neuroG Cancer Research Results
neuroG, neurogenesis: Click to Expand ⟱
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Neurogenesis is the process by which nervous system cells, the neurons, are produced by neural stem cells.
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Scientific Papers found: Click to Expand⟱
*angioG↑, angiogenic and neuroprotective effects of EGCG
*neuroG↑,
*NRF2↑, via upregulation of Nrf2 signaling pathway.
*neuroP↑, Exercise is known to have numerous neuroprotective and cognitive benefits, especially pertaining to memory and learning related processes.
*cognitive↑,
*memory↑,
*BDNF↑, relationship between exercise and hippocampal neurogenesis, and identifies a key molecule mediating this process, brain-derived neurotrophic factor (BDNF).
*neuroG↑, brain-derived neurotrophic factor (BDNF), that has been shown to modulate neurogenesis and how exercise influences BDNF levels
*BDNF↑, provide novel evidence that luteolin treatment, by restoring microglia alterations and transiently boosting BDNF/TrkB signaling
*Mood↑, Treatment with Luteolin Ameliorates Behavioral Deficits in Cdkl5 +/− Mice
*neuroG↑, Treatment with Luteolin Promotes Neurogenesis in the Hippocampus of Cdkl5 +/− Mice
*TrkB↑, Treatment with Luteolin Transiently Boosts BDNF/TrkB Signaling Pathways in the Cortex of
Cdkl5 +/− Mice
*neuroG↑, 2 weeks of naringin supplementation may have protective effects on impaired neurogenesis and BDNF levels after brain ischemia and reperfusion in rats
*BDNF↑,
*motorD↑, Naringin Improved Motor Function After Ischemia/Reperfusion
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Review, |
AD, |
NA |
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Review, |
Park, |
NA |
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*BBB↑, SF is able to cross the blood–brain barrier as well as to protect it
*BDNF↑, SF can protect against neuronal cell death by inhibiting apoptosis, by upregulating brain-derived neurotrophic factor (BDNF) it can enhance neuronal function and plasticity, and support neurogenesis.
*neuroG↑,
*NRF2↑, , Nrf2 inducers like SF that have no direct redox activity are often referred to as “indirect antioxidants”
*HO-1↑, (NQO1) (HO-1 or HMOX), as well as (Cat), (SOD), (Prx), (HSP), glutathione S-transferases (GST), thioredoxin reductase (Trx), glutathione synthetase (GS), glutathione peroxidases (GPx) and glutathione reductase in the brain
*Catalase↑,
*SOD↑,
*HSPs↑, It enhances the expression of HSP70, HSP90, and HSP40 in normal human fibroblasts
*GSTs↑,
*Trx↑,
*GPx↑,
*GSR↑,
*GSH↑, ability of SF to upregulate GSH in the brain is critical for antioxidant protection in youth but may become even more important with age.
*NQO1↑, SF administration to astrocytes increased NQO1 concentrations and protected against oxygen and glucose-induced astrocyte cell death
*GutMicro↑, the fact that SF modulates microbiome composition
*Inflam↓, reduces inflammation and enhances gut barrier integrity,
*neuroP↑, The effect of SF on the gut microbiome may also affect the production of short-chain fatty acids (SCFA) like butyrate, which have neuroprotective effects
*Hif1a↑, TQ can activate the HIF-1α pathway and its downstream genes such as VEGF, TrkB, and PI3K, which in turn enhance angiogenesis and neurogenesis.
*VEGF↑,
*TrkB↑,
*PI3K↑,
*angioG↑, which in turn enhance angiogenesis and neurogenesis.
*neuroG↑,
*motorD↑, TQ has the same effect as DMOG to activate HIF-1 α and can improve motor dysfunction after ischemic stroke
*cognitive↑, UA ameliorated cognitive impairment, prevented neuronal apoptosis, and enhanced neurogenesis in APP/PS1 mice.
*Apoptosis↓,
*neuroP↑,
*Aβ↓, UA attenuated Aβ deposition and peri-plaque microgliosis and astrocytosis in the cortex and hippocampus.
*AMPK↑, enhancing cerebral AMPK activation, decreasing the activation of P65NF-κB and P38MAPK, and suppressing Bace1 and APP degradation.
*NF-kB↓,
*MAPK↓,
*BACE↑,
*neuroG↑, triggering neurogenesis via anti-inflammatory signaling in APP/PS1 mice,
*Inflam↓,
*memory↑, UA ameliorates learning and memory deficits in APP/PS1 mice
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Review, |
AD, |
NA |
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Review, |
Stroke, |
NA |
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Review, |
ostP, |
NA |
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IBD, |
NA |
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*MitoP↓, Experimental models consistently show that UA increases mitophagy and mitochondrial function and blunts excessive inflammatory responses.
*Strength↑, UA is a promising strategy to target health and disease conditions of aging, especially those linked to mitochondrial and muscle dysfunction.
*PINK1↑, UA can activate. PTEN-induced kinase 1 (PINK1)/Parkin-dependent mitophagy starts with the stabilization of the kinase PINK1,
*PARK2↑, which recruits and phosphorylates the ubiquitin-conjugating protein Parkin.
*Inflam↓, anti-inflammatory effect of UA was reported for the first time as a decrease in mRNA and protein levels of the inflammatory marker cyclooxygenase 2 (COX2)
*COX2↓,
*IL1β↓, In neuronal tissues, UA treatment reduced levels of IL-1β, IL-6, and TNFα in the brains of the amyloid precursor protein/presenilin 1 (APP/PS1) mouse model of AD
*IL6↓,
*TNF-α↓,
*OS↑, impact on worm longevity showed that UA extends lifespan by 45%,
*cardioP↑, reduction in IRI markers, such as circulating creatine kinase and lactate dehydrogenase levels, and by fewer apoptotic cells in the heart
*memory↑, Increased learning, memory retention, neuronal survival, and neurogenesis in the hippocampus was achieved with UA administration in the APP/PS1 mouse model of AD
*neuroG↑,
*neuroP↑, UA was shown to have neuroprotective effects in the EAE mouse model of multiple sclerosis (MS)
*Cartilage↑, In a model of osteoarthritis, an age-related and disabling joint disease caused by a slow degeneration of cartilage,
*Inflam↓, UA has protective effects against a chronic DSS-induced model of IBD, leading to reduced levels of colon inflammation markers and to better mucosal integrity.
*RenoP↑, UA consistently reduced tubular damage induced by cisplatin, as shown by histopathology and by a reduction in circulating markers of kidney damage
*eff↑, When administered as nanoparticles to increase its bioavailability, UA even improved the survival of mice that received a lethal dose of cisplatin
*Dose↝, UA showed a favorable safety profile, with no observed side effects following either single oral administration of UA up to 2000 mg or multiple oral dosing (28 days) of UA up to 1000 mg daily.
*Half-Life↑, It showed a relatively long-half life (t1/2 = 17–22 hours),
*NRF2↑, Other mechanisms of action have been proposed for UA, such as the activation of the Ahr/Nrf2 pathway and its downstream antioxidative stress response
*GutMicro↑, A recent report also showed an impact of direct UA supplementation on gut microflora in obese rats
*memory↑, Urolithin A (Uro-A), a type of polyphenol derived from pomegranate, is known to improve memory function when ingested
*SIRT1↑, through the activation of longevity gene SIRT1.
*cognitive↑, therapeutic potential of Uro-A for cognitive health.
*BDNF↑, enhanced expression of several intestine-derived secretory factors, including BDNF, NT-4, (Figure S2), and ciliary neurotrophic factor (CNTF)
*Apoptosis↓, Uro-A prevents neuronal apoptosis and enhances neurogenesis, thereby inhibiting cognitive impairment in model mice
*neuroG↑,
*antiOx↑, Pomegranate (Punica granatum L.), is one such fruit that is well known for its medical usage due to its antioxidant properties.
*neuroG↑, pomegranate supplementation has been shown to impart cognitive aid by the protection of neurons and triggering neurogenesis through anti-inflammatory signaling pathway.
*Inflam↓,
*cognitive↑,
*neuroP↑, deficiency impairs memory and learning in AD. RA acts as a neuroprotective agent by regulating gene expression, and neuronal survival
memory↑,
*Inflam↓, VA deficiency is also associated with elevated inflammatory cytokines, promoting neuroinflammation involved in AD progression
*neuroG↑, RA also stimulates adult neurogenesis, potentially influencing cognition in AD [17].
*cognitive↑,
*Aβ↓, It also influences Aβ clearance and tau phosphorylation, key pathological features of AD [19].
p‑tau↓,
*BACE↓, VA deficiency enhances BACE1 activity, increasing Aβ production and promoting neurotic plaque formation, a hallmark of AD pathology [21]
Showing Research Papers: 1 to 11 of 11
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11
Pathway results for Effect on Cancer / Diseased Cells:
Synaptic & Neurotransmission ⓘ
p‑tau↓, 1,
Functional Outcomes ⓘ
memory↑, 1,
Total Targets: 2
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, Catalase↑, 1, GPx↑, 1, GSH↑, 1, GSR↑, 1, GSTs↑, 1, HO-1↑, 1, NQO1↑, 1, NRF2↑, 3, PARK2↑, 1, SOD↑, 1, Trx↑, 1,
Mitochondria & Bioenergetics ⓘ
PINK1↑, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1, SIRT1↑, 1,
Cell Death ⓘ
Apoptosis↓, 2, MAPK↓, 1,
Protein Folding & ER Stress ⓘ
HSPs↑, 1,
Autophagy & Lysosomes ⓘ
MitoP↓, 1,
Proliferation, Differentiation & Cell State ⓘ
neuroG↑, 11, PI3K↑, 1,
Migration ⓘ
Cartilage↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↑, 2, Hif1a↑, 1, VEGF↑, 1,
Barriers & Transport ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL1β↓, 1, IL6↓, 1, Inflam↓, 6, NF-kB↓, 1, TNF-α↓, 1,
Synaptic & Neurotransmission ⓘ
BDNF↑, 5, TrkB↑, 2,
Protein Aggregation ⓘ
Aβ↓, 2, BACE↓, 1, BACE↑, 1,
Drug Metabolism & Resistance ⓘ
Dose↝, 1, eff↑, 1, Half-Life↑, 1,
Clinical Biomarkers ⓘ
GutMicro↑, 2, IL6↓, 1,
Functional Outcomes ⓘ
cardioP↑, 1, cognitive↑, 5, memory↑, 4, Mood↑, 1, motorD↑, 2, neuroP↑, 5, OS↑, 1, RenoP↑, 1, Strength↑, 1,
Total Targets: 51
Scientific Paper Hit Count for: neuroG, neurogenesis
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
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