment consist of AChE reversible inhibitors, which balance cholinergic system and allow enough time to contact for information spread in the nervous system (51–53).