cognitive Cancer Research Results
cognitive, cognitive: Click to Expand ⟱
Scientific Papers found: Click to Expand⟱
*cognitive↓, Data from French cohort have demonstrated that aluminium in drinking water seems to have a deleterious effect and increased the risk of cognitive impairment when the silica concentrations were low.
*cognitive↓, high levels of aluminum appeared to have a deleterious effect when the silica concentration was low,
*Risk↑, These findings support the hypothesis that aluminum in drinking water is a risk factor for AD. This result was confirmed for AD (adjusted relative risk=2.20, 95 percent CI 1.24–3.89)
*cognitive↓,
*BioAv↑, As suggested by Taylor,30 it is plausible that there is an increase in aluminum absorption with age, so the effect of aluminum may be larger after 75 years than before.
*Risk↑, The unequivocal neurotoxicity of aluminum must mean that when brain burdens of aluminum exceed toxic thresholds that it is inevitable that aluminum contributes toward disease.
*cognitive↓, EVIDENCE NOW POINTS TO ALUMINUM AS A CONTRIBUTORY FACTOR IN ALL FORMS OF ALZHEIMER’S DISEASE
*neuroP↓, We also know that the addition of aluminum to feed or water exacerbates the many symptoms of Alzheimer’s disease in these animal models
*other↑, Postmortem analyses of their brain tissues revealed very high levels of aluminum.
*other↝, physical exercise can increase the perspiration volume many times and so improve the excretion of aluminum from the body.
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*neuroP↑, BAs-induced neuroprotection is proposed to be associated with the ability to reduce neurotoxic aggregates, decrease oxidative stress, and improve cognitive dysfunction.
*ROS↓,
*cognitive↓,
TumCP↓, BAs have been suggested as potential agents for the treatment of brain tumors due to their potential to attenuate cell proliferation, migration, metastasis, angiogenesis, and promote apoptosis during both in vitro and in vivo studies
TumCMig↓,
TumMeta↓,
angioG↓,
Apoptosis↑,
*Inflam↓, The anti-inflammatory activities of BAs have been investigated in many preclinical and clinical trials
IL1↓, BAs inhibit the production of pro-inflammatory cytokines such as interleukin-1 (IL-1), IL-2, IL-4, IL-6, and tumor necrosis factor-α (TNF-α) in several experimental studies.
IL2↓,
IL4↓,
IL6↓,
TNF-α↓,
P53↑, AKBA has been reported to induce apoptosis in pancreatic and gastric cancers, through tumor suppressor protein 53 (p53)-independent pathway, while reducing expression of protein kinase (PK) B and NF-kb
Akt↓,
NF-kB↓,
DNAdam↑, DNA fragmentation, and activation of caspase cascade
Casp↑,
COX2/PTGS2↓, regulated genes such as cyclooxygenase-2 (COX-2), matrix metallopeptidase-9 (MMP-9), C-X-C motif chemokine receptor 4 (CXCR4), and vascular endothelial growth factor (VEGF)
MMP9↓,
CXCR4↓,
VEGF↓,
*SOD↑, BAs against oxidative injury has been shown in several cell lines and animal models [12], [13], [21]. BAs exert protective effects through the normalization of antioxidant enzyme levels, such as superoxide dismutase (SOD), catalase, and glutathione p
*Catalase↑,
*GPx↑,
*NRF2↑, Moreover, it can activate nuclear factor erythroid 2-related factor-2 (Nrf2)/antioxidant response element-regulated pathways
AntiCan↑, Chlorogenic acid (5-caffeoylquinic acid, CGA), found in plants and vegetables, is promising in anticancer mechanisms.
*chemoP↑, CGA can overcome resistance to conventional chemotherapeutics and alleviate chemotherapy-induced toxicity by scavenging free radicals effectively.
TNF-α↓, CGA reduces inflammation levels in renal tissues by down-regulating tumor necrosis factor-alpha (TNF-α) and cyclooxygenase-2 (COX-2),
COX2/PTGS2↓,
IL6↓, Moreover, CGA exhibits a protective effect against 5-FU-induced ovarian tissue damage, reducing Interleukin 6 (IL-6) levels;
eff↑, CGA suppresses the expression of Programmed Cell Death Ligand 1 (PD-L1) on cancer cells, boosting the antitumor effect of the anti-PD-1 antibody and enhancing anticancer immunotherapy
PD-L1↓,
*cognitive↓, CGA, have shown promise in preventing cognitive dysfunction and suppressing amyloid β plaques
*Aβ↓,
*TAC↑, hyperlipidemic patients who ingested 200 mL of Mate tea (12.5 mg/mL) daily experienced a significant increase in serum total antioxidant status and the enzymatic activity of superoxide dismutase (SOD),
*SOD↑,
*eff↑, In blueberry jam production, the high-temperature processing of blueberries with sucrose promoted the formation of 11 CGA derivatives
*eff↑, roasting process (170 to 200 °C/10 to 30 min) of coffee beans promotes CGA transformation to four chlorogenic acid lactones
ChemoSen↑, CGA was found to increase the sensitivity of hepatocellular carcinoma cells to 5-FU treatment
tumCV↓, CGA was shown to collaborate by significantly reducing cell viability and growth through induction of apoptosis, attributed to inhibition of extracellular signal-regulated kinases (ERKs)
Apoptosis↑,
ERK↓,
chemoP↑, Protective Role of Chlorogenic Acid against Toxicity Induced by Chemotherapy
*GPx↑, figure4
*GSTs↑,
*GSH↑,
*SOD↑,
*Catalase↑,
*ROS↓,
*lipid-P↓,
*MDA↓,
*Casp3↓,
*HO-1↓,
cardioP↑, reported the cardioprotective effect of CGA against doxorubicin-induced cardiotoxicity in female Swiss albino mice.
radioP↑, The radioprotective potential of CGA against γ-radiation-induced chromosomal damage in male albino Swiss mice was initially demonstrated in 1993.
*TMAO↑, (HFD) promotes cardiovascular disease, in part because it is rich in quaternary amines such as choline, carnitine, and lecithin, which are converted to trimethylamine (TMA) by the gut microbes and increase levels of circulating TMAO
*cognitive↓, TMAO induces cognitive impairment via disrupting the BBB. TMAO treatment induced cognitive impairment and disrupted the BBB integrity in mice
*BBB↝, TMAO has been reported to regulate blood-brain barrier (BBB) integrity and suppress the expression of tight junction proteins (TJs) in the microvasculature.
*TJ↝,
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*TMAO↑, The gut microbiota’s role in metabolizing phytoestrogens suggests that these compounds can modulate the microbial community structure, potentially affecting the production of TMAO from dietary choline and carnitine [5].
*ROS↑, TMAO has the ability to induce oxidative stress in cells by promoting the production of reactive oxygen species (ROS).
*NADPH↑, TMAO has been shown to increase the activity of NADPH oxidase [30], an enzyme that generates ROS as part of its normal function.
*Ca+2↑, TMAO enters platelets and facilitates the release of calcium ions (Ca2+) from intracellular stores.
*AntiAg↓, Calcium serves as a critical secondary messenger in platelet activation, and its elevated levels promote platelet aggregation and thrombus formation
*cognitive↓, TMAO has been linked to cognitive decline and neurodegenerative disorders, including Alzheimer’s disease (AD). Through an integrated analysis of genetic, epigenetic, pathological, and biochemical data, Xu et al. identified a correlation between gut m
*TJ↓, However, excessive TMAO concentrations disrupt BBB integrity by inhibiting tight junction proteins, including claudin-5 and zonula occludens-1
*CLDN1↓,
*ZO-1↓,
*Inflam↑, TMAO also triggers neuroinflammation by activating the NLRP3 inflammasome,
*NLRP3↑,
*ER Stress↑, TMAO enhances the ER stress response by activating the PERK-eIF2α pathway, which is known to impair synaptic plasticity and neuronal function, processes strongly implicated in AD progression
*cognitive↓, TMAO has been identified as the most predictive biomarker for memory impairment and cognitive decline among 56 microbiota-derived metabolic markers
*Dose↝, use of cooking methods such as boiling or stewing instead of grilling, which can produce higher amounts of TMAO
*eff↑, Studies suggest that Lactobacillus plantarum ZDY04 could help reduce TMAO concentrations and prevent TMAO-induced atherosclerosis in animal models
*other↝, Currently, no medications specifically designed to reduce blood TMAO levels exist
*other↝, a review published in 2025 has highlighted the potential role of statins in lowering TMAO levels independently of their cholesterol-lowering effects
*other↝, scientific evidence suggests that statins selectively inhibit the growth of pathogenic bacteria, such as Clostridium and Ruminococcus, while promoting beneficial species, such as Bifidobacterium and Lactobacillus
*cognitive↓, 1-year administration of saffron extract capsules showed to be comparable with memantine in reducing cognitive decline in patients with moderate to severe AD.
*BioAv↑, Ferulic acid (4-hydroxy-3-methoxycinnamic acid) is abundant in some cereal grains and shows relatively higher absorption in the gastrointestinal mucosa compared to other phenolic acids
*cognitive↓, oral administration of ferulic acid (200 mg/d plus 40 mg of Angelica archangelica extract) daily for 48 weeks improved the mild cognitive impairment in populations aged 65−85 years old.
*Dose↝, ferulic acid (200 mg/d plus 40 mg of Angelica archangelica extract) daily for 48 weeks
*neuroP↑, ferulic acid might possess great neuroprotective potential in the neurodegenerative diseases.
*Aβ↓, ferulic acid reduced Aβ plaque deposits via inhibiting β-secretase (BACE1) activity and cleavage, as well as enhancing α-secretase (ADAM10) activity and cleavage in APP/PS1 mice
*BACE/β-secretase↓,
*ADAM10↑,
*Ac-histone H3↑, ferulic acid improved the cholinergic deficits as indicated by the increased ACh level in the cortex of Aβ1−42 -injected (i.c.v.) mice after ferulic acid treatmen
*BloodF↑, rerulic acid improved the cerebral blood flow (CBF) and insulin resistance, which helped to reduce the progression of AD pathology
*IRes↑,
*memory↑, while ferulic acid treatment (20 mg/kg, p.o.) improved the capillary hypofunction and reduced the memory deficits of APP/PS1 mice.
*Dose↝, Notably, the effective doses of ferulic acid in rodents were 5.3−30 mg/kg when administered for more than 4 weeks, which could be achieved through daily intake of appropriate amount of mung bean
*other↑, We showed that even low cumulative consumption of fruits/juices (>0.2 fruit‐years) or any consumption of herbal tea from Annonaceae worsen disease severity and cognitive deficits in degenerative parkinsonism including Parkinson's disease
*cognitive↓,
*Risk↑, consumption of at least 10 fruit‐years (ie, one fruit/day every day for 10 years) of an Annonaceae fruit, Annona muricata, increased the risk of AP. 2
*cognitive↓, Menopausal hormone therapy (MHT) reportedly increases the risk of cognitive decline in women over age 65 y.
*Stroke↑, Both hormone therapy regimens decreased fractures but increased stroke, thromboembolic events, gallbladder disease, and urinary incontinence.
Risk⇅, Estrogen plus progestin increased breast cancer and probable dementia, while estrogen alone decreased breast cancer.
*cognitive↓,
*cognitive↓, We found that long-term EMP exposure induced cognitive damage in rats.
*BACE/β-secretase↑, BACE1) and microtubule-associated protein 1 light chain 3-II (LC3-II) in EMP-exposed rats hippocampus were also higher than that of sham-exposed rats.
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*neuroP↑, Vitexin contributes to increasing neuroprotective factors and pathways and counteract the targets that induce neurodegeneration, such as redox imbalance, neuroinflammation, abnormal protein aggregation, and reduction of cognitive and/or motor impairm
*Inflam↓,
*cognitive↓,
*motorD↑,
*BACE/β-secretase↓, Vitexin has also been shown to limit the formation of beta-amyloid peptides by inhibiting the enzyme BACE1,
*LDH↓, This increase in viability was observed by reducing the levels of lactate dehydrogenase (LDH) in a dose-dependent manner, with a maximum increase in viability in vitexin treatment at 150 μg/mL
*AChE↓, potent inhibition of cholinesterase types (AChE and BChE) in RAW 264 cells,
*BChE↓,
*ROS↓, reduction of oxidative stress, neuroinflammation
Showing Research Papers: 1 to 15 of 15
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 15
Pathway results for Effect on Cancer / Diseased Cells:
Cell Death(tgid=5) ⓘ
Akt↓, 1, Apoptosis↑, 2, Casp↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
tumCV↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 1, P53↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↓, 1,
Migration(tgid=13) ⓘ
MMP9↓, 1, TumCMig↓, 1, TumCP↓, 1, TumMeta↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 1, VEGF↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 2, CXCR4↓, 1, IL1↓, 1, IL2↓, 1, IL4↓, 1, IL6↓, 2, NF-kB↓, 1, PD-L1↓, 1, TNF-α↓, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 1, eff↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
IL6↓, 2, PD-L1↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1, cardioP↑, 1, chemoP↑, 1, radioP↑, 1, Risk⇅, 1,
Total Targets: 31
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
IRes↑, 1, Stroke↑, 1, TMAO↑, 2,
Redox & Oxidative Stress(tgid=1) ⓘ
Catalase↑, 2, GPx↑, 2, GSH↑, 1, GSTs↑, 1, HO-1↓, 1, lipid-P↓, 1, MDA↓, 1, NRF2↑, 1, ROS↓, 3, ROS↑, 1, SOD↑, 3, TAC↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
Ac-histone H3↑, 1, LDH↓, 1, NADPH↑, 1,
Cell Death(tgid=5) ⓘ
Casp3↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↑, 2, other↝, 4,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1,
Migration(tgid=13) ⓘ
AntiAg↓, 1, Ca+2↑, 1, CLDN1↓, 1, TJ↓, 1, TJ↝, 1, ZO-1↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↝, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
Inflam↓, 2, Inflam↑, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↓, 1, ADAM10↑, 1, BChE↓, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 2, BACE/β-secretase↓, 2, BACE/β-secretase↑, 1, NLRP3↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 2, Dose↝, 3, eff↑, 3,
Clinical Biomarkers(tgid=22) ⓘ
BloodF↑, 1, LDH↓, 1,
Functional Outcomes(tgid=23) ⓘ
chemoP↑, 1, cognitive↓, 16, memory↑, 1, motorD↑, 1, neuroP↓, 1, neuroP↑, 3, Risk↑, 3,
Total Targets: 50
Scientific Paper Hit Count for: cognitive, cognitive
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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