APP Cancer Research Results

APP, amyloid precursor protein: Click to Expand ⟱
Source:
Type:
APP typically refers to the amyloid precursor protein, best known for its role in Alzheimer’s disease.
-APP is mainly distributed in the synapses of neurons in the brain and Aβ peptide was produced from APP proteolysis by β-secretase and γ-secretase complex.
-decreased APP in 5×FAD mice ameliorated their amyloid plaques and behavior activity.

• APP is found to be upregulated in some cancers such as certain breast cancers, colon cancers, and lung cancers. Elevated levels may influence processes such as cell proliferation, adhesion, migration, and even invasion.
Scientific Papers found: Click to Expand⟱
3864- ACNs,    Anthocyanins Potentially Contribute to Defense against Alzheimer’s Disease
- Review, AD, NA
*antiOx↑, ANTs are potent antioxidants that might regulate the free radical-mediated generation of amyloid peptides (Abeta-amyloids) in the brain
*Aβ↓,
*ROS↓,
*cognitive↑, Mulberries are a rich source of ANTs that induce antioxidant enzymes and promote cognition
*APP↓, In the cerebral cortex, blackcurrant and bilberry extract reduced APP levels in AD mouse models, but changes in the expression or phosphorylation of tau-protein were not observed
*BBB↑, ANTs cross the blood-brain barrier and protect brain tissue from Abeta toxicity
*Ca+2↓, Aronia melanocarpa. ANTs of this plant decrease intracellular calcium and ROS but increase ATP and mitochondrial potential.
*ATP↑,
*BACE/β-secretase↓, An-NPs also attenuate the protein expression of BACE-1 neuroinflammatory markers, such as phosphonuclear factor kB (p-NF-kB), tumor-necrosis factor (TNF-α), and inducible nitric oxide synthase (iNOS),
*p‑NF-kB↓,
*TNF-α↓,
*iNOS↓,

7396- Amla,    Enhancing cognitive memory function using Phyllanthus emblica polysaccharides via modulating autophagy and reshaping the gut microbiota
- in-vivo, AD, NA
*Inflam↓, Phyllanthus emblica polysaccharides (PEP) exhibit anti-inflammatory, antioxidant, and gut microbiota-modulating properties in colitis and obese mice.
*antiOx↓,
*GutMicro↑,
*cognitive↑, In vivo results showed that PEP administration significantly alleviated cognitive decline by reducing neuroinflammatory cytokines (TNF-α, IL-6, and IL-1β) and MDA levels while increasing anti-inflammatory factors (IL-4 and IL-10) and antioxidants (S
*TNF-α↓,
*IL6↓,
*IL1β↓,
*MDA↓,
*IL4↑,
*IL10↑,
*TAC↑,
*ATG5↑, Mechanistically, PEP upregulated autophagy-related proteins (Atg5, Beclin1, and LC3B) and LRP1 expression while downregulating AD-related proteins (BACE1, APP, Aβ, and phospho-TauSer404)
*Beclin-1↑,
*LC3B↑,
*LRP1↑,
*BACE/β-secretase↓,
*APP↓,
*Aβ↓,
*tau↓,

3678- BBR,    Network pharmacology study on the mechanism of berberine in Alzheimer’s disease model
- Review, AD, NA
*APP↓, BBR were decreased in the mRNA and protein expression of APP and presenilin 1 while PPARG was increased with a reduction in the NF-κB pathway.
*PPARγ↑, upregulated PPARG with decreasing its downstream NF-ΚB pathway
*NF-kB↓,
*Aβ↓, BBR played a protective role in the AD mice model via blocking APP processing and amyloid plaque formation.
*cognitive↑, berberine significantly reduced amyloid accumulation and improved cognitive impairment in APP/PS1 mice
*antiOx↑, via anti-oxidative stress, anti-neuroinflammation, inhibition of neuronal cell apoptosis, etc
*Inflam↓,
*Apoptosis↓,
*BioAv↑, BBR was found to be metabolized to dihydro-berberine by intestinal bacteria, whose bioavailability was five times higher than that of BBR
*BioAv↝, oral bioavailability (OB, >30%),
*BBB↑, blood-brain barrier (BBB, >0.3)
*motorD↑, BBR treated 5×FAD mice ameliorated their behavior activity including in locomotor activity and cognitive function compared to control.
*NRF2↑, BBR enhanced cellular antioxidant capacity, regulated antioxidant-related pathways such as Nrf2 and HO-1, and thereby reduced oxidative stress damage
*HO-1↑,
*ROS↓,
*p‑Akt↑, BBR significantly increased the phosphorylation levels of AKT and ERK
*p‑ERK↑,

3680- BBR,    Network pharmacology reveals that Berberine may function against Alzheimer’s disease via the AKT signaling pathway
- in-vivo, AD, NA
*Akt↑, Akt1 mRNA expression levels were significantly decreased in AD mice and significantly increased after BBR treatment (p < 0.05).
*neuroP↑, BBR may exert a neuroprotective effect by modulating the ERK and AKT signaling pathways.
*p‑ERK↑, Besides, AKT and ERK phosphorylation decreased in the model group, and BBR significantly increased their phosphorylation levels.
*Aβ↓, BBR has therapeutic potential in the treatment of AD by targeting amyloid beta plaques, neurofibrillary tangles, neuroinflammation, and oxidative stress
*Inflam↓,
*ROS↓,
*BioAv↑, oral bioavailability (OB) = 36.86%, drug-likeness (DL) = 0.78,
*BBB↑, blood brain barrier (BBB) = 0.57,
*Half-Life↝, half-life (HL) = 6.57. BBR half-life (t1/2) is in the mid-elimination group.
*memory↑, BBR improves the performance of memory and recognition tasks in AD mice
*cognitive↑,
*HSP90↑, Among the core targets, Akt1 (t = −5.01, p = 0.002), Hsp90aa1 (t = −3.66, p = 0.011), Hras (t = −2.99, p = 0.024) and Igf1 (t = 3.75, p = 0.019) mRNA levels were significantly increased after BBR treatment
*APP↓, BBR reduces Aβ levels by modulating APP processing and ameliorates Aβ pathology by inhibiting the mTOR/p70S6K signaling pathway
*mTOR↓,
*P70S6K↓,
*CD31/PECAM-1↑, it promotes the formation of brain microvessels by enhancing CD31, VEGF, N-cadherin, Ang-1 and inhibits neuronal apoptosis (Ye et al., 2021).
*VEGF↑,
*N-cadherin↑,
*Apoptosis↓,

3684- BBR,    Neuroprotective effects of berberine in animal models of Alzheimer’s disease: a systematic review of pre-clinical studies
- Review, AD, NA
*Inflam↓, berberine showed significant memory-improving activities with multiple mechanisms, such as anti-inflammation, anti-oxidative stress, cholinesterase (ChE) inhibition and anti-amyloid effects.
*antiOx↓,
*AChE↓,
*BChE↓, berberine exerts inhibitory effects on the four key enzymes in the pathogenesis of AD: acetylcholinesterase, butyrylcholinesterase, monoamine oxidase A, and monoamine oxidase B
*MAOA↓,
*MAOB↓,
*lipid-P↓, Fig3
*GSH↑,
*ROS↓,
*APP↓,
*BACE/β-secretase↓,
*p‑tau↓,
*NF-kB↓,
*TNF-α↓,
*IL1β↓,
*MAPK↓,
*PI3K↓,
*Akt↓,
*neuroP↑, neuroprotective effects of berberine have been extensively studied
*memory↑, berberine displayed significant effects in preventing memory impairment in these mechanistically different animal models, suggesting an over-all improvement of memory function by berberine

4300- BBR,    Effect of berberine on cognitive function and β-amyloid precursor protein in Alzheimer’s disease models: a systematic review and meta-analysis
- Review, AD, NA
*APP↓, Berberine can regulate APP expression and improve cognitive function in animal models of AD,
*cognitive↑,
*Aβ↓, Berberine is involved in regulating APP modification, which may inhibit Aβ production through BACE1 inhibition and regulation of γ-secretase substrates.
*BACE/β-secretase↓,
*tau?, berberine may be a good multi-targeted drug that can modulate AD related substances tau, PP-2A, Aβ, APP, or BACE-2.

7832- CA,  CGA,  MBS,    Neuroprotective Potential of Mung Bean (Vigna radiata L.) Polyphenols in Alzheimer's Disease: A Review
- Review, AD, NA
*BBB↑, both caffeic and chlorogenic acid could cross the BBB
*cognitive↑, caffeic acid (10−50 mg/kg/d, p.o.) improved the cognitive and memory impairments in Aβ25−35injected (i.c.v.) mice by the inhibition of oxidative stress
*memory↑,
*ROS↓,
*p‑tau↓, Aβ25−35-induced tau hyperphosphorylation was also suppressed by caffeic acid through reducing the calcium-dependent GSK-3β activation.
*GSK‐3β↓,
*MAPK↓, inhibited p38 MAPK activation to reduce neuroinflammation, suppressed p53 expression to downregulate caspase-3-mediated apoptosis, and decreased AChE activity.
*NeuroI↓,
*P53↓,
*Casp3↓,
*AChE↓,
*APP↓, by suppressing APP expression, β-secretase (BACE) activity, and GSK-3β activation, implying its neuroprotective activity under cerebral insulin resistance.
*BACE/β-secretase↓,
*neuroP↑,
*Dose↝, lowest effective dose of caffeic acid was 10 mg/kg in rats (Table 3), while its content range in the mung bean was 0.03−38.72 mg/100 g

3854- CAP,    Capsaicin consumption reduces brain amyloid-beta generation and attenuates Alzheimer’s disease-type pathology and cognitive deficits in APP/PS1 mice
- in-vivo, AD, NA
*Aβ↓, capsaicin, the pungent ingredient in chili peppers, reduced brain Aβ burden and rescued cognitive decline in APP/PS1 mice.
*cognitive↑, Our present findings further support the protective effects of chili consumption on cognition.
*APP↓, capsaicin shifted Amyloid precursor protein (APP) processing towards α-cleavage and precluded Aβ generation by promoting the maturation of a disintegrin and metalloproteinase 10 (ADAM10).
*MMP-10↝,
*p‑tau↓, capsaicin alleviated other AD-type pathologies, such as tau hyperphosphorylation, neuroinflammation and neurodegeneration.
*Inflam↓,
*neuroP↑,
*Risk↓, The incidence of AD in west China (3.99/1000 person-years) is lower than that in the east (5.58/1000 person-years)11, and in the west, the proportion of dishes with chili is higher and the pungency degree is greater than in the east
*TNF-α↓, reduced levels of proinflammatory factors, including TNF-α, IFN-γ, and IL-6
*IFN-γ↓,
*IL6↓,
*PPARα↑, apsaicin might activate ADAM10 via upregulating PPARα.

3701- Chol,    Lifelong choline supplementation ameliorates Alzheimer's disease pathology and associated cognitive deficits by attenuating microglia activation
- in-vivo, AD, NA
*Ach↑, Choline is also the precursor for acetylcholine, a neurotransmitter which activates the alpha7 nicotinic acetylcholine receptor (α7nAchR), and also acts as an agonist for the Sigma‐1 R (σ1R).
*Aβ↓, Lifelong choline supplementation significantly reduced amyloid‐β plaque load and improved spatial memory in APP/PS1 mice.
*memory↑,
*APP↓, Mechanistically, these changes were linked to a decrease of the amyloidogenic processing of APP, reductions in disease‐associated microglial activation, and a downregulation of the α7nAch and σ1 receptors.
*eff↑, Additional dietary choline is a putative treatment option that may prevent AD progression.
*neuroP↑, This suggests that additional choline in diet may be beneficial in preventing neuropathological changes associated with the aging brain.
*Dose↑, The tolerable upper limit (TUL) of choline unlikely to cause side effects for adult females and males (>19 years of age) is 3,500 mg/day, which is 8.24 times higher than the 425 mg/day recommendation for females and 6.36 times higher than the 550 mg/

6624- Cic,    Chicoric acid supplementation ameliorates cognitive impairment induced by oxidative stress via promotion of antioxidant defense system
- in-vivo, AD, NA - in-vivo, Park, NA
*neuroP↑, Chicoric acid attenuated neuron damage in d-gal-treated mice as revealed through histological examination in the hippocampus region of the mouse brain.
*TNF-α↓, The levels of inflammatory mediators, such as TNF-α and IL-1β, as well as malondialdehyde levels, were markedly reduced after chicoric acid treatment.
*IL1β↓,
*MDA↓,
*Catalase↑, activity of CAT and the level of GSH were significantly elevated in serum by chicoric acid
*GSH↑,
*NRF2↑, chicoric acid treatment noticeably activated the Nrf2 antioxidative defense system
*mtDam↓, reversing mitochondrial dysfunction, decreasing inflammation, and neuron apoptosis caused by oxidative stress.
*Inflam↓,
*Apoptosis↓,
*ROS↓, chicoric acid significantly quenched intracellular ROS to the normal level
*cognitive↑, suggested that chicoric acid supplementation ameliorated cognitive impairment induced by d-gal and SH-SY5Y cell apoptosis induced by H2O2
*Aβ↓, chicoric acid inhibited d-gal-induced Aβ1-42 accumulation in hippocampus of mice brain.
*BDNF∅, suggesting chicoric acid treatment did not restore the expression of BDNF in the hippocampus of aging mice.
*APP↓, chicoric acid treatment markedly decreased the expression of APP and BACE1 in the whole brain, which partly explains the inhibition by chicoric acid of Aβ1-42 accumulation in the cortex and hippocampus.
*BACE/β-secretase↓,

6779- EGCG,    Effectiveness of epigallocatechin gallate nanoparticles on the in-vivo treatment of Alzheimer's disease in a rat/mouse model: a systematic review
- Review, AD, NA
*BioAv↑, EGCG nanoparticles showed superior pharmacokinetic characteristics and improved blood-brain barrier permeability, and increased brain bioavailability compared to free EGCG.
*ROS↓, Additionally, nanoEGCG were more effective in modulating oxidative stress than free formulation and decreased AChE in the cortex and hippocampus of AlCl3-treated rats.
*AChE↓,
*Dose↝, formulated nanoparticles were given at a dose of 10 mg/kg. (rats)
*neuroP↑, Neuroprotective mechanisms of EGCG nanoformulations
*APP↓, Treating the AD rats with nanoEGCG significantly reduced the levels of APP, Aβ1–42, AChE, and GSK3β and elevated PDK1 levels
*GSK‐3β↓,
*PDK1↓,
*BBB↑, EGCG nanoparticles demonstrated better BBB penetration ability, higher bioavailability, and enhanced improvement of memory deficits over free EGCG in experimental animal models.
*memory↑,

3712- FA,    Ferulic Acid: A Hope for Alzheimer’s Disease Therapy from Plants
- Review, AD, NA
*antiOx↑, Ferulic acid (FA) is an antioxidant naturally present in plant cell walls with anti-inflammatory activities and it is able to act as a free radical scavenger.
*Inflam↓,
*ROS↓,
*Aβ↓, “FA could prevent the development of AD, not only through scavenging reactive oxygen species, but also through direct inhibition of the deposition of fibrils in the brain”
*HO-1↑, FA plays a cytoprotective role through the up-regulation of enzymes such as heme oxygenase-1, heat shock protein 70, extracellular signal-regulated kinase (ERK) 1/2, and serine/threonine kinase (Akt).
*HSP70/HSPA5↑,
*ERK↑,
*Akt↑,
*iNOS↓, , FA inhibits the expression and/or activity of cytotoxic enzymes, including inducible nitric oxide synthase, caspases, and cyclooxygenase-2
*COX2/PTGS2↓,
*cardioP↑, treatment of several age-related diseases, such as neurodegenerative disorders, cardiovascular diseases, diabetes, and cancer
*memory↑, reported that the long-term administration of FA to mice protected against learning and memory deficits induced by centrally administered β-amyloid
*IL2↓, FA is able to significantly reduce the interleukin-1β (IL-1β) cortical levels
*cognitive↑, FA reversed behavioral impairment, including hyperactivity, object recognition, spatial working, and reference memory.
*APP↓, it reduced amyloidogenic APP metabolism by modulation of β-secretase, attenuated neuroinflammation, and stabilized oxidative stress.
*SOD↑, superoxide dismutase (SOD), catalase (CAT) ERK 1/2, and Akt [95].
*Catalase↑,
*Akt↑,
*BioAv↑, A good strategy to increase the bioavailability and the cytoprotective effect of compounds such as FA is the formulation of new nanoparticles.

3715- FA,  CUR,  PS,    The Additive Effects of Low Dose Intake of Ferulic Acid, Phosphatidylserine and Curcumin, Not Alone, Improve Cognitive Function in APPswe/PS1dE9 Transgenic Mice
- in-vivo, AD, NA
*cognitive↑, Consequently, only the three-ingredient group exhibited a significant improvement in cognitive function compared to the control group
*IL1β↓, significant decrease in IL-1β and an increasing trend in acetylcholine were observed. In the Cur group, significant decreases in Aβ and phosphorylated tau and an increasing trend in BDNF were observed
*Ach↑,
*Aβ↓,
*p‑tau↓,
*BDNF↑,
*APP↓, FA inhibits AB production via down-regulation of APP and β-secretase,6) inhibits AB aggregation, 8) and protects nerve cells from Aβ-induced neurotoxicity

7833- GA,    Neuroprotective Potential of Mung Bean (Vigna radiata L.) Polyphenols in Alzheimer's Disease: A Review
- Review, AD, NA
*neuroP↑, Gallic acid (3,4,5-trihydroxybenzoic acid) showed neuroprotective activity against AD in various roden
*Dose↝, gallic acid (20 or 30 mg/kg) improved the cognitive impairments no matter it was administrated from the early (4 months), middle (9 months) or late-stage (12 months) of AD pathology
*ADAM10↝, related mechanisms involved modulation of the activity of α-secretase (ADAM10) and βsecretase (BACE-1) to inhibit the amyloidogenic cleavage of APP, disruption of the salt bridge between Aβ to suppress its aggregatio
*BACE/β-secretase↓,
*cl‑APP↓,
*Aβ↓,
*Ca+2↓, improvement of synaptic plasticity, as well as inhibition of Ca2+ influx, oxidative stress, and neuroinflammation.
*ROS↓,
*NeuroI↓,

3723- GBE,    Can We Use Ginkgo biloba Extract to Treat Alzheimer’s Disease? Lessons from Preclinical and Clinical Studies
- Review, AD, NA
*memory↑, GBE displayed generally consistent anti-AD effects in animal experiments, and it might improve AD symptoms in early-stage AD patients after high doses and long-term administration.
*antiOx↑, Antioxidant properties
*Casp3↓, ↓caspase-3
*APP↓, ↓APP
*AChE↓, ↓AChE activity
*Aβ↓, ↓Aβ oligomers
*5HT↑, ↑5-HT in the striatum
*SOD↓, ↓SOD ↓MDA ↓NO
*MDA↓,
*NO↓,
*GSH↑, ↓SOD ↑GSH ↓MDA
*Bcl-2↑, ↑Bcl-2 ↓Bax
*BAX↑,
*TNF-α↓, ↓TNF-α, IL-1β, ccl-2, iNOS, and IL-10
*IL1β↑,
*iNOS↓,
*IL10↓,
*p‑tau↓, ↓tau phosphorylation
*ROS↓, ↓ROS
*MAOB↓, ↓MAO-B enzyme activity
*cognitive↑, A total of 819 patients who had been diagnosed with AD, or that had AD-like symptoms, received lower SKT scores after GBE treatment for 12 to 24 weeks
*neuroP↑, Neuroprotective Mechanism Analysis
*Apoptosis↓, GBE Inhibits Cell Apoptosis

4302- Gins,    Panax ginseng: A modulator of amyloid, tau pathology, and cognitive function in Alzheimer's disease
- Review, AD, NA
*neuroP↑, highlighting neuroprotective mechanisms, such as the inhibition of Aβ production, enhanced Aβ clearance, and suppression of tau hyperphosphorylation.
*Aβ↓,
*p‑tau↓,
*cognitive↑, Research on P. ginseng and its bioactive ginsenosides has shown potential for improving cognitive function in AD models
*eff↑, particularly pronounced effects in individuals lacking apolipoprotein ε4 allele.
*PKA↑, Upregulates the PKA/CREB signaling pathway
*CREB↑,
*BACE/β-secretase↓, Inhibits BACE1 activity
*ADAM10↑, Enhances the expression of ADAM10 and reduces BACE1 expression through the activation of MAPK/ERK and PI3K/AKT
*MAPK↑,
*ERK↑,
*PI3K↑,
*Akt↑,
*NRF2↑, Activates the Nrf2/Keap1 signaling pathway
*PPARγ↓, Inhibits PPARγ phosphorylation and upregulates the expression of IDE
*IDE↑,
*APP↓, downregulates the expression of BACE1 and APP
*PP2A↑, Ginsenoside Rb1 enhances PP2A levels, thereby facilitating tau dephosphorylation and reducing p-tau levels observed in animal studies
*memory↑, The 400 mg dose of ginseng extract significantly improved “Quality of Memory” and “Secondary Memory” at all post-dose time points,

7482- H2,    Molecular Hydrogen Therapy: Mechanisms, Delivery Methods, Preventive, and Therapeutic Application
- Review, Var, NA - Review, IBD, NA - Review, Stroke, NA - Review, Sepsis, NA - Review, AD, NA
Dose↝, H2 can be administered exogenously and is also produced endogenously within the intestinal tract.
*Inflam↓, Anti‐Inflammatory Effect
*IL1β↓, diabetes combined with stroke, H₂ intervention downregulates the expression levels of proinflammatory factors (IL‐1β, IL‐6, TNF‐α), while activating the TLR4/NF‐κB signaling pathway to achieve neuroprotective effects
*IL6↓,
*TNF-α↓,
*neuroP↑,
*mTOR↓, sepsis model, H₂ regulates macrophage polarization (inhibiting the M1 phenotype/promoting the M2 phenotype) and inhibits (mTOR) phosphorylation, reducing the release of inflammatory mediators such as IL‐6, TNF‐α, and HMG
*IL10↑, while increasing the levels of anti‐inflammatory factors IL‐10 and Transforming Growth Factor‐beta (TGF‐β)
*TGF-β↑,
*Sepsis↓,
*NRF2↑, whereas Nrf2 induction suppresses these pathways via redox homeostasis modulation
*antiOx↑, figure 1
*Catalase↑,
*SOD↑,
*GPx↑,
*ROS↓, H₂ mediates ROS regulation through Nrf2, inhibiting NF‐κB/NLRP3 inflammasome activation and achieving an antioxidant–anti‐inflammatory synergistic effect
*HO-1↑, H2 can increase the expression of heme oxygenase‐1 (HO‐1) or activate the phosphatidylinositol‐3‐kinase (PI3K)–Akt signaling pathway to improve liver I/R injury
*PI3K↑,
*Akt↑,
*hepatoP↑,
*MPO↓, reduce myeloperoxidase (MPO) activity and IL‐1β/TNF‐α levels to alleviate myocardial injury
*cardioP↑,
CDK4↓, Studies have demonstrated that H2 inhibits CDK4 and CDK6 to restrict lung cancer progression
CDK6↑,
CD47↓, H₂ can reverse immune escape in lung cancer cells by inhibiting the expression of CD47 and activating the apoptosis program
PI3K↓, H2 promotes apoptosis by downregulating Akt phosphorylation and inhibiting the PI3K signaling pathway in non‐small cell lung cancer.
Akt↓,
Hif1a↓, inhalation of H2 suppresses Hypoxia‐Inducible Factor 1 Alpha Subunit (HIF‐1α)/NF‐κB signaling pathway activation and promotes apoptosis in HeLa cells
selectivity↑, This bidirectional regulatory capability allows H₂ to protect normal tissues from excessive apoptosis (such as inflammation‐induced cell death) while selectively inducing apoptosis in tumor cells.
*MMP↑, howed that after treating septic rats with HRS, the decline in mitochondrial membrane potential (MMP) and ATP content was improved.
*ATP↑,
*ER Stress↓, H₂ alleviated inflammation and organ damage by inhibiting ER stress and activating the autophagy pathway in septic mice
*CHOP/DDIT3↓, H2 could downregulate the expression of CHOP, caspase‐12, and GRP78, while inhibiting p38 and c‐Jun N‐terminal kinase (JNK) phosphorylation, and upregulating the LC3‐II/I ratio
*Casp12↓,
*GRP78/BiP↓,
*p38↓,
*p‑JNK↓,
*LC3‑Ⅱ/LC3‑Ⅰ↑,
*p‑eIF2α↓, HRW prevents IBD in mice by reducing levels of p‐eIF2α, ATF4, XBP1, and CHOP, key proteins in ER stress.
*ATF4↓,
*XBP-1↓,
*Imm↑, H₂ exhibit multidimensional characteristics, primarily enhancing immunity by protecting immune organs,
*IFN-γ↓, H2 treatment inhibited several T‐cell effector molecules, such as IFN‐γ, IL‐4, and GZMB
*IL4↓,
*GranB/GZMB↓,
NK cell↑, After inhaling H₂ for 2 weeks, patients with advanced non‐small cell lung cancer showed significant improvement in T‐cell exhaustion. (NK) subgroups was higher than the pretreatment percentag
radioP↑, HRS can protect against radiation‐induced immune dysfunction by restoring the number of CD4+ T and CD8+ T cells in the spleen.
*CD4+↑,
CD8+↑,
*Dose↝, Common delivery methods include inhalation, oral administration of HRW, injection of HRS, promotion of endogenous H2 production
*other↑, H2, which fall within the explosive range at concentrations ranging from 4 to 74%, it is essential to specify the concentration of H2 for inhalation therapy.
*Dose↝, China National Health Commission recommends the administration of oxygen–H2 mixture (33.3% O2 and 66.6% H2)
*antiPs↑, HRW baths exhibit inhibitory effects on inflammation and oxidative stress while demonstrating therapeutic benefits for conditions such as psoriasis
*BioAv↝, the solubility of H2 in water at room temperature and pressure is limited to a maximum of 0.8mM109, resulting in limited efficacy when orally administered.
*GutMicro↑, inhalation of H2 modulates the gut flora to ameliorate acute alcoholic liver injury. H2 altered the composition of the GM, leading to an increase in the relative abundance of Mycobacterium anisopliae and Mycobacterium thickum
Dose↝, CRC cell lines (ROK/SW480/HCT116) and xenograft mouse models,Inhalation of 66% H2 (66% H2 and 33% O2);Duration: 2 h a day for 21 days
*IBI↑, orally administered silicon H2 nanoparticles (SiH NPs) for targeted scavenging of ROS at inflammatory sites, thereby alleviating symptoms of IBD and restoring GM diversity by enhancing the abundance of beneficial bacteria.
TumCP↓, H2 inhibits tumor cell activity, proliferation, invasion, and migration through various molecular mechanisms, in a manner that depends on both dose and time.
TumCI↓,
TumCMig↓,
CD8+↑, H2 Improves Prognosis by Restoring Depleted CD8+ T Cells in Patients with CRC Cancer
PGC-1α↑, It has been shown that H2 can activate PGC‐1α to restore mitochondrial function and rescue depleted CD8+T cells
Akt↓, H2 Inhibits CRC Cell Proliferation by Suppressing the AKT/SCD1 Pathway
SCD1↓,
*MDA↓, The results showed that H2 water alone significantly improved detected antioxidant markers (SOD and CAT) and reduced MDA levels.
eff↑, combination of H2 water and 5‐fluorouracil significantly attenuated MDA levels more effectively than 5‐fluorouracil alone
*APP↓, H2 gas significantly inhibited the overexpression of APP, BACE1, and sAP, thereby reducing Aβ production.
*BACE/β-secretase↓,
*Aβ↓,
*cognitive↑, This intervention effectively halted the progression of AD, alleviating cognitive impairment, synaptic deficits, and neuronal death
*neuroP↑, regulation of GM(gutmicrobiome) by HRW considered a key mechanism underlying its neuroprotective effects.
NP/CIPN↓, mice with chemotherapy‐induced neuropathic pain caused by oxaliplatin, drinking HRW significantly reduced inflammation by inhibiting the LPS–TLR4 pathway and decreasing the expression of TNF‐α and IL‐6.
*Stroke↓, inhalation of 2% H2 gas significantly reduced levels of myocardial injury markers, such as creatine kinase‐MB and cardiac troponin‐T, while protecting myocardial tissue from further damage by inhibiting autophagy.
*NLRP3↓, daily inhalation of 2% H2 gas for 3 h over 28 days effectively suppressed the activation of the NLRP3 inflammasome, reduced cardiac fibrosis, and improved cardiac function
*ALAT↓, 4% H2 outperforming 67% H2 in reducing liver enzyme levels Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) and lipid accumulation.
*AST↓,
*LPS↓, inhalation of 4% H2 in an NAFLD rat model significantly lowered plasma LPS levels, inhibited the LPS/TLR4/NF‐κB signaling pathway to reduce liver inflammation
*hepatoP↑, drinking HRW, indicating its hepatoprotective effects
chemoP↑, injecting HRS in rats effectively reduced ALT and AST levels caused by doxorubicin, decreased ROS and MDA production, and regulated the Bax/Bcl‐2 ratio to alleviate inflammation and apoptosis.
*creat↓, mouse model of kidney injury induced by a high‐oxalate diet, HRW consumption markedly improved serum creatinine, blood urea nitrogen, and kidney injury markers such as kidney injury molecule‐1 (KIM‐1)
*Urea↓,
*RenoP↑,
*eff↑, higher concentrations of H2 gas (67%) produced more pronounced improvements in kidney histology and morphology compared with lower concentrations (4%)
Apoptosis↑, H2 gas increased apoptosis in A549 cells while reducing the expression of XIAP and BIRC3 proteins in studies on A549 cells and their nude mouse models.
XIAP↓,
IAP2/BIRC3↓,
TumVol↓, inhalation of 60% H2 gas significantly reduced tumor volume in experimental mice
MALAT1↓, In gastric cancer research, Zhu et al. [10] found that H2 gas downregulated the expression of lncRNA MALAT1 and EZH2 while upregulating miR‐124‐3p
EZH2↓,
miR-124-3p↓,
eff↑, combining platinum nanocolloid (Pt‐nc) with H2 gas effectively inhibited the growth of human promyelocytic leukemia HL60 cells
ChemoSen↑, combining H2 therapy with conventional treatments such as chemotherapy and radiotherapy, demonstrating improved efficacy and reduced side effects
*compII↑, allergic airway inflammation, showing that H2 increased ATP production as well as the activity of mitochondrial respiratory chain complexes I and III
*compIII↑,
*LDL↓, H2‐enriched water in humans, showing that supplementation with H2‐enriched water appeared to reduce serum low‐density lipoprotein cholesterol (LDL‐C) and apolipoprotein B (apoB) levels,
*Obesity↓, H2 may play a beneficial role in the prevention of potential metabolic syndrome
QoL↑, 82 patients with stage III and IV cancers receiving H2 inhalation therapy. They found that H2 inhalation improved the quality of life
PFS↑, Sixteen months of follow‐up found that progression‐free survival in the control group was lower than that in the H2 inhalation group alone, and significantly lower than that in the other three combination therapy groups.

3771- H2,    Molecular Hydrogen Neuroprotection in Post-Ischemic Neurodegeneration in the Form of Alzheimer’s Disease Proteinopathy: Underlying Mechanisms and Potential for Clinical Implementation—Fantasy or Reality?
- Review, AD, NA - Review, Stroke, NA
*cognitive↑, hydrogen improves cognitive and neurological deficits and prevents or delays the onset of neurodegenerative changes in the brain.
AntiCan↑, Chinese National Health and Medical Commission in 2020 recommended the use of inhaled hydrogen in addition to oxygen therapy for anti-cancer, anti-inflammatory and anti-oxidant treatments
*Inflam↓,
*antiOx↑,
*ROS↓, Hydrogen has been suggested as a new complementary therapy against stroke, which, e.g., reduces oxidative stress,
*neuroP↑, Molecular Hydrogen Neuroprotection in Post-Ischemic Brain Injury
*SOD↑, molecular hydrogen significantly increases SOD and GSH-Px activity, reduces malondialdehyde levels and infarct volume, relieves cerebral edema, improves neurological outcomes and alleviates cognitive deficits
*GPx↑,
*MDA↑,
*BBB↑, Molecular hydrogen has been shown to protect the permeability of the blood-brain barrier after focal and global cerebral ischemia
*OS↑, It was documented that hydrogen therapy significantly improved the 7-day survival rate of mice after global brain ischemia, from 8.3 to 50%
*Ca+2↓, In addition, hydrogen lowered the increased levels of intracellular Ca2+ caused by glutamate toxicity
*APP↓, Taken together, these results indicate that treatment with hydrogen-rich water prevents proteolysis of the amyloid protein precursor towards amyloid
*p‑tau↓, hydrogen-rich water significantly inhibited the phosphorylation of the tau protein

3767- H2,    The role of hydrogen therapy in Alzheimer's disease management: Insights into mechanisms, administration routes, and future challenges
- Review, AD, NA
*Inflam↓, Hydrogen therapy AD: inflammation, energy regulation, prevents neuronal damage.
*neuroP↑,
*toxicity↓, Hydrogen therapy's low side effects make it a complement to AD treatment. Even at high concentrations, hydrogen gas is still non-toxic, and has been widely used in the diving field.
*antiOx↑, hydrogen’s role as a natural antioxidant,
*ROS↓, Hydrogen has been shown to mitigate the amount of ROS released from mitochondria, thereby reducing mitochondrial DNA peroxidation and inhibiting the expression of NOD-like receptor thermal protein domain associated protein 3 (NLRP3), caspase-1, and I
*NLRP3↓,
*IL1β↓,
*mtDam↓, curtail mitochondrial damage, thereby bolstering ATP synthesis and fortifying the electron transport chain within mitochondria
*ATP↑,
*AMPK↑, activating AMPK and amplifying the downstream antioxidant response of forkhead box O3a (FOXO3
*FOXO3↑,
*SOD1↑, It elevates the levels of intracellular antioxidant enzymes, notably superoxide dismutase 1 (SOD1) and catalase (CAT), thereby serving as a neuroprotective agent that diminishes the risk and progression of AD
*Catalase↑,
*NRF2↑, Hydrogen slows AD progression by activating the cellular endogenous antioxidant system Nrf2;
*NO↓, Reduced inflammatory markers such as ROS, Nitric oxide (NO) and Malondialdehyde (MDA)
*MDA↓,
*lipid-P↓, drinking HRW significantly reduced lipid peroxidation in the brain of SAMP8 mice.
*memory↑, HRW inhibited the decline of learning and memory impairment
*ER(estro)↓, Decreased hormone levels, estrogen receptor (ER) β, and BDNF expression improve cognitive function in female transgenic AD mice.
*BDNF↑, upsurge in BDNF levels, which further ameliorated the cognitive impairments observed in mice affected by sepsis.
*cognitive↑,
*APP↓, The expression of APP, BACE1, and SAPPβ was proficiently suppressed, thereby curtailing the overproduction of Aβ in Alzheimer's
*BACE/β-secretase↓,
*Aβ↓,
*BP∅, inhaling hydrogen gas has no effect on blood pressure and other blood parameters (such as pH, body temperature, etc.),
*BBB↑, efficiently crossing the blood-brain barrier to perform their functions.

3769- H2S,    Research progress of hydrogen sulfide in Alzheimer's disease from laboratory to hospital: a narrative review
- Review, AD, NA
*APP↓, prevent the progress of the disease by affecting the amyloid precursor protein metabolism, anti-apoptosis, anti-inflammatory, and antioxidant pathways.
*Apoptosis↓,
*Inflam↓,
*antiOx↑,
*BP↓, H2S activates adenosine triphosphate-sensitive potassium channels, which in turn dilates blood vessels and lowers blood pressure, while improving myocardial ischemia-reperfusion injury
*NLRP3↓, activation of NLRP3 inflammatory bodies was inhibited
*ROS↓, catalase may be a key enzyme in the metabolism of H2S, which can convert H2S into sulfide, thereby achieving scavenging effect.
*Aβ↓, H2S can promote APP's non-amyloid metabolic pathway and reduce Aβ production.
*ER Stress↓, H2S may up-regulate brain-derived neurotrophic factor-TrkB pathway to suppress the stress of the endoplasmic reticulum,

7500- H2S,    Hydrogen sulfide ameliorates learning memory impairment in APP/PS1 transgenic mice: A novel mechanism mediated by the activation of Nrf2
- in-vivo, AD, NA
*neuroP↑, Hydrogen sulfide (H2S) has been recognized as a cytoprotectant, which improves learning memory impairment and exerts antioxidant effects in neurodegenerative disorders, including AD.
*memory↑,
*CBS↑, intraperitoneal (i.p.) injection of NaHS improved learning memory deficits, decreased the number of senile plaques, Aβ1-40 and Aβ1-42 levels, suppressed neurons loss, together with up-regulated the levels of cystathionine-β-synthase (CBS) and 3MST
*3MST/MPST↑,
*APP↓, the protein levels of beta-amyloid precursor (APP) and beta-secretase 1 (BACE1) were dramatically restrained after administration of H2S
*BACE/β-secretase↓,
*NRF2↑, H2S exerted antioxidant effects via up-regulation nuclear factor erythroid-2-related factor 2 (Nrf2), heme oxygenase-1(HO-1) and glutathione S-transferase (GST).
*HO-1↑,
*GSTs↑,
*Aβ↓, inhibition of Aβ production and activation of Nrf2/antioxidant response element (ARE) pathway.
*ARE↑,

7836- ISQ,    An Isoquinolinium Dual Inhibitor of Cholinesterases and Amyloid β Aggregation Mitigates Neuropathological Changes in a Triple-Transgenic Mouse Model of Alzheimer's Disease
- in-vivo, AD, NA
*AChE↓, In vitro studies revealed that 9Q exhibited over 80% inhibition of ChE activity at 100 μM and more than 30% inhibition of Aβ aggregation at 1 mM concentration.
*Aβ↓,
*BBB↑, Moreover 9Q was able to penetrate the blood-brain barrier (BBB) and enhance the cerebral acetylcholine level in triple transgenic AD (3xTg-AD) mice.
*Ach↑,
*cognitive↑, Following one month treatment with 9Q, the amyloid burden and the cognitive deficits in 3xTg-AD mice were significantly ameliorated.
*APP↓, decreased amyloidogenic APP processing, and reduced the tau pathology in 3xTg-AD mice.
*tau↓,
*eff↑, our results suggested that dual inhibition of cholinesterases and Aβ aggregation could be a promising approach in AD treatment.

2385- MET,    Metformin activates chaperone-mediated autophagy and improves disease pathologies in an Alzheimer disease mouse model
- in-vitro, AD, H4 - in-vitro, NA, HEK293 - in-vivo, NA, NA - in-vitro, NA, SH-SY5Y
*HK2↓, Metformin also induced degradation of two endogenous CMA substrates—HK2 and PKM2 (pyruvate kinase isozyme type M2), at both 20 mmol/L and 20 µmol/L doses of the drug
*PKM2↓,
*Dose↝, We chose these two doses due to the robustness of the 20 mmol/L dose and due to the clinical relevance of the 20 µmol/L dose, as the Metformin serum concentrations in patients receiving this drug are ~20 µmol/L
IKKα↑, Metformin activates TAK1-IKKα/β signaling
memory↑, Metformin-treated APP/PS1 mice showed improved learning and spatial memory
p‑Hsc70↑, Metformin treatment also significantly reduced the protein levels of APP and induced Hsc70 phosphorylation at Ser85, consistent with our findings in cell culture
APP↓, Metformin induced degradation of endogenous APP proteins in SH-SY5Y cell

3835- Moringa,    Moringa Oleifera Alleviates Aβ Burden and Improves Synaptic Plasticity and Cognitive Impairments in APP/PS1 Mice
- in-vivo, AD, NA
*antiOx↑, multiple effects such as Moringa oleifera (MO) that have strong anti-oxidative, anti-inflammatory, anticholinesterase, and neuroprotective virtues.
*Inflam↓,
*AChE↓,
*neuroP↑,
*Mood↑, MO improved behavioral deficits such as anxiety-like behavior and hyperactivity and cognitive, learning, and memory impairments.
*cognitive↑,
*memory↑,
*Aβ↓, MO treatment abrogated the Aβ burden to wild-type control mice levels via decreasing BACE1 and AEP and upregulating IDE, NEP, and LRP1 protein levels.
*BACE/β-secretase↓,
*AEP↓,
*IDE↑,
*NEP↑,
*LRP1↑,
*PSD95↑, MO improved synaptic plasticity by improving the decreased GluN2B phosphorylation, the synapse-related proteins PSD95 and synapsin1 levels, the quantity and quality of dendritic spines, and neurodegeneration in the treated mice
*STEP↓, These results suggest that MO modulates the PP2B/DARPP-32/PP1 axis to downregulate STEP activity thereby improving GluN2B Tyr1472 phosphorylation in APP/PS1 mice.
*APP↓, data suggest that MO downregulates the amyloidogenic processing of APP as well as improves Aβ clearance to decrease the Aβ burden in these mice.

3810- mushLions,    Key Mechanisms and Potential Implications of Hericium erinaceus in NLRP3 Inflammasome Activation by Reactive Oxygen Species during Alzheimer’s Disease
- Review, NA, NA
*neuroP↑, Hericium erinaceus administration reduced behavioral changes and hippocampal neuronal degeneration.
*p‑tau↓, it reduced phosphorylated Tau levels, aberrant APP overexpression, and β-amyloid accumulation.
*APP↓,
*Aβ↓,
*ROS↓, ericium erinaceus decreased the pro-oxidative and pro-inflammatory hippocampal alterations induced by AD
*Inflam↓,
*NLRP3↓, In particular, it reduced the activation of the NLRP3 inflammasome components, usually activated by increased oxidative stress during AD.

3943- Shank,    Protective Mechanisms of Nootropic Herb Shankhpushpi (Convolvulus pluricaulis) against Dementia: Network Pharmacology and Computational Approach
- Review, AD, NA
*neuroP↑, Experimental evidence suggests various neuroactive potentials of CP such as memory-enhancing, neuroprotective, and antiepileptic.
*memory↑,
*other↝, analysis predicted a total of five druglike phytochemicals from CP constituents, namely, scopoletin, 4-hydroxycinnamic acid, kaempferol, quercetin, and ayapanin
*AChE↓, scopoletin showed the highest binding affinity with PTGS1, NOS3, PPARG, ACHE, MAOA, MAOB, and TRKB
*MAOA↓,
*MAOB↓,
*TrkB↓,
*tau↓, CP treatment prevented protein and mRNA expressions of tau and amyloid precursor protein (APP) in scopolamine-induced rat brain
*APP↓,
*ROS↓, Scopoletin, a coumarin of CP, attenuated oxidative stress-mediated loss of dopaminergic neurons and increased the efficacy of dopamine in PD model
*Mood↑, In addition, CP improved anxiety, depression, and epileptic seizure

4314- VitB1/Thiamine,    Unraveling the molecular mechanisms of vitamin deficiency in Alzheimer's disease pathophysiology
- Review, AD, NA
*Risk↓, Its deficiency disrupts glucose metabolism, impairs neurotransmitter production and DNA synthesis, and increases the risk of AD and neurological deficits
*GlucoseCon↑,
*cognitive↑, Thiamine supplementation, especially benfotiamine, has been shown to improve cognitive function in mild AD, while higher dietary intake supports cognitive impairments
*ATP↑, Low thiamine impairs glucose metabolism, reducing ATP production and increasing ROS, leading to mitochondrial and synaptic dysfunction, key features of AD.
*ROS↓,
*NADPH↑, Thiamine aids in producing ribose-5-phosphate and NADPH, essential for nucleotide synthesis.
*Aβ↓, Low thiamine reduces antioxidant capacity, leading to ROS accumulation and oxidative damage to proteins, lipids, and DNA. This triggers neurodegeneration processes, including development of Aβ plaques
*APP↓, The increase in APP activates beta-site APP cleaving enzymes-1 (BACE1), promoting its cleavage and enhancing the secretion of the Aβ monomers.
*BACE/β-secretase↓,

4037- VitB12,  FA,    Mechanistic Link between Vitamin B12 and Alzheimer’s Disease
- Review, AD, NA
*antiOx↑, antioxidant properties of vitamin B12 are discussed to be accomplished by different mechanisms, including direct scavenging of ROS, particularly superoxide in the cytosol and mitochondria
*ROS↓,
*GSH↑, indirectly stimulating ROS scavenging by preservation of glutathione [
*Inflam↓, vitamin B12 might protect against inflammation-induced oxidative stress by modulating cytokine and growth factor production, including interleukin-6, tumour necrosis factor alpha (TNF-α) and epidermal growth factor.
*IL6↓,
*TNF-α↓,
*other↑, Vitamin B12 is an important cofactor of methionine-synthase, converting homocysteine into methionine.
*other↑, A folate and/or vitamin B12 deficiency with a reduction in genomic and non-genomic methylation processes caused by folate and/or vitamin B12 deficiency, might lead to decreased DNA stability
*other↑, methionine metabolism strongly depends on three important cofactors, namely, folate (vitamin B9), vitamin B6 and vitamin B12.
*Aβ↓, elevation of Aβ deposits in the hippocampus and cortex of an AD mouse model fed with a folate/vitamin B6/vitamin B12-deficient diet.
*memory↑, The simultaneous supplementation of folate and vitamin B12 attenuated the hyperhomocysteinemic-induced changes in APP processing and improved memory in these rats.
*p‑tau↓, Supplementation of folate and vitamin B12 also revealed positive effects on Aβ level and tau hyperphosphorylation in the retina of hyperhomocysteinemic three- to four-month-old rats
*APP↓, Notably, this increase in the APP, PS1 and BACE1 protein levels could be reverted by folate/vitamin B12 supplementation.
*BACE/β-secretase↓,
*ATP↑, C. elegans receiving a vitamin B12-containing diet showed a higher ATP level, decreased mitochondrial fragmentation and reduced oxidative species (ROS) than those without vitamin B12.
*neuroP↑, Significant neuroprotective effects of vitamin B12 were already apparent at 2 µM vitamin B12


Showing Research Papers: 1 to 28 of 28

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 28

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

CD47↓, 1,   miR-124-3p↓, 1,   PFS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

PGC-1α↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

SCD1↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   Apoptosis↑, 1,   IAP2/BIRC3↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

EZH2↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

p‑Hsc70↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK4↓, 1,  

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

PI3K↓, 1,  

Migration(tgid=13) ⓘ

APP↓, 1,   MALAT1↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IKKα↑, 1,   NK cell↑, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   Dose↝, 2,   eff↑, 2,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EZH2↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   chemoP↑, 1,   memory↑, 1,   NP/CIPN↓, 1,   QoL↑, 1,   radioP↑, 1,   TumVol↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 2,  
Total Targets: 35

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

3MST/MPST↑, 1,   CBS↑, 1,   compII↑, 1,   NeuroI↓, 2,   Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 2,   antiOx↑, 10,   ARE↑, 1,   Catalase↑, 4,   GPx↑, 2,   GSH↑, 4,   GSTs↑, 1,   HO-1↑, 4,   lipid-P↓, 2,   MDA↓, 5,   MDA↑, 1,   MPO↓, 1,   NRF2↑, 6,   ROS↓, 18,   SOD↓, 1,   SOD↑, 3,   SOD1↑, 1,   TAC↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 5,   compIII↑, 1,   MMP↑, 1,   mtDam↓, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   AMPK↑, 1,   CREB↑, 1,   GlucoseCon↑, 1,   HK2↓, 1,   LDL↓, 1,   NADPH↑, 1,   PDK1↓, 1,   PKM2↓, 1,   PPARα↑, 1,   PPARγ↓, 1,   PPARγ↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Akt↑, 5,   p‑Akt↑, 1,   Apoptosis↓, 5,   BAX↑, 1,   Bcl-2↑, 1,   Casp12↓, 1,   Casp3↓, 2,   GranB/GZMB↓, 1,   iNOS↓, 3,   p‑JNK↓, 1,   MAPK↓, 2,   MAPK↑, 1,   p38↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 3,   other↑, 4,   other↝, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↓, 1,   p‑eIF2α↓, 1,   ER Stress↓, 2,   GRP78/BiP↓, 1,   HSP70/HSPA5↑, 1,   HSP90↑, 1,   XBP-1↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   LC3B↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,  

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

ERK↑, 2,   p‑ERK↑, 2,   FOXO3↑, 1,   GSK‐3β↓, 2,   mTOR↓, 2,   P70S6K↓, 1,   PI3K↓, 1,   PI3K↑, 2,  

Migration(tgid=13) ⓘ

APP↓, 26,   cl‑APP↓, 1,   Ca+2↓, 3,   CD31/PECAM-1↑, 1,   LRP1↑, 2,   MMP-10↝, 1,   N-cadherin↑, 1,   PKA↑, 1,   TGF-β↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

ATF4↓, 1,   NO↓, 2,   VEGF↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 8,   IBI↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1,   COX2/PTGS2↓, 1,   IFN-γ↓, 2,   IL10↓, 1,   IL10↑, 2,   IL1β↓, 6,   IL1β↑, 1,   IL2↓, 1,   IL4↓, 1,   IL4↑, 1,   IL6↓, 4,   Imm↑, 1,   Inflam↓, 14,   LPS↓, 1,   NF-kB↓, 2,   p‑NF-kB↓, 1,   TNF-α↓, 8,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1,   AChE↓, 7,   ADAM10↑, 1,   ADAM10↝, 1,   BChE↓, 1,   BDNF↑, 2,   BDNF∅, 1,   MAOA↓, 2,   PSD95↑, 1,   tau?, 1,   tau↓, 3,   p‑tau↓, 9,   TrkB↓, 1,  

Protein Aggregation(tgid=19) ⓘ

AEP↓, 1,   Aβ↓, 22,   BACE/β-secretase↓, 14,   IDE↑, 2,   MAOB↓, 3,   NEP↑, 1,   NLRP3↓, 4,   PP2A↑, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

ER(estro)↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 4,   BioAv↝, 2,   Dose↑, 1,   Dose↝, 6,   eff↑, 4,   Half-Life↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   BP↓, 1,   BP∅, 1,   creat↓, 1,   GutMicro↑, 2,   IL6↓, 4,   Urea↓, 1,  

Functional Outcomes(tgid=23) ⓘ

antiPs↑, 1,   cardioP↑, 2,   cognitive↑, 18,   hepatoP↑, 2,   memory↑, 13,   Mood↑, 2,   motorD↑, 1,   neuroP↑, 19,   Obesity↓, 1,   OS↑, 1,   RenoP↑, 1,   Risk↓, 2,   STEP↓, 1,   toxicity↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

Sepsis↓, 1,  
Total Targets: 158

Scientific Paper Hit Count for: APP, amyloid precursor protein
4 Berberine
3 Hydrogen Gas
2 Ferulic acid
2 hydrogen sulfide
1 Anthocyanins
1 Phyllanthus emblica/Emblica officinalis/Amla / Indian Gooseberry
1 Caffeic acid
1 Chlorogenic acid
1 Mung Bean Sprouts
1 Capsaicin
1 Choline
1 Cichoric acid / Chicoric acid
1 EGCG (Epigallocatechin Gallate)
1 Curcumin
1 Phosphatidylserine
1 Gallic acid
1 Ginkgo biloba
1 Ginseng
1 isoquercitrin
1 Metformin
1 Moringa oleifera
1 Mushroom Lion’s Mane
1 Shankhpushpi
1 Vitamin B1/Thiamine
1 Vitamin B12
1 Folic Acid, Vit B9
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#:1300  State#:%  Dir#:1
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