TrkB Cancer Research Results

TrkB, Tropomyosin receptor kinase B: Click to Expand ⟱
Source:
Type:
Tropomyosin receptor kinase B (TrkB, encoded by the NTRK2 gene)

• TrkB is a high‐affinity receptor for brain-derived neurotrophic factor (BDNF) and neurotrophin-4 (NT-4).

• It has been implicated in promoting cell survival, proliferation, migration, and resistance to apoptosis.

• In several cancer types, increased TrkB expression has been associated with enhanced tumor aggressiveness and metastasis.
Scientific Papers found: Click to Expand⟱
4281- Api,    The neurotrophic activities of brain‐derived neurotrophic factor are potentiated by binding with apigenin, a common flavone in vegetables, in stimulating the receptor signaling
- in-vitro, AD, SH-SY5Y
*BDNF↑, Apigenin potentiates the neurotrophic activities of BDNF through direct binding, which may serve as a possible treatment for its curative efficiency in neurodegenerative diseases and depression.
*TrkB↑, activating the signaling cascade of high‐affinity BDNF receptor, Trk B.

4280- Api,    Protective effects of apigenin in neurodegeneration: An update on the potential mechanisms
- Review, AD, NA - Review, Park, NA
*neuroP↑, Apigenin, a flavonoid found in various herbs and plants, has garnered significant attention for its neuroprotective properties
*antiOx↑, shown to possess potent antioxidant activity, which is thought to play a crucial role in its neuroprotective effects
*ROS↓, Apigenin has been demonstrated to scavenge ROS, thereby reducing oxidative stress and mitigating the damage to neurons
*Inflam↓, apigenin has been found to possess anti-inflammatory properties.
*TNF-α↓, inhibit the production of pro-inflammatory cytokines, such as TNF-α and IL-1β, which are elevated in neurodegenerative diseases
*IL1β↓,
*PI3K↑, apigenin has been shown to activate the PI3K/Akt signaling pathway, which is involved in promoting neuronal survival and preventing apoptosis.
*Akt↑,
*BBB↑, Apigenin has additional neuroprotective properties due to its ability to cross the BBB and enter the brain
*NRF2↑, figure 1
*SOD↑, pigenin has also been shown to activate various antioxidant enzymes, such as superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx)
*GPx↑,
*MAPK↓, Apigenin inhibits the MAPK signalling system, which significantly reduces oxidative stress-induced damage in the brain
*Catalase↑, , including SOD, catalase, GPx and heme oxygenase-1 (HO-1) [37].
*HO-1↑,
*COX2↓, apigenin has the ability to inhibit the expression and function of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE-2), enzymes that produce inflammatory mediators
*PGE2↓,
*PPARγ↑, apigenin has the ability to inhibit the expression and function of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE-2), enzymes that produce inflammatory mediators
*TLR4↓,
*GSK‐3β↓, Apigenin can inhibit the activity of GSK-3β,
*Aβ↓, Inhibiting GSK-3 can reduce Aβ production and prevent neurofibrillary disorders.
*NLRP3↓, Apigenin suppresses nucleotide-binding domain, leucine-rich–containing family, pyrin domain–containing-3 (NLRP3) inflammasome activation by upregulating PPAR-γ
*BDNF↑, Apigenin causes upregulation of BDNF and TrkB expression in several animal models
*TrkB↑,
*GABA↑, Apigenin enhances GABAergic signaling by increasing the frequency of chloride channel opening, leading to increased inhibitory neurotransmission
*AChE↓, It blocks acetylcholinesterase and increases acetylcholine availability.
*Ach↑,
*5HT↑, Apigenin has been shown to increase 5-HT levels, decrease 5-HT turnover, and prevent dopamine changes.
*cognitive↑, Apigenin increases the availability of acetylcholine in the synapse after inhibiting AChE, thereby enhancing cholinergic neurotransmission and improving cognitive function and memory
*MAOA↓, apigenin acts as a monoamine oxidase (MAO) inhibitor and MAO inhibitors increase the levels of monoamines in the brain

3887- Api,    The flavonoid apigenin protects brain neurovascular coupling against amyloid-β₂₅₋₃₅-induced toxicity in mice
- in-vivo, AD, NA
*Inflam↓, anti-inflammatory, anticarcinogenic, and free radical-scavenging activities.
*ROS↓,
*Aβ↓, Recent studies revealed its protective effects against amyloid-β (Aβ)-induced neurotoxicity, but the mechanism was unclear. I
*memory↑, involving improvement of the learning and memory capabilities,
*AChE↓, improvement of cholinergic system involving the inhibition of AChE activity and elevation of ACh level, and modification of BNDF, TrkB, and phospho-CREB levels.
*Ach↑,
*Dose↑, Apigenin, at doses of 10 mg/kg and 20 mg/kg, promoted learning and memory
*BDNF↑, apigenin also increased BDNF level and up-regulated its receptor TrkB and pCREB in A25-35 -induced amnesic mice.
*TrkB↑,
*p‑CREB↑,
*BBB↑, Additionally, we found that treatment with apigenin was effective in preserving anatomical and functional integrity of the BBB per- meability.
*Ca+2?, A relevant effect of apigenin by suppressing the Ca 2+ influx through both voltage- and receptor-operated calcium channels might be attributed to the changes of rCBF

4276- BA,    Baicalin Attenuates Oxygen–Glucose Deprivation/Reoxygenation–Induced Injury by Modulating the BDNF-TrkB/PI3K/Akt and MAPK/Erk1/2 Signaling Axes in Neuron–Astrocyte Cocultures
- in-vivo, Stroke, NA
*BDNF↑, has been indicated to protect neurons by promoting brain-derived neurotrophic factor (BDNF).
*neuroP↑, neuroprotective mechanisms of baicalin against oxygen–glucose deprivation/reoxygenation
*TrkB↑, baicalin significantly increased the expressions of TrkB, PI3K/AKT, and MAPK/ERK.
*PI3K↑,
*Akt↑,
*MAPK↑,
*ERK↑,
*NO↓, elevation of NO and MDA was significantly attenuated by BCL treatment.
*MDA↓,
*SOD↑, BCL treatment increased the expression level of SOD
*TNF-α↓, OGD/R treatment significantly increased the expression levels of TNF-α, IL-1β, and IL-6 (p < 0.01). Compared with that in the OGD/R group, BCL robustly reduced the release of inflammatory cytokines
*IL1β↓,
*IL6?,

4267- Caff,    Caffeine‐mediated BDNF release regulates long‐term synaptic plasticity through activation of IRS2 signaling
- in-vivo, NA, NA
*cognitive↑, Caffeine has cognitive‐enhancing properties with effects on learning and memory, concentration, arousal and mood
*memory↑,
*Mood↑,
*BDNF↑, caffeine induces massive secretion of BDNF in cultured hippocampal neurons
*TrkB↑, These observations strongly suggest that TrkB activation is involved in CAFLTP.

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

4262- Chol,    Choline up-regulates BDNF and down-regulates TrkB neurotrophin receptor in rat cortical cell culture
- in-vitro, NA, NA
*TrkB↑, Further analysis of choline-exposed cell cultures showed an increased protein level of the TrkB ligand brain-derived neurotrophic factor (BDNF).
*BDNF↑,

4260- CHr,    Chrysin modulates the BDNF/TrkB/AKT/Creb neuroplasticity signaling pathway: Acting in the improvement of cognitive flexibility and declarative, working and aversive memory deficits caused by hypothyroidism in C57BL/6 female mice
- in-vivo, NA, NA
*BDNF↑, Chrysin modulates the BDNF/TrkB/AKT/CREB signaling pathway in the brain.
*TrkB↑,
*Akt↑,
*CREB↑,
*memory↑, Chrysin treatment effectively reversed these memory deficits, restored cognitive flexibility, and improved protein levels
*cognitive↑,

4171- CUR,    Curcumin produces neuroprotective effects via activating brain-derived neurotrophic factor/TrkB-dependent MAPK and PI-3K cascades in rodent cortical neurons
- in-vivo, NA, NA
*BDNF↑, treatment of curcumin increased BDNF and phosphor-TrkB
*TrkB↑,
*CREB↑, curcumin-induced increase in phosphorylated cyclic AMP response element binding protein (CREB), which has been implicated as a possible mediator of antidepressant actions
*Mood↑,
*neuroP↑, Therefore, we hypothesize the neuroprotection of curcumin might be mediated via BDNF/TrkB-MAPK/PI-3K-CREB signaling pathway.

4139- Ex,    Impact of physical exercise on the regulation of brain-derived neurotrophic factor in people with neurodegenerative diseases
- Review, AD, NA
*BDNF↑, recent studies are analyzed that indicate an increase in BDNF levels following physical activity, particularly in young adults.
*eff↑, with the most significant effects seen in aerobic and high-intensity exercises.
*eff↑, Both acute and prolonged exercise increase BDNF, but the effect is more sustained with regular, long-term regimens.
*cognitive↑, Prolonged aerobic exercise increases BDNF and improves vascular and cognitive functions, with positive effects observed in older adults.
*memory↑, In animal models, forced and voluntary exercise increased hippocampal BDNF, improving spatial memory and synaptic function.
*BrainVol↑,
*TrkB↑, The interaction of BDNF with its receptor TrkB is involved in the processes that lead to enhancements in learning and memory associated with exercise
*GABA↑, BDNF increases the expression of markers associated with GABAergic neurotransmission, such as GABA, GAD65, and GAD67

4247- GI,    6-Shogaol from Dried Ginger Protects against Intestinal Ischemia/Reperfusion by Inhibiting Cell Apoptosis via the BDNF/TrkB/PI3K/AKT Pathway
- vitro+vivo, NA, NA
*BDNF↑, activating BDNF/TrkB/PI3K/AKT signaling pathway and inhibiting II/R-induced cell apoptosis. The outcome is further validated both in vivo and in vitro.
*TrkB↑,
*PI3K↑,
*Akt↑,
*Apoptosis↓,
*Inflam↓, dried ginger, behaviors multiple biological activities, including anti-inflammation, antioxidation, and anti-apoptosis.
*antiOx↑,

4243- Gins,    Effects of Ginseng on Neurological Disorders
- Review, Stroke, NA - Review, AD, NA - Review, Park, NA
*BDNF↑, These results suggest that the active ingredient of ginseng may exert antidepressant effects through enhanced BDNF-TrkB signaling pathways
*TrkB↑,
*neuroP↑, Korean Red Ginseng attenuated long-term brain damage and protected neuro in a permanent cerebral ischemia model
*VEGF↑, but also can increase the expression of VEGF and BDNF in PC12 cells subjected OGD/reperfusion
*p‑tau↓, Ginsenoside Rb1 markedly decreased tau protein hyperphosphorylation through JNK/p38 MAPK pathway
*memory↑, ginseng extracts inhibited memory impairment of AD rats.

4241- HNK,    Effects of Honokiol on Neurological Injury and Cognitive Function in Mice with Intracerebral Hemorrhage by Regulating BDNF-TrkB-CREB Signaling Pathway
- in-vivo, Stroke, NA
*Apoptosis↓, Honokiol may alleviate hippocampal neuronal apoptosis and damage, and improve cognitive dysfunction in ICH mice by activating the BDNF-TrkB-CREB signaling pathway.
*cognitive↑,
*BDNF↑,
*TrkB↑,
*CREB↑,

4292- LT,    Luteolin for neurodegenerative diseases: a review
- Review, AD, NA - Review, Park, NA - Review, MS, NA - Review, Stroke, NA
*Inflam↓, luteolin, showing significant anti-inflammatory, antioxidant, and neuroprotective activity.
*antiOx↑,
*neuroP↑,
*BioAv↝, To increase the bioavailability of luteolin, several delivery methods have been developed; the most thoroughly studied include lipid carriers like liposomes and nanoformulations
*BBB↑, luteolin given intraperitoneally (ip) to mice can readily cross the blood-brain barrier (BBB) and enter the brain
*TNF-α↓, nhibiting pro-inflammatory mediators such as cyclooxygenase-2 (COX-2), nitric oxide (NO), TNF-α, IL-β, IL-6, IL-8, IL-31, and IL-33 in several in vitro models of AD
*IL1β↓,
*IL6↓,
*IL8↓,
*IL33↓,
*NF-kB↓, inhibition of the NF-кB pathway
*BACE↓, leads to the inhibition of a downstream target– β-site amyloid precursor protein cleaving enzyme (BACE1), which is a key mediator in forming Aβ fibrils in AD pathology
*ROS↓, anti-oxidant activity mainly by reducing ROS levels and increasing SOD activity in in vitro models of AD
*SOD↑,
*HO-1↑, increase the expression of antioxidant enzymes such as heme oxygenase-1 (HO-1) via the nuclear factor erythroid 2–related factor 2/ antioxidant responsive element (Nrf-2/ARE) complex activation
*NRF2↑,
*Casp3↓, reducing the levels of caspase-3 and − 9 and improving the B-cell lymphoma protein 2/Bcl-2-associated X protein (Bcl-2/Bax) ratio, as it was reported in in vitro models of AD
*Casp9↑,
*Bax:Bcl2↓,
*UPR↑, enhancing the unfolded protein response (UPR) pathway, leading to an increase in endoplasmic reticulum (ER) chaperone GRP78 and a decrease in the expression of UPR-targeted pro-apoptotic genes via the MAPK pathway.
*GRP78/BiP↑,
*Aβ↓, evidence that suggests that luteolin can directly influence the formation of Aβ plaques by selectively inhibiting the activity of N-acetyl-α-galactosaminyltransferase (ppGalNAc-T) isoforms
*GSK‐3β↓, inactivating the glycogen synthase kinase-3 alpha (GSK-3α) isoform, suppressing Aβ and promoting tau disaggregation
*tau↓,
*CREB↑, luteolin promoted phosphorylation and activation of cAMP response element-binding protein (CREB) leading to the increased miR-132 expression, and eventually neurite outgrowth in PC12 cells
*ATP↑, ROS production was decreased by 40%, MMP levels were restored close to control N2a levels (202%), and ATP levels were improved by 444%).
*cognitive↑, protective effect of luteolin against cognitive dysfunction was also reported in the streptozotocin
*BloodF↑, Luteolin increased regional cerebral blood flow values, alleviated the leakage of the lumen of vessels, and protected the integrity of BBB
*BDNF↑, increasing the level of brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptor (TrkB) expression in the cerebral cortex
*TrkB↑,
*memory↑, luteolin supplementation significantly ameliorated memory and cognitive deficits in 3 × Tg-AD mice.
*PPARγ↑, attenuated mitochondrial dysfunction via peroxisome proliferator-activated receptor gamma (PPARγ) activation.
*eff↑, combination of luteolin with another compound– l-theanine (an amino acid found in tea) also improved AD-like symptoms in the Aβ25–35-treated rats

4232- Lut,    Luteolin Treatment Ameliorates Brain Development and Behavioral Performance in a Mouse Model of CDKL5 Deficiency Disorder
- in-vivo, NA, NA
*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

4227- Lyco,    Lycopene Alleviates Depression-Like Behavior in Chronic Social Defeat Stress-Induced Mice by Promoting Synaptic Plasticity via the BDNF-TrkB Pathway
- in-vivo, NA, NA
*BDNF↑, suggesting that lycopene may enhance synaptic plasticity via the BDNF–TrkB/pTrkB signaling pathway.
*TrkB↑,
*PSD95↑, mRNA expression levels of PSD‐95 and Syn in the hippocampus of the CSDS + LYC group mice were substantially upregulated compared to the model group

4160- NAD,    The biochemical pathways of central nervous system neural degeneration in niacin deficiency
- Review, NA, NA
*BDNF↑, Recent evidences suggest that niacin administration may up-regulate the expression of BDNF-TrkB.
*TrkB↑,

4162- QC,    Quercetin attenuates cell apoptosis in focal cerebral ischemia rat brain via activation of BDNF-TrkB-PI3K/Akt signaling pathway
- in-vivo, Stroke, NA
*neuroP↑, Quercetin significantly improved neurological function, while it decreased the infarct volume and the number of TdT mediated dUTP nick end labeling positive cells in MCAO rats.
*BDNF↑, The protein expression of BDNF, TrkB and p-Akt also increased in the quercetin treated rats.
*TrkB↑,
*p‑Akt↑,

4214- Se,    Selenium ameliorates cognitive impairment through activating BDNF/TrkB pathway
- in-vivo, NA, NA
*memory↑, selenium supplementation can improve spatial learning and memory deficiencies in 3 × Tg-AD mice.
*other↑, Selenium supplementation increased selenium and GSH-Px levels in the brain tissue of 3 × Tg-AD mice and significantly enhanced neuronal conditions
*BDNF↑, the expression levels of proteins related to the BDNF/TrkB pathway significantly increased following selenium supplementation.
*TrkB↑,

4198- SFN,    Sulforaphane epigenetically enhances neuronal BDNF expression and TrkB signaling pathways
- vitro+vivo, AD, NA
*TrkB↑, Sulforaphane elevated levels of synaptic TrkB signaling pathway components, including CREB, CaMKII, ERK, and Akt in both primary cortical neurons and 3 × Tg-AD mice.
*CREB↑,
CaMKII ↑,
*ERK↑,
*ac‑H3↑, Sulforaphane increased global acetylation of histone 3 (H3) and H4, inhibited HDAC activity, and decreased the level of HDAC2 in primary cortical neurons
*ac‑H4↑,
*HDAC↓,
*HDAC2↓,
*BDNF↑, sulforaphane increased acetylated H3 and H4 at BDNF promoters, suggesting that sulforaphane regulates BDNF expression via HDAC inhibition.

4215- SY,    Safflower yellow alleviates cognitive impairment in mice by modulating cholinergic system function, oxidative stress, and CREB/BDNF/TrkB signaling pathway
- in-vivo, NA, NA
*memory↑, SY could shorten the escape latency and the time of the first crossing platform in the mice with memory acquisition and memory consolidation impairments, and increase the platform crossing times.
*AChE↓, SY decreased the AChE activities, increased the ChAT activities, and modulated oxidative stress markers (SOD, MDA, and GSH-PX) in scopolamine-induced mice
*ChAT↑,
*SOD↓,
*MDA↓,
*GPx↑,
*BDNF↑, SY could activated BDNF/TrkB/CREB signaling pathway and reduced neuronal damage.
*TrkB↑,
*CREB↑,
*ROS↓, SY can restore the function of the cholinergic system, inhibit oxidative stress

2138- TQ,    Thymoquinone has a synergistic effect with PHD inhibitors to ameliorate ischemic brain damage in mice
- in-vivo, Nor, NA
*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


Showing Research Papers: 1 to 22 of 22

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 22

Pathway results for Effect on Cancer / Diseased Cells:


Kinase & Signal Transduction(tgid=6) ⓘ

CaMKII ↑, 1,  
Total Targets: 1

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3,   Catalase↑, 2,   GPx↑, 3,   GSH↑, 1,   HO-1↑, 3,   MDA↓, 4,   NQO1↑, 1,   NRF2↑, 3,   ROS↓, 6,   SOD↓, 1,   SOD↑, 4,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 2,   OCR↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   CREB↑, 6,   p‑CREB↑, 1,   glucose↓, 1,   PFK↓, 1,   PPARγ↑, 2,  

Cell Death(tgid=5) ⓘ

Akt↑, 4,   p‑Akt↑, 1,   Apoptosis↓, 2,   Bax:Bcl2↓, 1,   Bcl-2↑, 1,   Casp3↓, 1,   Casp9↑, 1,   MAPK↓, 1,   MAPK↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 2,   ac‑H3↑, 1,   ac‑H4↑, 1,   other↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

GRP78/BiP↑, 1,   UPR↑, 1,  

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

ERK↑, 2,   GSK‐3β↓, 3,   HDAC↓, 1,   HDAC2↓, 1,   Nestin↑, 1,   neuroG↑, 2,   NOTCH1↑, 1,   PI3K↑, 5,   SOX2↑, 1,  

Migration(tgid=13) ⓘ

Ca+2?, 1,   Ki-67↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 1,   Hif1a↑, 1,   NO↓, 1,   VEGF↑, 2,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 3,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 1,   IL1β↓, 3,   IL33↓, 1,   IL6?, 1,   IL6↓, 1,   IL8↓, 1,   Inflam↓, 5,   NF-kB↓, 1,   PGE2↓, 1,   TLR4↓, 1,   TNF-α↓, 4,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1,   AChE↓, 4,   BDNF↑, 21,   BrainVol↑, 1,   ChAT↑, 1,   GABA↑, 2,   MAOA↓, 2,   NGF↑, 1,   PSD95↑, 1,   tau↓, 1,   p‑tau↓, 1,   TrkB↑, 22,  

Protein Aggregation(tgid=19) ⓘ

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

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   BioAv↝, 3,   Dose↑, 1,   eff↑, 3,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   BloodF↑, 1,   GutMicro↑, 1,   IL6?, 1,   IL6↓, 1,   Ki-67↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiDiabetic↑, 1,   cardioP↑, 1,   cognitive↑, 7,   memory↑, 9,   Mood↑, 3,   motorD↑, 1,   neuroP↑, 7,   Obesity↓, 1,   Weight↓, 1,   Wound Healing↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

Sepsis↓, 1,  
Total Targets: 100

Scientific Paper Hit Count for: TrkB, Tropomyosin receptor kinase B
3 Apigenin (mainly Parsley)
1 Baicalin
1 Caffeine
1 Centella asiatica / Gotu kola → asiaticoside
1 Choline
1 Chrysin
1 Curcumin
1 Exercise
1 Ginger/6-Shogaol/Gingerol
1 Ginseng
1 Honokiol
1 Luteolin
1 Lutein
1 Lycopene
1 nicotinamide adenine dinucleotide
1 Quercetin
1 Selenium
1 Sulforaphane (mainly Broccoli)
1 Safflower yellow
1 Thymoquinone
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#:1254  State#:%  Dir#:2
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