Asset Details
Do you wish to reserve the book?
P2X7 Receptors Amplify CNS Damage in Neurodegenerative Diseases
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
P2X7 Receptors Amplify CNS Damage in Neurodegenerative Diseases
Do you wish to request the book?
P2X7 Receptors Amplify CNS Damage in Neurodegenerative Diseases
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
P2X7 Receptors Amplify CNS Damage in Neurodegenerative Diseases
2020
Overview
ATP is a (co)transmitter and signaling molecule in the CNS. It acts at a multitude of ligand-gated cationic channels termed P2X to induce rapid depolarization of the cell membrane. Within this receptor-channel family, the P2X7 receptor (R) allows the transmembrane fluxes of Na+, Ca2+, and K+, but also allows the slow permeation of larger organic molecules. This is supposed to cause necrosis by excessive Ca2+ influx, as well as depletion of intracellular ions and metabolites. Cell death may also occur by apoptosis due to the activation of the caspase enzymatic cascade. Because P2X7Rs are localized in the CNS preferentially on microglia, but also at a lower density on neuroglia (astrocytes, oligodendrocytes) the stimulation of this receptor leads to the release of neurodegeneration-inducing bioactive molecules such as pro-inflammatory cytokines, chemokines, proteases, reactive oxygen and nitrogen molecules, and the excitotoxic glutamate/ATP. Various neurodegenerative reactions of the brain/spinal cord following acute harmful events (mechanical CNS damage, ischemia, status epilepticus) or chronic neurodegenerative diseases (neuropathic pain, Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, amyotrophic lateral sclerosis) lead to a massive release of ATP via the leaky plasma membrane of neural tissue. This causes cellular damage superimposed on the original consequences of neurodegeneration. Hence, blood-brain-barrier permeable pharmacological antagonists of P2X7Rs with excellent bioavailability are possible therapeutic agents for these diseases. The aim of this review article is to summarize our present state of knowledge on the involvement of P2X7R-mediated events in neurodegenerative illnesses endangering especially the life quality and duration of the aged human population.
Publisher
MDPI AG,MDPI
Subject
/ Central Nervous System Diseases - drug therapy
/ Central Nervous System Diseases - metabolism
/ Central Nervous System Diseases - pathology
/ Chronic Pain - physiopathology
/ Disease
/ Humans
/ Neurodegenerative Diseases - drug therapy
/ Neurodegenerative Diseases - metabolism
/ Neurodegenerative Diseases - pathology
/ Neurons
/ Proteins
/ Purinergic P2X Receptor Antagonists - pharmacology
/ Receptors, Purinergic P2X7 - deficiency
/ Receptors, Purinergic P2X7 - metabolism
/ Review
