gliosis : Related Words Words similar in meaning to gliosis
- glia«
- astrogliosis«
- scar«
- microglia«
- proliferation«
- astrocyte«
- gliotic«
- microgliosis«
- glial«
- reactive astrocyte«
- central nervous system«
- glial scar«
- glial cell«
- glial scar formation«
- neuron«
- severity«
- neurostatin«
- cns insult«
- molecule«
- cns trauma«
- neuropathologies«
- hypertrophy«
- injury«
- oligodendrocyte precursor cell«
- disease«
- degeneration«
- detrimental effect«
- oligodendrocyte«
- il-6«
- microgliosis response«
- microglial regulation«
- gliosis response«
- active microglia«
- active astrocyte«
- inflammatory cytokine«
- process«
- glial cell type«
- neurotoxic substance«
- astrocyte proliferation«
- cns pathology«
- activation«
- amyotrophic lateral sclerosis«
- mechanism«
- glial scarring«
- axon«
- macrophage«
- neuron survival«
- lesion site«
- cns injury«
- axonal regeneration«
- inflammatory molecule«
- retina«
- inflammatory factor«
- type«
- injury site«
- multiple sclerosis«
- scar formation«
- amyloid plaque«
- ifn-γ«
- excitotoxicity«
- complex array«
- therapeutic strategy«
- alzheimer«
- insult«
- neurotrophic factor«
- cell«
- trauma«
- myelin«
- gain«
- spectrum«
- damage«
- extreme form«
- protease«
- formation«
- cytokine«
- response«
- characteristic«
- expression«
- specific molecular trigger responsible«
- specific modulatory relationship«
- specific initial cns insult«
- similar cytokine receptor«
- significant astrogliosis«
- severe astrocyte proliferation«
- reversible neuronal injury«
- retinal gliosis«
- reduced glial scarring«
- promising therapeutic mechanism«
- potential molecular trigger«
- oxidative stress factor«
- oligodendrocytes«
- observed stage«
- notable microglial activation inhibitor«
- nonspecific reactive change«
- negative response inhibitory«
- multiple distinct nucleus«
- molecular trigger«
- molecular signaling mechanism«
- moderate gliosis«
- minor hypertrophy«
- microglial immunological surface receptor cr3«
- major hypertrophy«
- lesion condition«
- legion site«
- injury context«
- injured neuronal signal«
- initial cns insult«
- initial cns injury«
- inhibitory extracellular matrix«
- inhibitory barrier«
- increased degeneration«
- gliosis reaction«
- glial toxin«
- glial scar form«
- ganglion cell apoptosis«
- fibrous extracellular matrix component«
- extreme hypertrophy«
- extracellular αβ deposit«
- exogeneous perivascular cell«
- endogenous microglia«
- diffuse traumatic injury«
- detrimental effects«
- critical homeostatic activity«
- cns. reactive astrocyte«
- cns molecule«
- cns disease mechanism«
- cns cell type«
- cell cycle inhibitor olomoucine«
- brain barrier permeability«
- blood brain barrier function«
- autoimmune inflammatory«
- astroglial dysfunction«
- astrocyte production«
- aqp4 channel«
- altered cellular morphology«
- als. other«
- active microglia release anti«
- effect«
- inhibition«
- therapeutic route«
- such specificity«
- signaling event«
- secondary axotomy«
- rapid phagocytosis«
- postmortem tissue«
- oligodendrocyte injury«
- neurotoxic factor«
- neuroprotective ability«
- neural modulation«
- microglial response«
- massive retinal gliosis«
- local microglia«
- interleukin il-1«
- injured neuron«
- extracellular ion«
- excitotoxic glutamate«
- domain overlap«
- autoimmune inflammatory disorder«
- astroglial proliferation«
- astrocyte activation«
- addition«
- increase«
- aaa«
- degree«
- single molecular target«
- sensitive neural tissue«
- retinal ganglion cell death«
- glial cell responsible«
- experimental reduction«
- cytotoxic cytokine«
- cellular hypertrophy«
- astrocyte function«
- factor«
- synapse function«
- stat3 pathway«
- spinal cord result«
- prompt destruction«
- neurotransmitter concentration«
- macrophage inflammatory protein-1«
- dead neuron«
- cns condition«
- bergmann gliosis«
- specific molecular pathway«
- reactive astrogliosis«
- nitric oxide radical«
- injury condition«
- function essential«
- cytokine interleukin«
- reactive gliosis«
- limited reaction«
- axon connection«
- term clinical outcome«
- retinal injury«
- primary effector«
- neuron signal«
- müller cell«
- intraocular tumor«
- serum component«
- universal response«
- mhc antigen«
- initial insult«
- reactive process«
- negative connotation due«
- myelin debris«
- myelin damage«
- cns disease«
- chondroitin sulfate proteoglycans«
- axotomy«
- aid dementia complex«
- β-amyloid«
- irreversible injury«
- glutamate uptake«
- growth factor β«
- beneficial function«
- interferon-γ«
- limited event«
- toxic molecule«
- neuronal injury«
- microglial activation«
- leukemia inhibitory factor«
- different location«
- dependent fashion«
- temporal correlation«
- inflammatory signal«
- autoimmune attack«
- potential trigger«
- axon regeneration«
- fatal familial insomnia«
- acute trauma«
- molecular signal«
- ciliary neurotrophic factor«
- rapid transmission«
- remyelination«
- dense structure«
- neuronal damage«
- trophic factor«
- potential contributor«
- beneficial purpose«
- multiple system atrophy«
- cell debris«
- migration«
- potential therapeutic target«
- glial fibrillary acidic protein«
- cellular environment«
- widespread death«
- fast response time«
- acute condition«
- functional recovery«
- loss«
- molecular event«
- macrophage colony«
- gfap«
- β-lactam antibiotic«
- minocycline«
- vimentin«
- initial injury«
- widespread effect«
- neural signal«
- extracellular environment«
- cellular activity«
- neurotoxic effect«
- prion disease«
- intermediate filament«
- phenomenon«
- prostaglandin e2«
- neuroprotective effect«
- il-1«
- neural cell«
- il-8«
- korsakoff«
- inflammatory disorder«
- neuroprotection«
