GFAP Cancer Research Results

GFAP, Glial Fibrillary Acidic Protein: Click to Expand ⟱
Source:
Type: biomarker

GFAP - Glial Fibrillary Acidic Protein

Type: Intermediate filament protein / astrocyte marker / reactive astrogliosis biomarker

Function: GFAP is a type III intermediate filament protein expressed predominantly in astrocytes. It contributes to astrocyte cytoskeletal structure, mechanical stability, cellular remodeling, and responses to central nervous system injury. Increased GFAP expression is widely used as a marker of reactive astrocyte activation and astrogliosis.

Cancer: ↕ Context-dependent. GFAP is widely used as a marker of astrocytic differentiation in gliomas and astrocytomas, but total GFAP expression does not show a uniform relationship with tumor aggressiveness. Changes in GFAP isoforms, particularly the GFAPδ/GFAPα ratio, may be associated with more malignant astrocytoma phenotypes.

Alzheimer's Disease: ↑ Increased GFAP reflects reactive astrogliosis associated with Alzheimer's disease pathology. Elevated GFAP is observed in affected brain regions and increased circulating GFAP is strongly associated with cerebral amyloid pathology and progression toward cognitive impairment.
Scientific Papers found: Click to Expand⟱
7520- CAPE,    Neuroprotective Effect of Caffeic Acid Phenethyl Ester in A Mouse Model of Alzheimer's Disease Involves Nrf2/HO-1 Pathway
- in-vivo, AD, NA
*ROS↓, intraperitoneal administration of CAPE (10 mg/kg) after i.c.v. AβO-injection counteracted oxidative stress accompanied by an induction of Nrf2 and heme oxygenase-1 via the modulation of glycogen synthase kinase 3β in the hippocampus of mice.
*NRF2↑,
*HO-1↑,
*Apoptosis↓, CAPE treatment decreased AβO-induced neuronal apoptosis and neuroinflammation, and improved learning and memory, protecting mice against the decline in spatial cognition.
*Inflam↓,
*Learn↑,
*memory↑,
*cognitive↑,
*neuroP↑, CAPE could potentially be considered as a promising neuroprotective agent against progressive neurodegenerative diseases such as AD.
*p‑GSK‐3β↓, CAPE treatment reversed the effects of Aβ1-42O and significantly decreased (p<0.05 and p<0.001, 10 and 20 days post-injection) GSK3β inhibitory phosphorylation.
GFAP↓, CAPE treatment significantly decreased the number of reactive Iba-1 (p<0.001) and GFAP (p<0.001) cells in the hippocampus of Aβ1-42O treated mice

7484- H2,    Hydrogen Gas Attenuates Toxic Metabolites and Oxidative Stress-Mediated Signaling to Inhibit Neurodegeneration and Enhance Memory in Alzheimer's Disease Models
- in-vivo, AD, NA
*Dose↝, either 3% hydrogen gas (H2) or vehicle for 60 days.
*cognitive↑, H2 treatment significantly prevented cognitive deficits, oxidative stress, the accumulation of toxic metabolites, and the increase in inflammatory markers in 5xFAD mice.
*ROS↓, H2 treatment significantly attenuated ROS production in AβO-stimulated primary mouse astrocytes, showing a 1.2-fold reduction compared with vehicle
*Inflam↓, H2 Reduced OS and Decreased Neuroinflammation in AβO-Treated Astrocytes
*neuroP↑, H2 therapy can mitigate toxic metabolites in the astrocytic urea cycle, thereby reducing neurodegeneration and memory loss in AD.
*memory↑, H2 Inhalation Attenuates Memory Impairment in 5xFAD Mice
*Catalase↑, catalase activity increased by 20% following H2 treatment, although this increase was insignificant
*TNF-α↓, observed a significant reduction in TNF-α mRNA levels
*Aβ↓, Aβ plaque accumulation in GFAP decreased by 2.8-fold in the cortex
*GABA↓, GABA levels were markedly lower (p < 0.001) in the AβO-induced astrocytes treated with H2 than in those treated with vehicle
*H2O2↓, H2 treatment attenuated toxic metabolite accumulation, including Aβ, H2O2, and GABA, which were markedly reduced after H2
*GFAP↓, These suggest that astrocyte function was enhanced after H2 treatment due to reduced astrogliosis, denoted by the decrease in the GFAP level.
*antiOx↑, The antioxidant defense system is key to H2’s efficacy, which is modulated upstream by nuclear factor erythroid 2-related factor 2 (Nrf2)
*NRF2↑,

7902- VT,    Vitexin Protects Against Scopolamine-Induced Cognitive Impairment by Preserving Synaptic Integrity and Modulating Nrf2/HO-1 and NF-κB Signaling Pathways
- in-vivo, AD, NA
*Dose↝, Sco (2 mg/kg/day, i.p.), Sco + vitexin (30 mg/kg/day, oral), Sco + donepezil (1.5 mg/kg/day, i.p.), vitexin alone, and donepezil alone
*Learn↑, co significantly impaired spatial learning and memory while increasing anxiety-like behaviors. Vitexin treatment markedly improved these deficits, with efficacy comparable to donepezil
*memory↑,
*AChE↓, Sco elevated acetylcholinesterase activity, lipid peroxidation, and oxidative/nitrosative stress markers (TOS, OSI, MDA, Peroxynitrite, NO, and NOS) while decreasing total antioxidant status (TAS). Vitexin reversed these changes.
*lipid-P↓,
*TOS↓,
*MDA↓,
*ONOO↓,
*NO↓,
*NOS2↓,
*TAC↑,
*BDNF↑, Sco reduced hippocampal BDNF, GDNF, PSD95, and synaptophysin levels and increased GFAP, IL-6, TNF-α, NF-κB p65, and COX-2 expression. Vitexin restored neurotrophic and synaptic proteins, suppressed astrocyte activation and inflammatory signaling, a
*GDNF↑,
*PSD95↑,
*GFAP↓,
*NF-kB↓,
*COX2/PTGS2↓,
*NRF2↑, and activated the Nrf2/HO-1 pathway.
*HO-1↑,
*neuroP↑, vitexin exerts significant neuroprotective and synaptoprotective effects against Sco-induced cognitive impairment by simultaneously restoring redox balance
*NeuroI↓, suppressing neuroinflammation, and preserving synaptic integrity.


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

GFAP↓, 1,  
Total Targets: 1

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

GDNF↑, 1,   GFAP↓, 2,   Learn↑, 2,   NeuroI↓, 1,   ONOO↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↑, 1,   H2O2↓, 1,   HO-1↑, 2,   lipid-P↓, 1,   MDA↓, 1,   NRF2↑, 3,   ROS↓, 2,   TAC↑, 1,   TOS↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

p‑GSK‐3β↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   Inflam↓, 2,   NF-kB↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   BDNF↑, 1,   GABA↓, 1,   PSD95↑, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 2,  

Clinical Biomarkers(tgid=22) ⓘ

NOS2↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 2,   memory↑, 3,   neuroP↑, 3,  
Total Targets: 32

Scientific Paper Hit Count for: GFAP, Glial Fibrillary Acidic Protein
1 Caffeic Acid Phenethyl Ester (CAPE)
1 Hydrogen Gas
1 Vitexin
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1647  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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