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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.
Neuroimaging in Nuclear Medicine
Published in Michael Ljungberg, Handbook of Nuclear Medicine and Molecular Imaging for Physicists, 2022
Anne Larsson Strömvall, Susanna Jakobson Mo
In Alzheimer´s disease (AD), the most common form of dementia, amyloid plaques, mainly composed of clumps of β-amyloid (a part of a protein occurring in the synapse) and neurofibrillary tangles, are formed by aggregation of an intracellular protein type called tau. In AD the degenerative process causes damage to nerve-cells communicating with the neurotransmitter acetylcholine. In the brain, acetylcholine is important for cognitive functions, including memory. As the neurons die and the function in affected areas is decreased, the regional blood flow and glucose metabolism will be lower than in normally functioning areas. Typically, the parietal and temporal lobes are affected in Alzheimer´s disease, causing memory loss as well as, for example, difficulties in time and space orientation.
Toxic Responses of the Nervous System
Published in Stephen K. Hall, Joana Chakraborty, Randall J. Ruch, Chemical Exposure and Toxic Responses, 2020
The neurotransmitter system of the neuron represents yet another target for certain neurotoxic substances. A classic example of neurotoxicity due to disruption of the neurotransmitter system involves inhibition of acetylcholinesterase by various organophosphorus insecticides. During normal impulse conduction, the neurotransmitter, acetylcholine, is released from synaptic end bulbs of an axon into the synapse. The neurotransmitter molecules then interact with receptors on the dendrite of an opposing neuron to continue impulse conduction. An endogenous enzyme, acetylcholinesterase, then inactivates the acetylcholine molecules. However, when present in the synaptic region, organophosphorus compounds bind with the endogenous acetylcholinesterase molecules rendering the enzyme ineffective. Consequently, the acetylcholine transmitter accumulates in the synapse and inappropriately continues impulse conduction. The signs and symptoms of organophosphate poisoning are predictable based on this mechanism of action and include increased salivation, lacrimation, and sweating; ataxia, tremors, muscle fasciculations, and convulsions; constriction of the pupils; bronchial constriction; and increased peristalsis with consequent development of nausea, vomiting, abdominal cramps, and diarrhea. In fatal organophosphorus poisoning, death is due to asphyxiation resulting from respiratory failure. However, in most acute exposures, full recovery occurs following cessation of the exposure.
Mechanism of peripheral nerve modulation and recent applications
Published in International Journal of Optomechatronics, 2021
Heejae Shin, Minseok Kang, Sanghoon Lee
In the ANS, sensory information obtained from organs (pain, bladder distension, etc.) is sent to the brain using this action potential, and based on this information, action potentials are exchanged between neurons in the brain, and after the inside process, the final decision is made. Then, this decides the form of an action potential and sends it back to the organ or hormone system to modulate the organs (some signals return via the spinal cord). In the SNS, muscle cells and axon terminals (end of the neuron) are connected (neuromuscular junction). When an action potential arrives at the neuron terminal, acetylcholine (ACh), a neurotransmitter, is released, and ACh consequently activates muscle fibers through an internal process that causes muscle contraction.[18] If the action potential (information) is not properly generated or transmitted, incorrect information is sent to the function of a part of the body, which can lead to a malfunction of the organ and, in severe cases, cause disease.[19–22]
Effects to perfluorooctane sulfonate (PFOS) on the mollusk Unio ravoisieri under laboratory exposure
Published in Chemistry and Ecology, 2018
Imen Amraoui, Noureddine Khalloufi, Samir Touaylia
AChE catalyses the acetylcholine hydrolysis into choline and acetic acid. AChE inhibition by neurotoxic agents causes permanent transmission of the nerve impulse leading to paralysis and death [86]. AChE activity is a specific biomarker of pesticide exposure [87,88]. AChE activity was inhibited in the bivalve Arcanoae, Venus verrucosa and Mytilus edulis exposed to an organophosphorus pesticide [89,90]. Singh and Agarwal [91] showed that AChE activity was inhibited in gastropod Lymnaea acuminate following permethrin contamination. Our study revealed that PFOS did not modify AChE activity in gill and digestive gland of U. ravoisieri. The same profile was observed by Kim et al. [30] in fish Cyprinus carpio where AChE activity was not influenced by PFOS exposure. In contrast, contamination of Daphnia magna with PFOS resulted in AChE inhibition [31].
Open source modular ptosis crutch for the treatment of myasthenia gravis
Published in Expert Review of Medical Devices, 2018
Trust Saidi, Sudesh Sivarasu, Tania S. Douglas
Advances during the last century have resulted in various treatments for MG. Cholinesterase inhibitors are used to retard the degradation of acetylcholine at the neuromuscular junction [46]. There are challenges in the use of cholinesterase inhibitors such as pyridostigmine bromide and neostigmine [7,47]. Although pyridostigmine bromide is the most common first treatment and is considered effective particularly during the early phases of the disease, most patients experience muscarinic side effects of nausea, abdominal cramping, and diarrhea [7,34]. Neostigmine is rarely used because of its poor tolerability and pharmacodynamic profile [7]. Consequently, cholinesterase inhibitor treatment is inadequate for the vast majority of MG patients, and as a result, immunosuppressive corticosteroids, particularly prednisone, is prescribed [48]. Although corticosteroids are inexpensive and rapid-acting drugs for immunomodulation in MG [49], their use is limited by multiple side effects such as osteoporosis, diabetes mellitus, infection, gastric ulcer, and glaucoma [50].