Term
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Definition
| many didffernts factors comming together tocause common mechanisms of injury in neruosn leadign to cell death |
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Term
| general stratetigeis for neruoprotection: in mitochodnria, immune repsone , excitooxitiy, and oxidative stress |
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Definition
mitochondria- boost energy produciton and block proapopotoic signlas
immune repsone- antibodies, block immune resposnee, anti inflammatoyr agents, reduce microglial activation
excitotoxicity: reduce glutamate actions (inhibit uptake block nmda receptors)
oxidative stress- antixoidants, prevent formation of ros,rns, prevent cyotkine produciton |
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Term
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Definition
| aonal damage iwth retrogade dying back |
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Term
| factors that cause necrosis and manifestations |
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Definition
| cellular swelling mitochodnrial sweelling icnresed ionic influxes (especially calcium), mitochondrial dysfunciton loss of energy stores, produciton of ros and rns , oxidation of proteins , and other celular portions and loss of itnegraity of cell membrane. |
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Term
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Definition
| programemd cel death. Requiresnew protein sytnehesis and ATp. Activated via cytorochrome C which is realeased and leads to activation of caspases. Caspasesdegrade intercelluar proteins leadign to death |
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Term
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Definition
necrosis: loss of membrane itnegrity, cellular and mtiochondrial s welling, ends with cel lysis, loss of ion regulation, andl oss of atp
apoptosis: membrane blebbing, cell shrinkage, cell gets fragmented int osmall bodies, openign of mitochodnrial permeability pore. SUe of atp required |
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Term
| causes of neruoifnlammation |
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Definition
| can be bacteria or virus or directly damge to neuron. Cause release of cyotkiens etc. which are direclty neurotoxic and cause activation fo mcirgolia |
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Term
| neurosn myay rpecipitate neurodegenraiton and immuen resposne or vice versa (with immune repsonse being iniating factor) |
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Definition
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Term
| major players in neurodegeneratio and their sources |
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Definition
ROS (mitochondria e trnasport chain and microglia nadph oxidase).
Reactive nitrogen species- neurons wbcs and cyotkiens.
cyotkiens /cheokiens
foreign substances
mutant or over produciton fo proteins asosciated iwth neurodenegariton
Caspases. |
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Term
| neuropreoticetive stargeties agaisnt ors and rns |
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Definition
remove superoxides via superoide dismutase.
increase glutathion levels to remove peroxide.
free radical scavengers
reducei ron load via cehlators
Block No synthesis |
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Term
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Definition
| can cause cel ldeath either by causing necrosis, or altering mtiochodnrrial membrane permeabililty leading to apoptoosis |
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Term
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Definition
| microglia, astrocytes, neurons, they ahver ecpetors for htese factors as well. |
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Term
| microglia quiescent state vs activated state |
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Definition
queiscent : extensive branching and low levles of profinalmamtory cyotkiens
When activated- becoem abmoiboid so can phagocytose, upregulate receptors to enhacne repsosne ,adn increase cyotkine levels |
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Term
| mciroglial activation by damaged neuron debirs benenficail actions |
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Definition
| phagocytosis, and antiifnlammtory moelcuels Ros/RNS and profinallamtory moecluels (can be harmful if there for oo long) |
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Term
| astrocyte play extrmely impornt neuroprotective role |
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Definition
| provide metabolis suport for neurons, conolr electrolyete and water hemoestasis, rpovide neurtorpohic factors, remove haardous stuff such as excess glutamte from the area. And improtnat for antiodinatns, and siruptino fo astrocytes ma ybe destrimental to neurosn |
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Term
| various stages of astrogliosis |
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Definition
normal :non overlapping
Moderate to severe- as go from moderate to severe show increased overlapping , hypertrophy adn staining with GFAP and more proliferation |
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Term
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Definition
| can exsit in various states depending on environment |
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Term
| advantage and idsadtanvate of glial sca |
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Definition
| inhbiit migraiton of pathogens or immunecells to restrict spreado f infection or ifnalmamtion, hwoever, imapriaxonal and dendtritic regeneration |
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Term
| priamrys timulus allowing cells to enter cns |
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Definition
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Term
| mitochodnrial dysfunction general causes |
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Definition
mitcohodnrial dysfunciotn sieen in many enurgdegnerative disroders.
Dysfucnitonal mitochodnria inrease ROS production . Calcium influx leadign to cellclualr distuction, loss of mitochodnrdial transition porte activatign apotptosis. loss energy supplies ledads to reduciton cl membrane potential eladign to excitotoxicity. |
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Term
| targets for interventin in apotposis |
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Definition
| blcok death recpetors, blco k activation fo caspases, block cytochrome C release. |
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Term
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Definition
playes rominet roel in stroke LAS and ischemia. Caused by glutamte andnmda re ceptors. Icnrease in glutamte in extracelluar space.
loss of energy stores can reduce celular membranpeotenial causign relase of magnesium block. Thsi will ilcnrease itnracellular calcium causing caspaseissues and produciton of ROS and RNS. lack of ATp will most likely cause death via Radicals and necrosis. wheras normal atp wil lcause apoptotiss |
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Term
| nmda receptor details slide 39 of neuroprotection |
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Definition
| ahs a glutamte recognition site, glycitine recognistion site and polyamien site (modulates glycinewsite). Aslso pcp siteh wich acts like magnesium pore, but not really useful due to pyschotropic efefcts. |
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Term
| unfolded misfolded prtoein resposne |
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Definition
| increasei nmisfolded proteins may overwehlm autophagy system resullting in inadequate reponse. Misfolded aggregates form creating fibbiilary aggregates which impair protein degrading sys tems. (most neurodegenetive diseases). |
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Term
| neuroprotetciive strategies for protein misfolding |
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Definition
target specifi proteins or pathways in specific disiease tor educe produciton of misofolded proteins.
target general neurodegenerative processes which are common to most forms of degneration-
change lifestyle |
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Term
| Lewy bodies: slide 53 lewy body |
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Definition
| hallmarks of PD= intracellular inclusions in enurons which stain densley for synuclein and ubuiquitin |
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Term
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Definition
| all factors nerudoegenratino come itno pla: proteosome autopahy, protein aggregation , icnlusion bodies ,neurifinflammaiton apoptosis defective motchiondria oxidative stress excitoocity, comrpomsied calciumha ndling |
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Term
| alpha synuclein formation |
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Definition
| phosophorylation leads to unfolding which leads to formation of b sheets which form aggregates and impair proetsomal fucniton, and autophagy. can also block kinate and try to silence transcipriton fo htis mutant form |
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Term
| alkpha snucleins and immune repsonse |
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Definition
| relase of alpha synuclins can activate t lmphocytes and potentiate immune reposne lead to release of neurtoxins and free radicals etc. |
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Term
| alpha synuclin as biomareker |
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Definition
| levels of alph synuclein are low in pD patietns |
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Term
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Definition
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Term
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Definition
| may contribute tooxidative dmage in PD patients |
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Term
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Definition
| promiennt in PD pattietns , reduced levels of PPAR gamma protein levels |
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Term
| evidence o immune repsonsei nPD disease ,i nshort, pD can be caused by eeverything. |
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Definition
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Term
| excercise and diet are neuroprotective |
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Definition
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Term
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Definition
| not loss of fucnitno ,but gain of toxic fucntion |
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Term
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Definition
| excitotoxicity in cells gluatamte . defective satrocyte glutatme uptake |
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