BDNF Cancer Research Results

BDNF, brain-derived neurotrophic factor: Click to Expand ⟱
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Brain-Derived Neurotrophic Factor (BDNF) is a key neurotrophin (a type of growth factor) involved in brain health, and its role in Alzheimer’s Disease (AD) has been extensively studied.
-AD patients often have lower BDNF levels in key brain regions, such as the hippocampus and cortex.
-This reduction correlates with cognitive decline and brain atrophy.
-BDNF normally protects neurons from Aβ toxicity
-Exercise and cognitive training have been shown to boost BDNF levels and may slow cognitive decline.
- natural compounds (like curcumin or flavonoids) may also upregulate BDNF.
Scientific Papers found: Click to Expand⟱
4163- ACNs,  Flav,    Dietary levels of pure flavonoids improve spatial memory performance and increase hippocampal brain-derived neurotrophic factor
- in-vivo, AD, NA
memory↑, enhancement of spatial memory in 18 month old rats.
*BDNF↑, These behavioral changes were paralleled by increases in hippocampal brain-derived neurotrophic factor
*cognitive↑, flavonoids are likely causal agents in mediating the cognitive effects of flavonoid-rich foods.

4282- ALA,    Effect of add-on alpha lipoic acid on psychopathology in patients with treatment-resistant schizophrenia: a pilot randomized double-blind placebo-controlled trial
- Trial, NA, NA
*antiOx↑, Alpha lipoic acid (ALA) is a naturally occurring antioxidant that plays an important role in the functioning of enzymes involved in mitochondrial oxidative metabolism
*Inflam↓, act as antioxidant and anti-inflammatory agents
*lipid-P↓, ALA supplementation has been shown to decrease lipid peroxidation in healthy controls but not in patients with schizophrenia
*adiP↑, ALA has also been shown to improve adiponectin levels, prevent weight gain or weight loss
*cognitive∅, no significant difference between placebo and the ALA groups in scores of cognitive functions
*BDNF↑, median BDNF levels increased from 5.06 to 5.50 ng/mL

4283- ALC,    Rapid-acting antidepressant-like effects of acetyl-l-carnitine mediated by PI3K/AKT/BDNF/VGF signaling pathway in mice
- in-vivo, NA, NA
*BDNF↑, In addition, ALC (100 mg/kg, i.p.) also reversed depressive-like behavior and the down-regulation of phosphorylated AKT (pAKT), brain-derived neurotrophic factor (BDNF) and neuropeptide VGF in the hippocampus and prefrontal cortex of mice induced by
*p‑Akt↑,
*PI3K↑,

5262- aLinA,    The Role of Alpha-Linolenic Acid and Other Polyunsaturated Fatty Acids in Mental Health: A Narrative Review
- Review, AD, NA
*neuroP↑, The evidence suggests that PUFAs are beneficial for mental health, brain function, and behavior. ALA, EPA, and DHA have very significant neuroprotective properties, particularly in inducing changes to the synaptic membrane and modulating brain cell s
*Risk↓, DHA is a primary component of neuronal membranes in regions critical to memory and cognition, such as the hippocampus and cortex, and low levels of DHA are associated with an increased risk of cognitive decline [16,22].
*cognitive↑, Omega-3 supplementation has shown promise in delaying cognitive decline and neurodegeneration, potentially due to its anti-inflammatory and antioxidative properties, as well as its role in neurogenesis and brain-derived neurotrophic factor (BDNF) enh
*Inflam↓,
*antiOx↑,
*BDNF↑,

4279- Api,    The Beneficial Role of Apigenin against Cognitive and Neurobehavioural Dysfunction: A Systematic Review of Preclinical Investigations
- Review, NA, NA
*antiOx↑, potent antioxidant and has been shown to exhibit anti-inflammatory, antitumorigenic and antimicrobial activities
*Inflam↓,
*BBB↑, Its ability to cross the blood–brain barrier is important as it contributes to its pharmacological activity against neurological disorders
*5HT↑, Apigenin improved serotonin, dopamine and epinephrine levels, which were altered in depressive animals
*CREB↑, Apigenin further regulates the cAMP-CREB-BDNF signalling pathway and N-methyl-D-aspartate (NMDA) receptors, which play important roles in neuronal survival, synaptic plasticity, cognitive function and mood behaviour
*BDNF↑, Apigenin improved BDNF levels and enhanced ERK1/2 and CREB expression
*memory↑, All the studies showed that apigenin improved learning and memory, except for two studies.
*motorD↑, In the open field test, apigenin improved locomotor activity
*Mood↑, The splash test revealed that apigenin improved grooming activity and locomotion in streptozotocin-induced depressive-like behaviour in a mouse model via an improvement in grooming activity.
*cognitive↑, The studies included in this systematic review showed that apigenin improved cognitive function and neurobehaviour in impaired or stressed animals.
*ROS↓, inhibition of ROS production

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

3884- Api,    Neuroprotective, Anti-Amyloidogenic and Neurotrophic Effects of Apigenin in an Alzheimer’s Disease Mouse Model
- in-vivo, AD, NA
*memory↑, Three-month oral treatment with apigenin rescued learning deficits and relieved memory retention in APP/PS1 mice.
*Aβ↓, Apigenin also showed effects affecting APP processing and preventing Aβ burden due to the down-regulation of BACE1 and β-CTF levels, the relief of Aβ deposition, and the decrease of insoluble Aβ levels.
*BACE↓, we observed BACE1 level reduction treated with apigenin.
*antiOx↑, apigenin exhibited superoxide anion scavenging effects and improved antioxidative enzyme activity of superoxide dismutase and glutathione peroxidase.
*BDNF↑, apigenin restored neurotrophic ERK/CREB/BDNF pathway in the cerebral cortex.
*p‑CREB↑, After long-term apigenin treatment, coupled with the elevation of BDNF level, enhanced phosphorylated ERK1/2 and CREB expression were detected in the cerebral cortex
*p‑ERK↑,
*ROS↓, apigenin exhibited superoxide anion scavenging effects and improved antioxidative enzyme activity of superoxide dismutase (SOD) and GSH-Px.
*SOD↑,
*GPx↑,
*neuroP↑, observations are correlated with a prospective neuroprotective, anti-amyloidogenic and neurotrophic effects in AD deficits.

3819- Aroma,    Aromatherapy improves cognitive dysfunction in senescence-accelerated mouse prone 8 by reducing the level of amyloid beta and tau phosphorylation
- Human, AD, NA - in-vitro, AD, NA
*cognitive↑, benefits of aromatherapy on the cognitive function of patients with AD utilizing various aromatic essential oils
*Dose↝, The mice were exposed to a mixture of lemon and rosemary oil at nighttime as well as to a mixture of lavender and orange oil in the daytime for 2 months.
*Aβ↓, brain levels of Aβ and abnormally phosphorylated tau were considerably lower in the aromatherapy group, while the levels of BDNF were marginally higher.
*tau↓,
*BDNF↑,
*motorD↑, fig 1

4278- ART/DHA,    Artemisinin Ameliorates the Neurotoxic Effect of 3-Nitropropionic Acid: A Possible Involvement of the ERK/BDNF/Nrf2/HO-1 Signaling Pathway
- in-vivo, NA, NA
*IL6↓, ART effectively suppressed neuroinflammatory (IL-6) and apoptotic markers (caspase 3 and 9), increasing BDNF levels and restoring the p-ERK1/2, Nrf2, and HO-1 expression.
*Casp3↓,
*Casp9↓,
*BDNF↑,
*ERK↑,
*NRF2↑,
*HO-1↑,
*neuroP↑, ART could exert its neuroprotective effect via antioxidant, anti-inflammatory, and antiapoptotic properties with a possible involvement of the ERK/BDNF/Nrf2/HO-1 pathway.
*antiOx↑,
*Inflam↓,

4810- ASTX,    Effects of Astaxanthin on the Proliferation and Migration of Breast Cancer Cells In Vitro
- in-vitro, BC, MDA-MB-231 - in-vitro, Nor, MCF10
TumCP↓, application of ASX significantly reduced proliferation rates and inhibited breast cancer cell migration compared to control normal breast epithelial cells.
TumCMig↓,
selectivity↑,
*BDNF↑, ASX increases brain derived neurotropic factor (BDNF) protein levels, while concurrently decreasing oxidative stress levels [6]
*ROS↓,
*TNF-α↓, ASX decreases the amount of inflammatory markers such as TNF-α, IL-6, and IFN-γ via NFκβ inhibition [7].
*IL6↓,
*IFN-γ↓,
*NF-kB↓,
BAX⇅, In the triple-negative cell line MDA-MB-231 both BAX and BCL-2 mRNA levels were reduced following ASX treatments. while BAX levels were elevated following treatment with 50 μM ASX.
Bcl-2↓,
*antiOx↑, ASX is a marine-based ketocarotenoid that has potent antioxidant characteristics
radioP↑, Incorporation of ASX into anticancer therapy will help control tumor growth and potentially reduce the impact of radiation therapy and chemotherapy associated side effects.
ChemoSen↑,

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?,

2605- Ba,  BA,    Potential therapeutic effects of baicalin and baicalein
- Review, Var, NA - Review, Stroke, NA - Review, IBD, NA - Review, Arthritis, NA - Review, AD, NA - Review, Park, NA
cardioP↑, cardioprotective activities.
Inflam↓, Decreasing the accumulation of inflammatory mediators and improving cognitive function
cognitive↑,
*hepatoP↑, Decreasing inflammation, reducing oxidative stress, regulating the metabolism of lipids, and decreasing fibrosis, apoptosis, and steatosis are their main hepatoprotective mechanisms
*ROS?, Reducing oxidative stress and protecting the mitochondria to inhibit apoptosis are proposed as hepatoprotective mechanisms of baicalin in NAFLD
*SOD↑, Baicalin could reduce the levels of ROS and fatty acid-induced MDA, and increase superoxide dismutase (SOD) and glutathione amounts compared to the control.
*GSH↑,
*MMP↑, Moreover, baicalin could partially restore mitochondrial morphology and increase ATP5A expression and mitochondrial membrane potential (Gao et al., 2022).
*GutMicro↑, After baicalein treatment, a remodelling in the overall structure of the gut microbiota was observed
ChemoSen↑, Besides, a combination of baicalin and doxorubicin could elevate the chemosensitivity of MCF-7 and MDA-MB-231 breast cancer cells
*TNF-α↓, Baicalin can protect cardiomyocytes from hypoxia/reoxygenation injury by elevating the SOD activity and anti-inflammatory responses through reducing TNF-α, enhancing IL-10 levels, decreasing IL-6, and inhibiting the translocation of NF-κB to the nucl
*IL10↑,
*IL6↓,
*eff↑, Studies show that baicalin and baicalein may be effective against IBD by suppressing oxidative stress and inflammation, and regulating the immune system.
*ROS↓,
*COX2↓, baicalein can improve the symptoms of ulcerative colitis by lowering the expression of pregnane X receptor (PXR), (iNOS), (COX-2), and caudal-type homeobox 2 (Cdx2), as well as the NF-κβ and STAT3
*NF-kB↓,
*STAT3↓,
*PGE2↓, Administration of baicalin (30-90 mg/kg) could decrease the levels of prostaglandin E2 (PEG2), myeloperoxidase (MPO), IL-1β, TNF-α, and the apoptosis-related genes including Bcl-2 and caspase-9
*MPO↓,
*IL1β↓,
*MMP2↓, Rheumatoid arthritis RA mouse model by supressing relevant proinflammatory cytokines such as IL-1b, IL-6, MMP-2, MMP-9, TNF-α, iNOS, and COX-2)
*MMP9↓,
*β-Amyloid↓, Alzheimer’s disease (AD) : reduce β-amyloid and trigger non-amyloidogenic amyloid precursor proteins.
*neuroP↑, For instance, administration of baicalin orally for 14 days (100 mg/kg body weight) exhibited neuroprotective effects on pathological changes and behavioral deficits of Aβ 1–42 protein-induced AD in vivo.
*Dose↝, administration of baicalin (500 mg/day, orally for 12 weeks) could improve the levels of total cholesterol, TGs, LDLC and apolipoproteins (APOs), and high-sensitivity C-reactive protein (hs-CRP) in patients with rheumatoid arthritis and coronary arte
*BioAv↝, the total absorption of baicalin depends on the activity of intestinal bacteria to convert baicalin to baicalein as the first step.
*BioAv↝, Kidneys, liver, and lungs are the main organs in which baicalin accumulates the most.
*BBB↑, Baicalin and baicalein can pass through the blood brain barrier (BBB)
*BDNF↑, mechanism of action for baicalein is illustrated in Figure 3. Activation of the BDNF/TrkB/CREB pathway, inhibition of NLRP3/Caspase-1/GSDMD pathway,

4274- BBR,    Berberine exerts antidepressant effects in vivo and in vitro through the PI3K/AKT/CREB/BDNF signaling pathway
- in-vivo, NA, NA
*IL1β↓, serum levels of IL-1β, IL-6, TNF-α and CRP in CRS mice were significantly increased, while berberine and fluoxetine could down-regulate the expression of the above cytokines.
*IL6↓,
*TNF-α↓,
*CRP↓,
*CREB↑, The results showed that the mRNA and protein expression (or phosphorylation) levels of CREB (Fig. 4B, D) and BDNF (Fig. 4C, E) were decreased in the hippocampus of CRS mice, which could be reversed by berberine treatment
*BDNF↑,

4275- BBR,    Pharmacological effects of berberine on mood disorders
- Review, NA, NA
*antiOx↑, Berberine has multiple therapeutic actions, including antioxidant, anti‐inflammatory, antitumour, antimicrobial, hepatoprotective, hypolipidemic, and hypoglycemic actions.
*Inflam↓,
*hepatoP↑,
*eff↑, recent studies show that berberine has a protective effect on central nervous system disorders, such as Alzheimer's, cerebral ischaemia, mental depression, schizophrenia, and anxiety
*5HT↑, Chronic administration of berberine (5 mg/kg, ip) for 15 days significantly increased the levels of norepinephrine (29%), serotonin (19%) as well as dopamine (52%)
*Mood↑, An antidepressant effect of berberine results from elevation of brain‐derived neurotrophic factor (BDNF) levels.
*BDNF↑,

4273- BetA,    BDNF_improve_cerebral_blood_flow_and_recover_memory_deficits_in_permanent_BCCAO_induced_vascular_dementia_in_rats">Betulinic acid, a natural PDE inhibitor restores hippocampal cAMP/cGMP and BDNF, improve cerebral blood flow and recover memory deficits in permanent BCCAO induced vascular dementia in rats
- in-vivo, NA, NA
*neuroP↑, BA demonstrated a neuroprotective effect in a dose-dependent manner.
*BDNF↑, BA was able to re-establish cerebral blood flow, restore behavioral parameters and showed significant improvements in the as cAMP,cGMP and BDNF levels, restrain the oxidative stress and inflammatory parameters
*ROS↓,
*Inflam↓,
*cognitive↑, its ability to restore cognitive impairment and hippocampal neurochemistry in VaD.

4277- BM,    Reversion of BDNF, Akt and CREB in Hippocampus of Chronic Unpredictable Stress Induced Rats: Effects of Phytochemical, Bacopa Monnieri
- in-vivo, NA, NA
*BDNF↑, restored the normal level of BDNF, total and phospho-Akt, total and phospho CREB in the hippocampus of CUS induced rats as compared to vehicle treated control rats
*p‑CREB↑,

4272- Bor,    Neuroprotective properties of borax against aluminum hydroxide-induced neurotoxicity: Possible role of Nrf-2/BDNF/AChE pathways in fish brain
*NRF2↑, BX clearly activating the Nrf-2/ROS signaling pathway.
*ROS↓,
*antiOx↑, BX supported antioxidant capacity without leading apoptosis, lipid peroxidation, inflammatory response and DNA damage.
*lipid-P↑,
*Inflam↓,
*DNAdam↓,
*BDNF↑, BX also increased the BDNF levels and AChE activity.
*neuroP↑, BX exerted a neuroprotective effect against AH-induced neurotoxicity via down-regulating cytokine-related pathways, minimising DNA damage, apoptosis
*GSH↑, as well as up-regulating GSH, AChE, BDNF and antioxidant enzyme levels.

4270- Bos,    Boswellic acids ameliorate neurodegeneration induced by AlCl3: the implication of Wnt/β-catenin pathway
- in-vivo, AD, NA
*memory↑, BA significantly improved learning and memory impairments induced by AlCl3 treatment.
*AChE↓, BA treatment significantly decreased acetylcholinesterase levels and reduced amyloid-beta (Aβ) expression
*Aβ↓,
*TNF-α↓, BA ameliorated the increased expression of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β), inhibited lipid peroxidation, and increased total antioxidants in the brain.
*IL1β↓,
*lipid-P↓,
*TAC↑,
*BDNF↑, Indeed, BA significantly suppressed AlCl3-induced decrease of brain-derived neurotrophic factor, pGSK-3β (Ser 9), and β-catenin.
*β-catenin/ZEB1↑,
*Dose↑, BA (250 mg/kg) showed a significant protective effect compared to a lower dose.

4269- Bos,    Boswellia serrata gum resin aqueous extract upregulatesBDNF but not CREB expression in adult male rat hippocampus
- in-vivo, NA, NA
*BDNF↑, Gene expression analysis revealed a significant increase in BDNF but not CREB expression in rats treated with both 50 and 100 mg/kg doses in comparison with the control group.
*CREB∅,

4263- CA,    Neuroprotective Effects of Carnosic Acid: Insight into Its Mechanisms of Action
- Review, AD, NA
*neuroP↑, neuroprotective effect of CA on neuronal cells subjected to ischemia/hypoxia injury via the scavenging or reduction of ROS (reactive oxygen species) and NO (nitric oxide) and inhibition of COX-2 and MAPK pathways
*ROS↓,
*NO↓,
*COX2↓,
*MAPK↓,
*NRF2↑, CA is known to activate the Keap1/Nrf2 pathway, thereby resulting in the production of cytoprotective proteins.
*GSH↑, activation of GSH metabolism
*HO-1↑, activation of Nrf2 target genes, including heme oxygenase 1 (HO-1) and thioredoxin reductase 1 (TXNRD1)
*5HT↑, Observations of increased serotonin and BDNF suggest that CA may represent a novel therapeutic avenue for depressive behaviors that should be further explored.
*BDNF↑, 10 μM CA results in a 1.5-fold increase in levels of BDNF
*PI3K↑, CA has been shown to mediate the activation of the PI3K/Akt/NF-κB pathway
*Akt↑,
*NF-kB↑,
*BBB↑, CA was shown to ameliorate brain edema and blood-brain barrier (BBB) disruption
*SIRT1↑, CA was also shown to increase SIRT1
*memory↑, CA was shown to significantly improve short-term and spatial memory attributes in rat models of AD
*Aβ↓, CA also delayed the deposition of Aβ and protected cells against Aβ-induced cholinergic and mitochondrial dysfunction in a Caenorhabditis elegans model of AD
*NLRP3↓, CA also inhibits the nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) inflammasome, which plays a critical role in the pathogenesis of neurodegenerative disorders, including AD and PD and COVID-19

4264- CA,    Carnosic Acid Mitigates Depression-Like Behavior in Ovariectomized Mice via Activation of Nrf2HO-1 Pathway
- in-vivo, NA, NA
*NRF2↑, CA treatment alleviated depressive behavior, induced the expression of Nrf2, HO-1, thioredoxin-1, and brain-derived neurotrophic factor, and enhanced serotonin levels.
*HO-1↑,
*Trx1↑,
*BDNF↑,
*5HT↑,
*ROS↓, CA also suppressed oxidative stress, reduced TNF-α, IL-1β, and iNOS mRNA expression, and ameliorated OVX-induced histopathological changes.
*TNF-α↓,
*IL1β↓,
*iNOS↓,

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↑,

4268- Caff,    Modulatory effect of coffee fruit extract on plasma levels of brain-derived neurotrophic factor in healthy subjects
- Study, NA, NA
*BDNF↑, green coffee caffeine powder (N677), grape seed extract powder (N31) increased levels of plasma BDNF by about 31 % under these experimental conditions, whereas treatment with WCFC(whole coffee fruit concentrate powder) increased it by 143 %

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.

4161- Caff,    Chronic caffeine prevents changes in inhibitory avoidance memory and hippocampal BDNF immunocontent in middle-aged rats
- in-vivo, AD, NA
*BDNF↑, Caffeine treatment substantially reduced i) age-related impairments in the two types of memory in an inhibitory avoidance paradigm, and ii) parallel increases in hippocampal BDNF levels.
*cognitive↑, modifications in BDNF and related proteins in the hippocampus contribute to the pro-cognitive effects of caffeine on age-associated losses in memory encoding.
*memory↑,

4266- CAP,    Capsaicin effects on brain-derived neurotrophic factor in rat dorsal root ganglia and spinal cord
- in-vivo, NA, NA
*BDNF↑, The percentage of BDNF-immunoreactive neurons in the L5 DRG was found to increase significantly 1 day after capsaicin injection

5925- CAR,    Neuroprotective effects of carvacrol against Alzheimer’s disease and other neurodegenerative diseases: A review
- Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*Inflam↓, anti-inflammatory, antioxidant, and AChEI properties
*antiOx↑,
*AChE↓,
*BBB↑, Carvacrol is able to cross the blood brain barrier easily, notably improving its therapeutic efficacy in neurodegenerative disorders
*cardioP↑, prevention of many chronic diseases, such as cancer as well as infectious, cardiovascular and neurodegenerative diseases
*neuroP↑, Extensive researches have revealed carvacrol neuroprotective properties
*memory↑, memory-enhancing activities
*TAC↑, Carvacrol has antioxidant activity and was shown to act as a dietary phyto-additive to boost animal antioxidant status (sharifi-Rad et al., 2018
*ROS↓, carvacrol could protect neuronal injuries against Aluminum-induced oxidative stress leading to lipid peroxidation
*lipid-P↓,
*MDA↓, carvacrol has been indicated to reduce malondialdehyde (MDA) and neuronal cell necrosis, and increase superoxide dismutase (SOD) and catalase (CAT) activity levels in the hippocampus (
*SOD↑,
*Catalase↑,
*NRF2↑, carvacrol activated nuclear factor-erythroid 2-related factor 2 (Nrf2) as an endogenous antioxidant
*cognitive↑, Carvacrol administration (25, 50, and 100 mg/kg) during 21 days attenuated memory impairments and enhanced cognition compared to the control group.
*IL1β↓, Carvacrol administration diminished the expression of interleukin-1β (IL-1β), cyclooxygenase-2 (COX-2), and tumor necrosis factor-α (TNF-α).
*COX2↓,
*TNF-α↓,
*TLR4↓, carvacrol could significantly decrease Toll-like receptor 4 (TLR4) and increase brain-derived neurotrophic factor (BDNF) expression.
*BDNF↑,
*PKCδ↑, carvacrol and thymol might have protective ability on cognitive function in AD by activation of PKC pathway
*5LO↓, Carvacrol inhibited AChE and lipoxygenase activity that supports its anti-inflammation and anti-Alzheimer effects
*TRPM7↓, Reduced caspase-3 levels, and TRPM7 channels inhibitor
*GSH↑, Antioxidant activity, Increased glutathione
*other↑, revealed a remarkable neuroprotective action of carvacrol in cerebral ischemia in animal models
*Ferroptosis↓, via ferroptosis inhibition by elevating GPx4 expression
*GPx4↑,

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↓,

6001- Chit,    Recent advances in engineering chitosan-based nanoplatforms in biotherapeutic multi-delivery for multi-targeted disease treatments: Promises and outlooks
- Review, Var, HepG2 - Review, AD, NA
TumVol↓, chitosan-based nanoparticles reduced tumors (doxorubicin (DOX) + survivin siRNA and curcumin + siRNA).
toxicity↓, Their initial studies reveal low toxicity and long-term medication delivery.
Half-Life↑,
eff↑, that allows drug release in reductive cellular environments (especially cancer cells with elevated glutathione levels),
selectivity↑, This clever nanocarrier reacts to intracellular cues and delivers its therapeutic payload mostly to cancer cells while protecting healthy tissues
Dose↝, These co-delivery systems take advantage of chitosan's mucoadhesive properties and protection against enzymatic degradation, enabling oral or nasal administration routes that traditionally pose challenges for peptide delivery
*BDNF↑, Chitosan nanoparticles delivering a combination of brain-derived neurotrophic factor (BDNF) protein and Nrf2 plasmid DNA have been shown to support synaptic plasticity, inhibit oxidative stress, and slow neurodegeneration.
*NRF2↑,
*ROS↓,
*neuroP↑,
*memory↑, In preclinical trials, such strategies improved memory retention, cognitive performance, and neuronal survival in rodent models
*cognitive↑,
*Obesity↓, obese non-human primates illustrated how chitosan-based codelivery of metformin and fibroblast growth factor 21 (FGF21) plasmid DNA targeted adipose tissue to achieve a 40 % reduction in visceral fat

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↑,

4261- Chol,  VitB12,  FA,  VitB2,    B-Vitamin and Choline Supplementation Changes the Ischemic Brain
- Study, Stroke, NA
*BDNF↑, this study suggests that supplementation with folic acid, vitamin B12, riboflavin, and choline may promote post-stroke neuroplasticity through increasing levels of BDNF.
*homoC↓, Choline reduces levels of homocysteine by converting it to methionine (Niculescu and Zeisel, 2002).

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↑,

4259- Cin,    The Potential of Cinnamon as Anti-Depressant
- Review, NA, NA
*Inflam↓, Active components such as Phenol, Cinnamaldehyde, Turmerone, Proanthocyanidin and Linalool as well as Eugenol can provide antidepressant effects through anti- inflammatory prevention.
*BDNF↑, Cinnamaldehyde will be metabolized in the body and produce a metabolite, namely NaB (Sodium Benzoate Metabolite) which can increase BDNF (Brain-derived neurotrophic factor)
*TNF-α↓, cinnamon extract inhibited the action of the pro-inflammatory cytokine TNF-α in the brain hippocampus
*lipid-P↓, Cinnamon also has active substances such as Linalool and Eugenol. Both of these active substances have the function of reducing the oxidation of lipids.
*Mood↑, active ingredient components contained in cinnamon have anti-depressant effects which can be used as an alternative treatment for depressed patients

4258- CoQ10,    Neuroprotective effects of coenzyme Q10-loaded exosomes obtained from adipose-derived stem cells in a rat model of Alzheimer's disease
- in-vivo, AD, NA
*memory↑, Exo+CoQ10 significantly improved STZ-induced memory impairment compared to CoQ10 and Exo groups alone.
*BDNF↑, BDNF expression increased in the STZ-induced rats after Exo+ CoQ10, when compared to the CoQ10 and Exo groups.
*cognitive↑, this study, Exo+ COQ10 enhanced cognition and memory deficiency in Alzheimer's disease by boosting BDNF and SOX2 levels in the hippocampus.
*SOX2↑,

4257- CoQ10,    Dietary intake of coenzyme Q10 reduces oxidative stress in patients with acute ischemic stroke: a double-blind, randomized placebo-controlled study
- Trial, Stroke, NA
*MDA↓, Significant reductions in serum MDA and IL-6 levels, alongside increased SOD and BDNF levels, were observed in the CoQ10 group.
*IL6↓,
*SOD↑,
*BDNF↑,
*ROS↓, A 30-day regimen of CoQ10 (600 mg/day) resulted in reduced oxidative stress and inflammation, alongside increased BDNF, suggesting potential neuroprotective benefits for post-stroke rehabilitation.
*Inflam↓,
*neuroP↑,

4208- Cro,    Antidepressant Effect of Crocus sativus Aqueous Extract and its Effect on CREB, BDNF, and VGF Transcript and Protein Levels in Rat Hippocampus
- in-vivo, NA, NA
*BDNF↑, The protein levels of BDNF, CREB and p-CREB were significantly increased in saffron treated rats.
*CREB↑,
*p‑CREB↑,

4158- Cro,    Antidepressant effects of crocin and its effects on transcript and protein levels of CREB, BDNF, and VGF in rat hippocampus
- in-vivo, AD, NA
*CREB↑, 25 and 50 mg/kg of crocin increased the levels of CREB and BDNF significantly and dose dependently.
*BDNF↑,
*Mood↑, crocin has antidepressant-like action by increasing CREB, BDNF and VGF levels in hippocampus

4176- CUR,    Effects of curcumin (Curcuma longa) on learning and spatial memory as well as cell proliferation and neuroblast differentiation in adult and aged mice by upregulating brain-derived neurotrophic factor and CREB signaling
- in-vivo, AD, NA
*BDNF↑, Upregulating Brain-Derived Neurotrophic Factor and CREB Signaling
*CREB↑,

4175- CUR,    Effects of curcumin on learning and memory deficits, BDNF, and ERK protein expression in rats exposed to chronic unpredictable stress
- in-vivo, NA, NA
*BDNF↑, CUS reduced hippocampal BDNF and ERK levels, while curcumin effectively reversed these alterations
*ERK↑, related to its aptitude to promote BDNF and ERK in the hippocampus.

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.

3795- CUR,    Curcumin: A Golden Approach to Healthy Aging: A Systematic Review of the Evidence
- Review, AD, NA
*antiOx↑, Curcumin, a natural compound with potent antioxidant and anti-inflammatory properties
*Inflam↓,
*AntiAge↑, Its potential anti-aging properties are due to its power to alter the levels of proteins associated with senescence, such as adenosine 5′-monophosphate-activated protein kinase (AMPK) and sirtuins
*AMPK↑,
*SIRT1↑,
*NF-kB↓, preventing pro-aging proteins, such as nuclear factor-kappa-B (NF-κB) and mammalian target of rapamycin (mTOR)
*mTOR↓,
*NLRP3↓, Moreover, curcumin, by inhibiting the NF-κB pathway, can directly restrain the assembly or even inhibit the activation of the NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome
*NADPH↓, by inhibiting nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and elevating the activity of antioxidant enzymes and consequently lowering reactive oxygen species (ROS)
*ROS↓,
*COX2↓, (COX-2), granulocyte colony-stimulating factor (G-CSF), and monocyte chemotactic protein-1 (MCP-1) can be decreased by curcumin
*MCP1↓,
*IL1β↓, by decreasing IL-1β, IL-17, IL-23, TNF-α, and myeloperoxidase, enhancing levels of IL-10, and downregulating activation of NF-κB
*IL17↓,
*IL23↓,
*TNF-α↓,
*MPO↓,
*IL10↑,
*lipid-P↓, curcumin showed a significant decline in lipid peroxidation and increased superoxide dismutase levels, in addition to a reduction in Aβ aggregation and tau hyperphosphorylation through the regulation of GSK3β, Cdk5, p35, and p25
*SOD↑,
*Aβ↓,
*p‑tau↓,
*GSK‐3β↓,
*CDK5↓,
*TXNIP↓, Curcumin also has an inhibitory role on the thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome pathway
*NRF2↑, well as upregulation of Nrf2, NAD(P)H quinine oxidoreductase 1 (NQO1), HO-1, and γ-glutamyl cysteine synthetase (γ-GCS) in brain cells.
*NQO1↑,
*HO-1↑,
*OS↑, significant improvement in OS, and a positive evolution in memory and spatial learning
*memory↑,
*BDNF↑, Besides that, it promoted neurogenesis through increasing brain-derived neurotrophic factor (BDNF) levels
*neuroP↑, Curcumin can promote neuroprotection
*BACE↓, Figure 7
*AChE↓, figure 7
*LDL↓, and reduced total cholesterol and LDL levels.

3797- CUR,    Curcumin reverses cognitive deficits through promoting neurogenesis and synapse plasticity via the upregulation of PSD95 and BDNF in mice
- in-vitro, NA, NA
*cognitive↑, Our results showed that curcumin administration rescued the impaired cognition of mice, shown as enhanced BrdU+ and dendritic spine in hippocampus.
*BDNF↑, At the molecular level, curcumin was found to promote the expression of brain-derived neurotrophic factor (BDNF) and postsynaptic density protein 95 (PSD95).
*PSD95↑,
*memory↑, Studies have shown that curcumin improves the spatial learning and memory abilities of the Alzheimer’s disease model mice

4333- Cyste,    Cystamine protects from 3-nitropropionic acid lesioning via induction of nf-e2 related factor 2 mediated transcription
- vitro+vivo, AD, NA
*NRF2↑, We found that cystamine activates Nrf2/ARE both in cell culture and in brain tissue and then probed the mechanism of activation in cell culture.
*ARE↑,
*neuroP↑, findings provide strong evidence that Nrf2 signaling may be an effective target for prevention of neurodegeneration.
*BDNF↑, cystamine has been shown to increase levels of brain derived neurotrophic factor (BDNF) in the striatum of HD knock-in mice and in primate blood.
*GSH↑, One effect of cystamine in cell culture is to increase glutathione (GSH) levels

4331- Cyste,    Cystamine and cysteamine increase brain levels of BDNF in Huntington disease via HSJ1b and transglutaminase
- in-vivo, HD, NA - NA, AD, NA
*BDNF↑, Cystamine increases BDNF secretion from the Golgi region that is blocked by reducing HSJ1b levels or by overexpressing transglutaminase.
*neuroP↑, We demonstrate that cysteamine, the FDA-approved reduced form of cystamine, is neuroprotective in HD mice by increasing BDNF levels in brain.

4178- DHA,    The salutary effects of DHA dietary supplementation on cognition, neuroplasticity, and membrane homeostasis after brain trauma
- in-vivo, NA, NA
*BDNF↑, We found that DHA supplementation, which elevates brain DHA content, normalized levels of brain-derived neurotrophic factor (BDNF), synapsin I (Syn-1), cAMP-responsive element-binding protein (CREB), and calcium/calmodulin-dependent kinase II (CaMKII
*CREB↑,
*cognitive↑, potential of dietary DHA to counteract broad and fundamental aspects of TBI pathology that may translate into preserved cognitive capacity.
*SOD↑, DHA diet also counteracted the FPI-reduced manganese superoxide dismutase (SOD) and Sir2 (a NAD+-dependent deacetylase).

4177- DHA,    Dietary omega-3 fatty acids normalize BDNF levels, reduce oxidative damage, and counteract learning disability after traumatic brain injury in rats
- in-vivo, NA, NA
*BDNF↑, Supplementation of omega-3 fatty acids in the diet counteracted all of the studied effects of FPI, that is, normalized levels of BDNF and associated synapsin I and CREB, reduced oxidative damage, and counteracted learning disability.
*CREB↑,
*ROS↓,
*cognitive↑,

4256- dietMed,    Association between Mediterranean dietary pattern with sleep duration, sleep quality and brain derived neurotrophic factor (BDNF) in Iranian adults
- Study, Nor, NA
*Sleep↑, Higher adherence to MDS among individuals with overweight or obesity reduced the odds of having short sleep;
*BDNF↑, Participants with higher adherence to MDS had lower odds for low BDNF values; however, this relation was not statistically significant.

4180- dietSTF,    Brain-derived neurotrophic factor, but not body weight, correlated with a reduction in depression scale scores in men with metabolic syndrome: a prospective weight-reduction study
- Human, Obesity, NA
*BDNF↑, Zung SDS only significantly improved in men with increased fasting BDNF levels after a lifestyle intervention.


Showing Research Papers: 1 to 50 of 179
Page 1 of 4 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 179

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death ⓘ

BAX⇅, 1,   Bcl-2↓, 1,  

Migration ⓘ

TumCMig↓, 1,   TumCP↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 2,   Dose↝, 1,   eff↑, 1,   Half-Life↑, 1,   selectivity↑, 2,  

Functional Outcomes ⓘ

cardioP↑, 1,   cognitive↑, 1,   memory↑, 1,   radioP↑, 1,   toxicity↓, 1,   TumVol↓, 1,  
Total Targets: 16

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 12,   ARE↑, 2,   Catalase↑, 2,   Ferroptosis↓, 1,   GPx↑, 2,   GPx4↑, 1,   GSH↑, 5,   GSR↑, 1,   HO-1↑, 5,   lipid-P↓, 5,   lipid-P↑, 1,   MDA↓, 3,   MPO↓, 2,   NQO1↑, 1,   NRF2↑, 10,   ROS?, 1,   ROS↓, 16,   SOD↑, 9,   TAC↑, 2,   Trx1↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,  

Core Metabolism/Glycolysis ⓘ

adiP↑, 1,   AMPK↑, 1,   CREB↑, 10,   CREB∅, 1,   p‑CREB↑, 4,   homoC↓, 1,   LDL↓, 1,   NADPH↓, 1,   PPARγ↑, 1,   SIRT1↑, 2,  

Cell Death ⓘ

Akt↑, 4,   p‑Akt↑, 1,   Casp3↓, 1,   Casp9↓, 1,   Ferroptosis↓, 1,   iNOS↓, 1,   MAPK↓, 2,   MAPK↑, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 2,   other↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 3,   p‑ERK↑, 1,   GSK‐3β↓, 2,   mTOR↓, 1,   PI3K↑, 4,   SOX2↑, 1,   STAT3↓, 1,   TRPM7↓, 1,  

Migration ⓘ

5LO↓, 1,   Ca+2?, 1,   CDK5↓, 1,   MMP2↓, 1,   MMP9↓, 1,   PKCδ↑, 1,   TXNIP↓, 1,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 2,  

Barriers & Transport ⓘ

BBB↑, 6,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 5,   CRP↓, 1,   IFN-γ↓, 1,   IL10↑, 2,   IL17↓, 1,   IL1β↓, 8,   IL23↓, 1,   IL6?, 1,   IL6↓, 5,   Inflam↓, 13,   MCP1↓, 1,   NF-kB↓, 3,   NF-kB↑, 1,   PGE2↓, 2,   TLR4↓, 2,   TNF-α↓, 10,  

Synaptic & Neurotransmission ⓘ

5HT↑, 5,   AChE↓, 5,   BDNF↑, 50,   GABA↑, 1,   MAOA↓, 1,   NGF↑, 2,   PSD95↑, 1,   tau↓, 1,   p‑tau↓, 1,   TrkB↑, 8,  

Protein Aggregation ⓘ

Aβ↓, 7,   BACE↓, 2,   NLRP3↓, 3,   β-Amyloid↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 2,   Dose↑, 2,   Dose↝, 2,   eff↑, 2,  

Clinical Biomarkers ⓘ

CRP↓, 1,   GutMicro↑, 1,   IL6?, 1,   IL6↓, 5,  

Functional Outcomes ⓘ

AntiAge↑, 1,   cardioP↑, 1,   cognitive↑, 16,   cognitive∅, 1,   hepatoP↑, 2,   memory↑, 13,   Mood↑, 6,   motorD↑, 3,   neuroP↑, 17,   Obesity↓, 1,   OS↑, 1,   Risk↓, 1,   Sleep↑, 1,  
Total Targets: 112

Scientific Paper Hit Count for: BDNF, brain-derived neurotrophic factor
11 Exercise
10 Hydrogen Gas
9 Magnetic Fields
6 Curcumin
6 Lycopene
6 Silymarin (Milk Thistle) silibinin
5 Apigenin (mainly Parsley)
5 Sulforaphane (mainly Broccoli)
4 Ellagic acid
4 Ginseng
4 Honokiol
4 Huperzine A/Huperzia serrata
4 Lutein
4 Resveratrol
4 Vitamin D3
4 Zinc
3 Carnosic acid
3 Caffeine
3 Ferulic acid
3 Naringin
3 Piperine
3 Urolithin
2 flavonoids
2 Aromatherapy
2 Baicalin
2 Berberine
2 Boswellia (frankincense)
2 Choline
2 Folic Acid, Vit B9
2 Coenzyme Q10
2 Crocetin
2 Cysteamine
2 Docosahexaenoic Acid
2 diet Short Term Fasting
2 Ginger/6-Shogaol/Gingerol
2 Luteolin
2 Zeaxanthin
2 Magnesium
2 Phenylbutyrate
2 Propolis -bee glue
2 Quercetin
2 Sesame seeds and Oil
2 Taurine
2 Ursolic acid
1 Anthocyanins
1 Alpha-Lipoic-Acid
1 Acetyl-l-carnitine
1 alpha Linolenic acid
1 Artemisinin
1 Astaxanthin
1 Baicalein
1 Betulinic acid
1 Bacopa monnieri
1 Boron
1 Capsaicin
1 Carvacrol
1 Carnosine
1 chitosan
1 Vitamin B12
1 Vitamin B2,Riboflavin
1 Chrysin
1 Cinnamon
1 dietMediterranean
1 2-DeoxyGlucose
1 Calorie Restriction Mimetics
1 EGCG (Epigallocatechin Gallate)
1 Phosphatidylserine
1 Fisetin
1 Galantamine
1 Ginkgo biloba
1 Lecithin
1 Magnolol
1 Magnetic Field Rotating
1 Moringa oleifera
1 Methylsulfonylmethane
1 Mushroom Lion’s Mane
1 nicotinamide adenine dinucleotide
1 probiotics
1 Pterostilbene
1 Salvia officinalis
1 Rosmarinic acid
1 Selenium
1 Shikonin
1 Selenite (Sodium)
1 Safflower yellow
1 Thymoquinone
1 Vitamin B6,pyridoxine
1 Vitamin E
1 Vitamin K2
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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