NGF Cancer Research Results

NGF, Nerve Growth Factor: Click to Expand ⟱
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Nerve Growth Factor (NGF) plays a crucial role in the development, maintenance, and survival of certain neurons. Its connection to Alzheimer’s disease (AD) has been well-studied, particularly because of its importance in cholinergic neurons of the basal forebrain, which are notably affected in AD.
-Loss of NGF signaling contributes to cholinergic deficits, a hallmark of AD pathology
Scientific Papers found: Click to Expand⟱
4265- CA,    Potential applications of nanomedicine for treating Parkinson's disease
- Review, Park, NA
*NRF2↑, Carnosic acid (CA) is defined as a natural product synthesized by plants of the Lamiaceae family, known for its potent Nrf2-ARE activating properties and neuroprotective role in early brain injury.
*ARE↑,
*neuroP↑,
*motorD↑, It enhances motor and cognitive function while modulating inflammatory markers in the central nervous system.
*cognitive↑,
*SOD↑, enhancement in the expression of superoxide dismutase, glutathione reductase, γ-glutamate-cysteine ligase modifier subunit, and γ-glutamate-cysteine ligase catalytic subunit, induction of caspase 3 cleavage
*GSR↑,
*NGF↑, Carnosic acid is a phenolic diterpene that promotes the synthesis of NGF in the glioblastoma cell lines and also enhances BDNF production in the dopaminergic neurons.
*BDNF↑,

3875- Carno,    Ionophore Ability of Carnosine and Its Trehalose Conjugate Assists Copper Signal in Triggering Brain-Derived Neurotrophic Factor and Vascular Endothelial Growth Factor Activation In Vitro
- in-vitro, AD, NA
*IronCh↑, copper tuning effect on the ability of l-carnosine and, particularly its conjugate, to activate tyrosine kinase cascade pathways.
*CREB↑, As previously mentioned, Car (10 mM) is able: (i) to activate CREB and CREB related pathways, including BDNF expression and release, by activating Ca2+-related pathways in Caco-2 cell line
*BDNF↑,
*NGF↑, Car induces expression and secretion of NGF and BDNF in U-87 MG cells,
*antiOx↑, while antioxidant, oxygen free-radical scavenge
*ROS↓,

6650- Cen,    Therapeutic Potential of Centella asiatica and Its Triterpenes: A Review
- Review, AD, NA
*BioAv↝, madecassoside, asiaticoside, madecassic acid, and asiatic acid are widely distributed in the body and madecassoside, asiaticoside may exert their biological activity through converted into aglycone (madecassic acid, and asiatic acid).
*BioAv↝, C. asiatica enhances the function of the nervous system. It dissolves in methanol, ethanol, and water.
*MDA↓, Male Wistar rats – MDA ↓, GSH ↑, SOD ↑, AChE↓
*GSH↑,
*SOD↑,
*AChE↓,
*memory↑, Male SD rats; hippocampal cell – Spatial working memory↑, Ki-67 cells↑
*Ki-67↑,
*Catalase↑, Male SD rats MAPK SOD↑, LPO↑, CAT↑, GSH↑, dopamine↑, glutamate↑, Syn1↑, Stx1A↑, PI3K↑, PDK1↑, PEBP↓, VMAT2↑, TH ↑, MAPK ↑, BDNF↑, NGF↑
*PI3K↑,
*BDNF↑,
*NGF↑,
*ROS↓, Water extract of CA Tg2576 mice – ROS↓, NRF2↑, GCLC↑, HMOX1↑, NQO1↑, ATP↑, Mt-ND1↑, Mt-ATP6↑, Mt-CO1↑, Mt-CYB↑, oxygen consumption rate↑
*NRF2↑,
*HO-1↑,
*NQO1↑,
*ATP↑,
*OCR↑,
*TNF-α↓, Ethanolic extract of CA Male SD rats – TNF-α↓, BDNF↑
*PP2A↑, Ethanolic extract of CA Male albino Wistar rats PP2A/GSK-3B PP2A↑, GSK-3B↓, Bcl-2↑
*GSK‐3β↓,
*Bcl-2↑,
*TrkB↑, Standardized extract of CA Male Wistar rats – NR2A↑, NR2B↑, BDNF↑,TrkB↑
*NOTCH1↑, Asiatic acid Male SD rats – Notch1↑, SOX2↑, DCX↑, Nrf2↑, nestin↑, p21 positive cells↓, MDA↓
*SOX2↑,
*Nestin↑,
*MDA↓,
*MAOA↓, Asiaticoside-D Worms – MAO-A↓, MAO-B↓
*MAOB↓,
*GPx↑, Previous studies found that C. asiatica and its triterpenoids could effectively increase SOD and GPX activities, activate nuclear factor erythroid-2-related factor 2, improve the cognitive impairment of animals,
*cognitive↑,
*ROS↓, C. asiatica and its triterpenoids could reduce ROS production
*neuroP↑, they reduced related nerve cell apoptosis, increased synaptic density, and improved the survival rate of neural cells
*glucose↓, Methanol extract of CA Male SD rats – Blood glucose ↓, food and water intake ↓, ALT↓, AST↓, PFK ↑, GS ↑, GP↑, glycogen content ↑
*ALAT↓,
*AST↓,
*PFK↓,
*Weight↓, inhibit weight gain
*Inflam↓, (4) ameliorate inflammation,
*AntiDiabetic↑, C. asiatica extract and related components (asiatic acid, madecassoside) for the treatment of endocrine diseases such as diabetes, obesity and osteoporosis are excellent.
*Obesity↓,
*Wound Healing↑, The C. asiatica extract and its triterpenoids had certain therapeutic and relieving effects on acne, baldness, vitiligo, atopic dermatitis, and wounds. C. asiatica extract can effectively promote wound healing in diabetic patients
*cardioP↑, C. asiatica has a positive effect on cardiovascular diseases.
*GutMicro↑, C. asiatica and its triterpenoids also have therapeutic effects on digestive disorders, which is mainly reflected by improved liver fibrosis, colitis, and gastric mucosal damage; and even reduced Helicobacter pylori gastric colonization
*Sepsis↓, Asiatic acid can improve the side effects caused by antibiotics, reverse multidrug resistance (MDR), and reduce sepsis.
*BioAv↑, C. asiatica cream containing 5.12% asiaticoside and 5.1% madecassoside can be completely absorbed by the skin and effectively improve pigmentation and may be used in treating hypertrophic scars

7230- EGb 761,    Ginkgo biloba extract (EGb 761) promotes peripheral nerve regeneration and neovascularization after acellular nerve allografts in a rat model
- in-vivo, Nor, NA
*Dose↝, i.p. injection of EGb 761 for 10 days (
*NGF↑, rats in the EGb 761 group significantly increased the number of myelinated fibers and the average diameter of the nerves within the graft.
*angioG↑, EGb 761 treatment increased the expression of several angiogenesis-related genes, including Vegf, SOX18, Prom 1, and IL-6.
*VEGF↑,
*SOX18↑,
*CD133↑,
*IL6↑,

6780- EGCG,    The pharmacological activity of epigallocatechin-3-gallate (EGCG) on Alzheimer's disease animal model: A systematic review
- Review, AD, NA
*neuroP↑, Regulation of α-, β-, γ-secretase activity, inhibition of tau phosphorylation, anti-oxidation, anti-inflammation, anti-apoptosis, and inhibition of AchE activity are reported as the main neuroprotective mechanisms.
*tau↓,
*antiOx↑,
*Inflam↓,
*Apoptosis↓,
*AChE↓,
*TNF-α↓, Inhibiting TNF-α/JNK pathway
*JNK↓,
*NGF↑, Increasing the level of NGF. EGCG (2 mg/kg) mouse
*SOD↑, figure 7
*GPx↑, EGCG enhanced the activity of T-SOD and GSH-Px and reduced MDA content in the hippocampus.
*MDA↓,
*NO↓,
*ROS↓,
*iNOS↓,
*COX2/PTGS2↓, anti apoptosis
*BAX↓, EGCG prevented LPS-induced elevation of GFAP, iNOS, and COX-2.
*CHOP/DDIT3↓,
*GRP78/BiP↓,
*Bcl-2↑,
*Dose↑, The highest safe dose for more than a month of treatment allowed by FDA is 800 mg of EGCG daily with food.
*BioAv↑, In preclinical and phase I clinical trials, it has been shown that bioavailability of EGCG is increased when it is consumed on a fasting basis.
*hepatoP↓, However, the rate of hepatotoxicity is also increased

6981- Form,    Formononetin: a review of its source, pharmacology, drug combination, toxicity, derivatives, and drug delivery systems
- Review, Var, NA - Review, AD, NA - Review, PSA, NA
BioAv↝, FMN has only one phenolic hydroxyl group, so it is poorly soluble in water and easily soluble in organic solvents such as methanol, ethyl acetate, and ether.
*memory↑, It had been found that FMN, isolated from Sophora secundiflora, could improve memory problems by restoring the level of oxidative stress in brain tissues and modulating acetylcholinesterase activity. I
*ROS↓, findings suggest that FMN can inhibit oxidative stress in the liver and restore mitochondrial function
*AChE↓,
*NF-kB↓, FMN, the expression levels of the above three decreased and NF-κB activation was inhibited, which may be related to the release of FMN blocking kelch-like ECH-associated protein-1 (Keap1) and activating the nuclear factor erythroid 2-related factor 2
*Keap1↝,
*NRF2↑,
*Inflam↓, FMN exerted anti-neuroinflammatory effects by targeting peroxisome proliferator-activated receptor coactivator-1α (PGC-1α) and bidirectionally regulating NF-κB signaling pathway and Nrf2/Heme oxygenase-1 (HO-1) signaling pathway,
*PGC-1α↝,
*HO-1↓,
*p‑tau↓, thereby inhibiting tau protein hyperphosphorylation.
*cognitive↑, Significantly FMN improve cognitive dysfunction in mice caused by high-fat feeding
*BDNF↑, increased BDNF and 5-hydroxytryptamine (5-HT) levels, and mitigated the progression of depression in mice.
*5HT↑,
*Stroke↓, It could significantly reduce the level of inflammatory factors, increase the number of dendritic spines in neurons, and increase the expression of βIII-tubulin, growth-associated protein 43 (GAP-43), nerve growth factor (NGF) and BDNF.
*PARP1↓, FMN significantly reduced PARP1, PARG, apoptosis-inducing factor (AIF), cysteinyl aspartate-specific protease 3 (caspase-3) and p53 protein in rats with cerebral ischemia-reperfusion injury
*AIF↓,
*Casp3↓,
NP/CIPN↓, FMN had a favorable ameliorative effect on oxaliplatin-induced peripheral neuropathy and did not affect the chemotherapeutic function of oxaliplatin.
*neuroP↑, The neuroprotective mechanism of FMN is shown in Figure 2.
*NGF↑,
*TNF-α↓,
*IL1β↓,
*IL18↓,
*IL6↓,
*VCAM-1↓,
*pol-M2 MC↑,
*hepatoP↑, could reduce hepatotoxicity and improve liver function through inflammatory molecular pathways.
*AST↓, reduce serum AST, ALT, TNF-α and IL-1β levels. I
*ALAT↓,
*LC3II↑, the levels of LC3II, Beclin1, p62, cyclooxygenase-2 (COX2), COX4, MMP and adenosine triphosphate (ATP) were increased
*Beclin-1↑,
*p62↑,
*COX2/PTGS2↑,
*MMP↑,
*ATP↑,
*GSH↑, activity of antioxidant proteins glutathione (GSH), catalase (CAT), GSH-PX in the FMN treatment group recovered, and the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) decreased.
*Catalase↑,
*GPx↑,
*MDA↓,
*antiPs↑, it was found that the interferon (IFN) signaling pathway was inhibited, which could effectively reduce the expression of related inflammatory chemokines, and significantly improve the erythema, scales and thickness of skin lesions in the psoriasis m
*AntiDiabetic↑, FMN effectively mitigated alloxan-induced pancreatic β-cell and DNA damage, lowered blood glucose levels, and increased insulin content.
*glucose↓,
*Insulin↑,
*GutMicro↑, FMN could act as a prebiotic to regulate intestinal microbial flora, thereby improving host metabolism and preventing obesity
*Obesity↓,
COX2/PTGS2↓, FMN effectively inhibited the proliferation of KYSE170 and KYSE150 cells by significantly reducing the mRNA and protein expression levels of COX-2 and cyclin D1, while inducing G1 phase arrest.
cycD1/CCND1↓,
TumCCA↑,
EGFR↓, FMN binds to both WT and mutant EGFR, reducing EGFR kinase activity and inhibiting downstream signaling.
GSK‐3β↑, This, in turn, activated GSK-3β and decreased the expression of myeloid leukemia sequence 1 (Mcl-1), without causing significant toxicity to the vital organs of mice.
Mcl-1↓,
*toxicity↓,
TumCP↓, FMN inhibited the proliferation and growth of cervical cancer cells by inhibiting the expression of HIF-1-α and VEGF.
Hif1a↓,
VEGF↓,
ERK↓, can achieve antiproliferative and invasive effects through effective inhibition of the oncogenic ERK1/2 pathway and the Lamin A/C signaling pathway,
LAMs↓,
Cyt‑c↑, FMN, as a candidate anticancer drug, could release cytochrome C (cyto C) directly through the mitochondrial pathway and activate the cascade reaction of caspase-9, caspase-3 and PARP, which ultimately lead to FaDu cell death
Casp9↑,
Casp3↑,
PARP↑,
TumCD↑,
mitA↑, FMN inhibited mitosis by inactivating the BACH1/p53 signaling pathway, promoted the release of cyto C
BACH1↓,
P53↓,
ROS↑, FMN delivered ROS to mitochondria to release cyto C and activated caspase-3 and caspase-9 cascade reactions to induce apoptosis in MCF7 cells
PD-1↓, FMN has the potential to serve as a PD-1/PD-L1 inhibitor for clinical use
NF-kB↓, FMN mainly interfered with PD-L1 activation by inhibiting the STING-NF-κB signaling pathway
*Bacteria↓, possess other pharmacological activities, such as antibacterial, antiviral, and antiallergic
*AntiViral↑,
*mt-ROS?, FMN effectively reduced the accumulation of ROS and mitochondrial damage in hair cells by activating the PI3K/AKT-Nrf2 signaling pathway, restored the balance of GSH/GSSG.
*PI3K↓,
*chemoP↑, FMN was a potential therapeutic agent for cisplatin-induced ototoxicity.
ChemoSen↑, Therefore, combination therapy had better control effects on multiple targets and a lower risk of drug resistance, which had great application prospects for treating cancer.
eff↑, combination of FMN (30 μM) and sulforaphane (20 μM) exhibited a significant synergistic effect
*toxicity↓, Therefore, it was proved that FMN was safe and non-toxic and could be used for pharmacological and therapeutic purposes.
*BioAv↑, water solubility problem of FMN, succinylated FMN using Bacillus amyloliquefaciens FJ18 to form the compound FMN-7-O-β-D (6″-O-succinyl)-D-glucoside (FMP), which compared to FMN, the water solubility was increased more than 106-fold.
*BioAv↑, To solve those problems, structural modification and nano-delivery systems can be used as a promising solution
*eff↑, FMN can be combined with other treatments, such as immunotherapy, to enhance the therapeutic effect and improve the prognosis of patients;

4210- Hup,    A Synopsis of Multitarget Potential Therapeutic Effects of Huperzine A in Diverse Pathologies–Emphasis on Alzheimer’s Disease Pathogenesis
- Review, AD, NA
*neuroP↑, Several studies have reported both cholinergic and non-cholinergic effects of this compound on AD with significant neuroprotective properties.
*AChE↓, Hup A is a potent reversible inhibitor of AChE. By its action on AChE, it enhances the ACh levels which enhances learning and memory.
*Ach↑,
*memory↑,
*NGF↑, Increased levels of ACh augments NGF/BDNF and M1mAChR mediated sAPPα levels which further provides neuroprotection.
*BDNF↑,

7565- HYP,    Potential Implications of Hyperoside on Oxidative Stress-Induced Human Diseases: A Comprehensive Review
- Review, AD, NA
*Inflam↓, exhibits a multitude of biological functions including anti-inflammatory, antidepressant, antioxidative, vascular protective effects and neuroprotective effects,
*antiOx↑,
*neuroP↑,
*lipid-P↓, Anti-oxidant Saccharomyces Cerevisiae 5, 20 mg/L Decreased LPO and the level of ROS
*ROS↓,
*IL1β↓, HT22 cells 20 μM Alleviates the level of IL-1β, IL-6, IL-8, TNF-α, ROS, MDA, Bax, and caspase-3; increases the expression of CAT, SOD, GSH, Bcl-2, BDNF, TrkB, and NGF.
*IL6↓,
*IL8↓,
*TNF-α↓,
*MDA↓,
*BAX↓,
*Casp3↓,
*Catalase↑,
*SOD↑,
*GSH↑,
*BDNF↑,
*TrkB↑,
*NGF↑,
*BDNF↑, Male Albino Swiss mice 0.94 mg/kg, 3.75 mg/kg Mediated by monoaminergic system and the upregulation of BDNF level
*NF-kB↓, Inhibited the activation of NF-κB, lessened the expression of iNOS,
*AChE↓, ICR mice 2.5 mg/kg Inhibited AchE activity
*H2S↑, SD rats 1, 10, 100 μM Upregulation of H2S,
Casp3↑, Anti-lung cancer A549 cells, Balb/c-nude mice 15, 20, 25 μM in vitro 15, 20, 25 mg/kg in vivo Activation of caspase-3 to motivate apoptosis and inactivation of NF-κB to inhibit inflammatory
Apoptosis↑,
NF-kB↓,
AMPK↑, A549 cells 10, 50, 100 μM Upregulation of AMPK signal pathway and HO-1 expression to suppressed the survival and proliferation of A549 cells
HO-1↑,
MAPK↑, A549 cells, H466 cells, C57BL/6J mice – Upregulated the expression of p38 MAPK, caspase 3, caspase 9, cleaved caspase 3, cleaved caspase 9 and Bax, downregulated the expression of Cu/Zn SOD, CAT, Nrf2, NQO1, HO-1 and Bcl-2
cl‑Casp3↑,
cl‑Casp9↑,
BAX↑,
SOD?,
Catalase↓,
NRF2↓,
NQO1↓,
HO-1↓,
Bcl-2↓,
TumCCA↑, A549 cells 10, 20, 50, 100, 200, 400 μg/mL Inhibited the process of G1/S phase to inhibit proliferation
FOXO1↑, NCI-H1975 cells, PC-9 cells, Nude male mice 30, 60, 90, 120, 150 μM in vitro, 25 mg/kg in vivo Upregulation of FoxO1
TumAuto↑, A549 cells 0.5, 1, 2 mM Induced autophagy through inhibiting the Akt/mTOR/p70S6K signal pathway
Akt↓,
mTOR↓,
P70S6K↓,
BMP7/OP1↓, HepG2 cells 5, 10, 20, 40, 80 μM Inhibiting the BMP-7
*cardioP↑, Cardiovascular Protective Effect
*hepatoP↑, Hepatoprotective
*antiCG↑, The report indicates hyperoside possesses antithrombotic activities and offer bases for development of a novel anticoagulant
*AntiThr↑,
*Diar↓, Antidiarrheal Activity
*AntiFungal↑, Antifungal Activity
*CYP2D6↓, hyperoside is a potent selective CYP2D6 inhibitor in HLMs, and might cause herb-drug interactions when co-administrated with CYP2D substrates.
*PDGFR-BB↓, In diabetic rats’ model, hyperoside inhibited the platelet-derived growth factor-BB (PDGF-BB)/platelet-derived growth factor-B receptor (PDGFR-β) ligand binding
*PDGFRB↓,
*toxicity↓, In research conducted in Wistar rats, the researchers demonstrated that in a long-term oral administration lasted for 6 months, hyperoside has a good safety. And the possible target organ of toxicity is kidney and the damage is reversible
*Half-Life↑, hyperoside also showed a long half-life for 4 hours and the safety experiments also proves that it has good safety.

7560- HYP,    Hyperoside: A Review of Its Structure, Synthesis, Pharmacology, Pharmacokinetics and Toxicity
- Review, Nor, NA - Review, AD, NA
*RenoP↓, Thirdly, long-term use of hyperoside is toxic to the kidneys, but the damage is reversible
Casp3↑, Up-regulates caspase-3, caspase-8, Bax, p53 and MDA contents; decreases GSH, SOD and CAT activities; decreases VEGF and Bcl-2 levels; and inhibits cell growth. HeLa 100 μmol/L
Casp8↑,
MDA↑,
GSH↓,
SOD↓,
Catalase↓,
VEGF↓,
Bcl-2↓,
TumCG↓,
p‑Akt↓, Down-regulates BMP-7 expression, AKT phosphorylation and PI3K expression; induces cell cycle arrest; and inhibits cell proliferation. Human HepG2 5, 10, 20, 40 and 80 μM
PI3K↓,
TumCCA↑,
TumCP↓,
BMP7/OP1↓,
*ZO-1↑, up-regulates ZO-1 and claudin5 protein expression; maintains the integrity of the blood–brain barrier; and may protect neural function in CIR-injured mice. CIR injury induced by MCAO in mice 50 mg/kg
*BBB↝,
*p‑Akt↑, increases the phosphorylation of AKT and GSK-3β; alleviates early brain injury after subarachnoid haemorrhage; and promotes nerve function recovery in rats.
*GSK‐3β↑,
*SOD↑, increases SOD and CAT activities and GSH content; increases SIRT1 gene expression; down-regulates NF-κB mRNA
*Catalase↑,
*GSH↑,
*SIRT1↑,
*NF-kB↓,
*IL1β↓, Down-regulates IL-1β, IL-6, IL-8, TNF-α, ROS, MDA, Bax and caspase-3 levels; increases CAT, SOD and GSH activities; up-regulates Bcl-2, BDNF, TrkB, SIRT1 and NGF expression; reduces LPS-induced inflammation, oxidative stress and apoptosis; and protec
*IL6↓,
*IL8↓,
*TNF-α↓,
*ROS↓,
*MDA↓,
*BAX↓,
*Casp3↓,
*Bcl-2↑,
*BDNF↑,
*TrkB↑,
*NGF↑,
*Apoptosis↓,
*cardioP↑, Cardioprotective Activity of Hyperoside.
*AST↓, Decreases the levels of AST, CK, CK-MB and c-TnT in rats; the rate of cardiomyocyte apoptosis;
*hepatoP↑, Hepatoprotective Activity of Hyperoside.
*AST↓, Decreases liver index, AST, ALT, MDA and Bach1 complex levels and alleviates the pathological damage of acute liver injury mice.
*ALAT↓,
*MDA↓,
*BACH1↓,
*neuroP↑, Brain-Protective Activity of Hyperoside.
*Stroke↓, Down-regulates TNF-α, IL-1β, IL-6, ICAM-1, VCAM-1, TLR4, COX-2, NF-κB, caspase-3, caspase-9, Bax and Bcl-2 expression and prevents CIR injury. Middle cerebral artery occlusion/reperfusion rat model
*ICAM-1↓,
*VCAM-1↓,
*TLR4↓,
*COX2/PTGS2↓,
*RenoP↑, Renal-Protective Activity of Hyperoside.
*NLRP3↓, Suppresses NLRP3, caspase-1 and ASC expression and prevents acute kidney injury induced by lipopolysaccharide. Mouse acute kidney injury model
*Casp1↓,
*ASC↓,
*BioAv↓, low oral bioavailability
*BioAv↑, hyperoside is compatible with other traditional Chinese medicines and they can improve its bioavailability and oral absorption.
*toxicity↓, Firstly, an acute toxicity test of hyperoside showed that its LD50 > 5000 mg/kg

3745- MFrot,  MF,    The neurobiological foundation of effective repetitive transcranial magnetic brain stimulation in Alzheimer's disease
- Review, AD, NA
*neuroP↑, neuroprotective actions aimed at mitigatingoxidative stress and inflammation, and intense stimulation of neu-rotrophic factors
*ROS↓,
*Inflam↓,
*5HT↑, increase in serotoninand its metabolites and a change in the properties of serotonergicreceptors.
*cFos↑, in rats, a single session of bothLF- (1 Hz) and HF-rTMS (10 Hz) enhanced c-Fos expression in all exam-ined cortical areas
*Aβ↓, rTMS enhances neuronal viability and counteracts oxidative stressors, such as Aβ and glutamate toxicity, in vitro
*memory↑, downregulation results in memory impairments
*BDNF↑, long-term change in synaptic proteinexpression due to BDNF-TrkB pathway activation following rTMSprotocols
*Ach↑, rTMSincreases ACh levels by modulating AChE activity.
*AChE↓,
*cognitive↑, HF-rTMS (20 Hz) and LF-rTMS (1 Hz)—in termsof neurotransmitter circuits and neurogenic signaling. 142 While bothprotocols improved cognition-related behaviors
*BDNF↑, Notably, rTMS could enhance BDNF and NGF expression irrespec-tive of frequency,
*NGF↑,
*β-catenin/ZEB1↑, both LF-rTMS (1 Hz) and HF-rTMS (10 Hz)protocols enhanced cognitive performance through the activation of β-catenin via the regulation of glycogen synthase kinase-3β (GSK-3β) andTau
*p‑Akt↓, 3 weeks, iTBS reducedinflammation and increased anti-inflammatory molecules, specificallylinked to reversing the downregulation of phosphorylated forms ofAkt and the mammalian target of rapamycin.
*mTOR↓,
*MMP1↓, 6 months, patients showed significant reductions in plasma levels of MMP1, MMP9, and MMP10, along with increases in TIMP1 and TIMP2
*MMP9↓,
*MMP-10↓,
*TIMP1↑,
*TIMP2↑,

3814- mushLions,    Lion's Mane (Hericium erinaceus) Exerts Anxiolytic Effects in the rTg4510 Tau Mouse Model
- in-vitro, AD, NA
*neuroP↑, Despite neurocognitive and neurobiological effects of H. erinaceus being seen in both healthy and transgenic mice,
*cognitive↑, Tau mice given H. erinaceus had significantly shorter latencies to enter the center of the open field (OF) (p < 0.05) and spent significantly more time in the open arms of the elevated zero maze (EZM) (p < 0.001) compared to tau control mice
*cognitive∅, While H. erinaceus had anxiolytic effects, no improvements were seen in spatial memory or activities of daily living.
*BBB↑, cross the blood brain barrier (BBB)
*NGF↑, Additional benefits of H. erinaceus include the promotion of nerve growth factor (NGF)
*BDNF↑, promotion of brain-derived neurotrophic factor (BDNF), improvement of cognitive function
*NO↓, reduction in nitric oxide (NO)
*memory↑, Mice receiving H. erinaceus had improved recognition memory and exploratory behavior in the novel object recognition task; this increased exploratory behavior toward novel objects was indicative of lower levels of anxiety
*Aβ↓, Researchers have also found that H. erinaceus can reduce Aβ plaque formation in the APPswe/PS1dE9 mouse model receiving erinacine

7517- Poly,    Modulation of neurotrophic signaling pathways by polyphenols
- Review, Nor, NA
*NRF2↑, antioxidant activity of polyphenols reflected in the activation of Nrf2 pathway
*HO-1↑, upregulation of detoxification enzymes such as heme oxygenase-1
*NGF↑, stilbenoid compound resveratrol (a polyphenol present in grapes and red wine, Figure 3)79 cause a significant enhancement of neurotrophin (nerve growth factor [NGF] and brain-derived neurotrophic factor [BDNF]
*BDNF↑,
*neuroP↑, including neuroprotective activity
p‑CREB↑, Ferulic acid has also been reported to increase CREB phosphorylation in the hippocampus

3948- Shank,    Neuroprotective role of Convolvulus pluricaulis on aluminium induced neurotoxicity in rat brain
- in-vivo, AD, NA
*AChE↓, Daily administration of CP (150 mg/kg) for 3 months along with aluminium chloride (50 mg/kg) decreased the elevated enzymatic activity of acetylcholine esterase and also inhibited the decline in Na(+)/K(+)ATPase activity which resulted from aluminium
*ChAT↑, Oral administration of CP preserved the mRNA levels of muscarinic receptor 1 (M1 receptor), choline acetyl transferase (ChAT) and Nerve Growth Factor-Tyrosine kinase A receptor (NGF-TrkA).
*NGF↑,
*CDK5↓, It also ameliorated the upregulated protein expression of cyclin dependent kinase5 (Cdk5) induced by aluminium.
*neuroP↑, , indicative of its neuroprotective effects.
*MDA↓, Data showed co-treatment of CP to alu- minium treated rats led to a significant reduction in MDA by ∼23% and protein carbonyl by ∼71% as compared to group II.

4321- VitE,    Unraveling the molecular mechanisms of vitamin deficiency in Alzheimer's disease pathophysiology
- Review, AD, NA
*ROS↓, Vitamin E (Tocotrienols and alpha-tocopherol), is a fat-soluble vitamin that protects neural cells from oxidative stress
*cardioP↑, promotes cardiovascular health by preventing clotting
*lipid-P↓, It prevents lipid peroxidation, supports docosahexaenoic acid (DHA) transport, and enhances cognition, reduces AD progression, highlighting its importance in maintaining cognitive function and preventing neurodegeneration
*cognitive↑,
*neuroP↑,
*Aβ↓, vitamin E influences gene expression by upregulating genes involved in Aβ clearance, a key factor in AD
*NGF↑, Vitamin E deficiency downregulates nerve growth factor (NGF) and sodium-dependent dopamine transporter, both essential for neuroprotection, neuronal survival, and neurotransmission


Showing Research Papers: 1 to 14 of 14

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 14

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

BMP7/OP1↓, 2,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 2,   GSH↓, 1,   HO-1↓, 1,   HO-1↑, 1,   MDA↑, 1,   NQO1↓, 1,   NRF2↓, 1,   ROS↑, 1,   SOD?, 1,   SOD↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,   p‑CREB↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 2,   Casp3↑, 3,   cl‑Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   cl‑Casp9↑, 1,   Cyt‑c↑, 1,   MAPK↑, 1,   Mcl-1↓, 1,   TumCD↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,   PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   mitA↑, 1,   TumCCA↑, 3,  

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

ERK↓, 1,   FOXO1↑, 1,   GSK‐3β↑, 1,   mTOR↓, 1,   P70S6K↓, 1,   PI3K↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

BACH1↓, 1,   LAMs↓, 1,   TumCP↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↓, 1,   Hif1a↓, 1,   VEGF↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   NF-kB↓, 2,   PD-1↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 1,   ChemoSen↑, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,  

Functional Outcomes(tgid=23) ⓘ

NP/CIPN↓, 1,  
Total Targets: 54

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

antiCG↑, 1,   CYP2D6↓, 1,   Stroke↓, 2,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3,   ARE↑, 1,   Catalase↑, 4,   GPx↑, 3,   GSH↑, 4,   GSR↑, 1,   HO-1↓, 1,   HO-1↑, 2,   Keap1↝, 1,   lipid-P↓, 2,   MDA↓, 8,   NQO1↑, 1,   NRF2↑, 4,   ROS↓, 9,   mt-ROS?, 1,   SOD↑, 5,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↓, 1,   ATP↑, 2,   Insulin↑, 1,   MMP↑, 1,   OCR↑, 1,   PGC-1α↝, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 3,   CREB↑, 1,   glucose↓, 2,   H2S↑, 1,   PFK↓, 1,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

p‑Akt↓, 1,   p‑Akt↑, 1,   Apoptosis↓, 2,   BAX↓, 3,   Bcl-2↑, 3,   Casp1↓, 1,   Casp3↓, 3,   iNOS↓, 1,   JNK↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 2,   AntiThr↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↓, 1,   GRP78/BiP↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↑, 1,   LC3II↑, 1,   p62↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

PARP1↓, 1,  

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

CD133↑, 1,   cFos↑, 1,   GSK‐3β↓, 1,   GSK‐3β↑, 1,   mTOR↓, 1,   Nestin↑, 1,   NOTCH1↑, 1,   PDGFRB↓, 1,   PI3K↓, 1,   PI3K↑, 1,   SOX2↑, 1,  

Migration(tgid=13) ⓘ

BACH1↓, 1,   CDK5↓, 1,   Ki-67↑, 1,   MMP-10↓, 1,   MMP1↓, 1,   MMP9↓, 1,   TIMP1↑, 1,   TIMP2↑, 1,   VCAM-1↓, 2,   ZO-1↑, 1,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 1,   NO↓, 2,   PDGFR-BB↓, 1,   SOX18↑, 1,   VEGF↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   BBB↝, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

ASC↓, 1,   COX2/PTGS2↓, 2,   COX2/PTGS2↑, 1,   ICAM-1↓, 1,   IL18↓, 1,   IL1β↓, 3,   IL6↓, 3,   IL6↑, 1,   IL8↓, 2,   Inflam↓, 5,   pol-M2 MC↑, 1,   NF-kB↓, 3,   TLR4↓, 1,   TNF-α↓, 5,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 2,   AChE↓, 7,   BDNF↑, 12,   ChAT↑, 1,   MAOA↓, 1,   NGF↑, 14,   tau↓, 1,   p‑tau↓, 1,   TrkB↑, 3,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 3,   MAOB↓, 1,   NLRP3↓, 1,   PP2A↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 5,   BioAv↝, 2,   Dose↑, 1,   Dose↝, 1,   eff↑, 1,   Half-Life↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 3,   AST↓, 4,   GutMicro↑, 2,   IL6↓, 3,   IL6↑, 1,   Ki-67↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiDiabetic↑, 2,   antiPs↑, 1,   cardioP↑, 4,   chemoP↑, 1,   cognitive↑, 6,   cognitive∅, 1,   hepatoP↓, 1,   hepatoP↑, 3,   memory↑, 5,   motorD↑, 1,   neuroP↑, 12,   Obesity↓, 2,   RenoP↓, 1,   RenoP↑, 1,   toxicity↓, 4,   Weight↓, 1,   Wound Healing↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   AntiViral↑, 1,   Bacteria↓, 1,   Diar↓, 1,   Sepsis↓, 1,  
Total Targets: 140

Scientific Paper Hit Count for: NGF, Nerve Growth Factor
2 Hyperoside
1 Carnosic acid
1 Carnosine
1 Centella asiatica / Gotu kola → asiaticoside
1 Ginkgo biloba-EGb 761
1 EGCG (Epigallocatechin Gallate)
1 Formononetin
1 Huperzine A/Huperzia serrata
1 Magnetic Field Rotating
1 Magnetic Fields
1 Mushroom Lion’s Mane
1 Polyphenols
1 Shankhpushpi
1 Vitamin E
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#:1360  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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