glutamate excitotoxicitycausesneuronal cell death 10.3.2.8
Núñez G. bcl - x is expressed in embryonic and postnatal neural tissues and functionsto preventneuronal cell death
811 - 3 , 1995 González - García , García , Ding , OShea , Boise , Thompson , Núñez : " bcl - x is expressed in embryonic and postnatal neural tissues and functionsto preventneuronal cell death
Excitotoxicity , the effect of glutamate receptor activationto triggerneuronal cell death
the ability of a compoundto preventneuronal cell death
J Clin Microbiol ( 1995 ) 1.47 bcl - x is expressed in embryonic and postnatal neural tissues and functionsto preventneuronal cell death
different mechanisms by whichcan causeneuronal cell death
excessive activation of glutamate receptors ... increased intracellular calciumtriggersneuronal cell death
Excessive glutamatecausesneuronal cell death
glutamate , NMDA , and(passive) caused byneuronal cell death
understanding the mechanisms used by NRG1to preventneuronal cell death
distinct mechanisms in different neurodegenerative diseases(passive) are caused byneuronal cell death
Several neurodegenerative diseasescan causeneural cell death
over - activation of glutamate receptors [ 1,2(passive) caused byneuronal cell death
overstimulation of glutamate receptors(passive) caused byneuronal cell death
over - stimulation of the glutamate receptors(passive) caused byneuronal cell death
Abstract ] negative regulation of endoplasmic reticulum stress - induced intrinsic apoptotic signaling pathway Source : UniProtKB " bcl - x is expressed in embryonic and postnatal neural tissues and functionsto preventneuronal cell death
Overactivation of glutamate receptors leads to calcium overloadingtriggeringneuronal cell death
the three types of SOD1 mutant genes ( FIG(passive) caused byneuronal cell death
transient brain ischemia(passive) caused byneuronal cell death
the ability of glutamate receptor activationto triggerneuronal cell death
toxic levels of glutamate and is useful in strokes and epilepsy(passive) caused byneuronal cell death
an excessive production and accumulation of reactive oxygen species ( ROS(passive) is caused byneuronal cell death
It has also shown protection against excitotoxicitythereby preventingneuronal cell death
excitatory neurotransmitters such as glutamate(passive) caused byneuronal cell death
decreased uptake of glutamatecausesneuronal cell death
imbalanced levels of glutamate(passive) caused byneuronal cell death
excessive amounts of glutamatecan triggerneuronal cell death
an excess of glutamate ( 5(passive) caused byneuronal cell death
excessive activation of glutamate receptors due to increasing levels of extracellular glutamate at the lesion site(passive) caused byneuronal cell death
ischemia or other events knownto causeneuronal cell death
the identified mechanism ... neurodegenerative diseases and injurycauseneuronal cell death
Elliott Mufson on Gambogic amide , a selective agonist for TrkA receptor that possesses robust neurotrophic activitypreventsneuronal cell death
Ye K. Gambogic amide , a selective agonist for TrkA receptor that possesses robust neurotrophic activitypreventsneuronal cell death
toxic levels of glutamate which is associated with Alzheimer 's disease(passive) caused byneuronal cell death
toxic levels of glutamate , which makes it useful in strokes and epilepsy too(passive) caused byneuronal cell death
glutamate efflux under ischemic conditions(passive) caused byneuronal cell death
several reasons like glutamate toxicity [ 110(passive) caused bythe neuronal cell death
glutamate toxicity and inhibits an enzyme that degrades the SHOP(passive) caused byneuronal cell death
chemotherapeutic agents(passive) caused byneuronal cell death
to Alzheimer ’s disease and dementialeadsto Alzheimer ’s disease and dementia
The dementia of Alzheimer 's disease(passive) is caused byThe dementia of Alzheimer 's disease
to neurodegenerative diseases such as Parkinson 's disease and Alzheimer 's diseaseleadingto neurodegenerative diseases such as Parkinson 's disease and Alzheimer 's disease
to Alzheimer 's disease Findingsleadingto Alzheimer 's disease Findings
significantly to ischemic brain injurycontributedsignificantly to ischemic brain injury
to neurodegenerative diseases and most commonly Alzheimer ’s disease [ 6 , 9leadingto neurodegenerative diseases and most commonly Alzheimer ’s disease [ 6 , 9
the death of injured brain cells - Progesteronepreventsthe death of injured brain cells - Progesterone
nervous system disorders including Parkinson 's disease and Alzheimer 's diseasecan causenervous system disorders including Parkinson 's disease and Alzheimer 's disease
Parkinson ’s disease , like trichloroethylene and perchloroethylenecauseParkinson ’s disease , like trichloroethylene and perchloroethylene
to the debilitating symptoms associated with diseases like Parkinson ’s and Alzheimerleadsto the debilitating symptoms associated with diseases like Parkinson ’s and Alzheimer
to edema , hemorrhage , and necrosis when encephalitis is presentleadingto edema , hemorrhage , and necrosis when encephalitis is present
to the progressive mental decline in both Down syndrome and Alzheimer diseasecontributesto the progressive mental decline in both Down syndrome and Alzheimer disease
from stroke , seizures , and other age - related diseases.(8 , 9 ) Oroxylin A ... also from Chinese skullcapresultsfrom stroke , seizures , and other age - related diseases.(8 , 9 ) Oroxylin A ... also from Chinese skullcap
to dementia , which would be similar to alzheimers diseasecould leadto dementia , which would be similar to alzheimers disease
to degenerative brain diseaseswill leadto degenerative brain diseases
to Alzheimer ’s Disease ... using a very simple compound that blocks free radicals and inflammationleadsto Alzheimer ’s Disease ... using a very simple compound that blocks free radicals and inflammation
brain atrophy(passive) caused bybrain atrophy
to increased inflammation through the activation of astrocytes and microglialeadsto increased inflammation through the activation of astrocytes and microglia
from ischemic insult such as from a cerebral strokeresultingfrom ischemic insult such as from a cerebral stroke
to Alzheimer 's diseaseMemantineleadingto Alzheimer 's diseaseMemantine
under the same conditions as autophagy[30 ... essentially leading to the destruction of cancer cellscan be triggeredunder the same conditions as autophagy[30 ... essentially leading to the destruction of cancer cells
to the progressive infarct development and associated functional impairments after cerebral ischemia or brain traumacontributesto the progressive infarct development and associated functional impairments after cerebral ischemia or brain trauma
to Alzheimers disease 11leadingto Alzheimers disease 11
from either acute insults due to ischemia , trauma , excitotoxicity , or chronic neurodegenerative diseasesresultingfrom either acute insults due to ischemia , trauma , excitotoxicity , or chronic neurodegenerative diseases
inflammation and BCP treatmentcould triggerinflammation and BCP treatment
from oxidative stress , inflammation , and failure of the blood brain barrierresultingfrom oxidative stress , inflammation , and failure of the blood brain barrier
to dopamine deficiency Defective gene for synuclein on Chrleadingto dopamine deficiency Defective gene for synuclein on Chr
to Alzheimer 's diseaseGlaucoma treatment timeleadingto Alzheimer 's diseaseGlaucoma treatment time
from early necrosis or delayed apoptosisresultingfrom early necrosis or delayed apoptosis
a gradual and progressive neurodegenerative disease(passive) caused bya gradual and progressive neurodegenerative disease
memory loss and other deficiencies in brain functioncausesmemory loss and other deficiencies in brain function
from ischemic insult or from acute damage , such as traumatic brain injury , associated with glutamate - induced neuronal excitotoxicity , or for treating type 2 diabetes in a patient or preventing type 2 diabetes in a subject , as well as in identifying inhibitors of GSK-3resultingfrom ischemic insult or from acute damage , such as traumatic brain injury , associated with glutamate - induced neuronal excitotoxicity , or for treating type 2 diabetes in a patient or preventing type 2 diabetes in a subject , as well as in identifying inhibitors of GSK-3