cognitive Cancer Research Results
cognitive, cognitive: Click to Expand ⟱
Scientific Papers found: Click to Expand⟱
*cognitive↑, The odds of IADL impairment increased significantly with decreasing intake of vitamins B2, B6, and B12
*neuroP↑, possible long-term neuroprotective effect of dietary fibre, n-3 polyunsaturated fats, and B-group vitamins, and support dietary intervention to prevent cognitive decline.
*other↝, Recent cognitive decline was associated with lower intakes of poultry, fish, and animal fats, as well as higher intakes of dairy dessert and ice-cream.
*other⇅, IADL impairment was associated with lower intake of vegetables
*cognitive↑, Vitamin B12 deficiency causes treatable dementia and vitamin B12 supplementation has been reported to improve cognitive function
*memory↑, Kobe et al. reported that low vitamin B12 concentration within the normal range is poorer memory performance which is an effect that is partially mediated by hippocampal microsurgical integrity examined by MRI
*Mood↑, The improvement in cognitive function may have been associated with improvement in mood disorders, at least in part
*cognitive↑,
*Dose↝, 100mg nightly
*5HT↑,
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*other↝, exact causes of neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS) are not fully understood, researchers believe that regulating the 5-HT system could help alleviate symptoms
*cognitive↑, 5-HT-related drugs may also improve the most prominent cognitive impairment issues in AD.
*memory↑, 5-HT6 receptor antagonists (such as idalopirdine) have the potential to improve memory and learning abilities in clinical trials.
*Ach↑, 5-HT4 receptor agonists can enhance acetylcholine release, which helps improve cognitive function and memory formation.
*5HT↑, Moreover, the 5-HTP group showed a significant increase in serum serotonin levels.
*cognitive↑, 5-HTP supplementation can enhance cognitive performance and reduce symptoms of depression in Singaporean older adults, potentially through serotonergic modulation.
*BBB↑, 5-HTP could cross the blood-brain barrier and synthesize serotonin, thereby effectively elevating serotonin levels
*Mood↑, Prior studies have also observed the effect of 5-HTP on mood regulation, especially improvements in patients with depression
*cognitive↑, Improved recognition of positive emotions with TRP in older participants supports the use of a TRP-rich diet to compensate for age related decline in social-cognitive processes.
*Dose↝, they took cellulose capsules containing either 200 mg 5-HTP (extracted from Griffonia simplicifolia) or placebo (cellulose and mannitol) with a 200 ml mixture of fruit juice (15–20%) and water.
*cognitive↑, the neurotransmitter serotonin plays a significant role in cognition.
*other↑, Low glycemic index foods seem to improve attention, memory and functional capacity, while those rich in simple sugars are associated with difficulty in concentration and attention.
*other↓, Low levels of serotonin have been linked to decreased learning, reasoning and memory.
*cognitive↑, It is advisable to consume diets with an adequate ratio (5:1) of omega-6: 3 fatty acids (Mediterranean diet) given that they are associated with better memory capacity and lower risk of cognitive deterioration.
*eff↑, Vitamins B1, B6, B12, B9 (folic acid) and D, choline, iron and iodine exert neuroprotective effects and improve intellectual performance.
*eff↑, In parallel, antioxidants (vitamins C, E, A, zinc, selenium, lutein and zeaxanthin) have a very important role in the defense against oxidative stress associated with mental deterioration and in the improvement of cognition.
*cognitive↑, Previous studies have found that cognitive impairment and neuronal damage were effectively alleviated by blueberry extract (BBE) in AD mice
*LDH↓, including decreased neuron viability and increased levels of lactate dehydrogenase and reactive oxygen species, was effectively reversed by PCA
*ROS↓,
*neuroP↑, proved PCA may be the main bioactive metabolite of BBE for neuroprotective effects, providing a basis for dietary intervention in AD.
*memory↑, We observed improved performances for the blueberry group on measures of lexical access, p = 0.003, and memory interference, p = 0.04, and blueberry-treated participants reported reduced memory encoding difficulty in daily life activities
*cognitive↑, The cognitive findings indicated improved executive ability in this middle-aged sample.
*ROS↓, reduced oxidative stress, preservation of tissue function with aging, and with extended lifespan
*antiOx↑, Blueberries contain polyphenolic compounds, most prominently anthocyanins, which have antioxidant and anti-inflammatory effects.
*Inflam↓,
*memory↑, anthocyanins have been associated with increased neuronal signaling in brain centers mediating memory function as well as improved glucose disposal, benefits that would be expected to mitigate neurodegeneration.
*neuroP↑, preliminary study suggest that moderate-term blueberry supplementation can confer neurocognitive benefit
*cognitive↑, At 12 weeks, we observed improved paired associate learning (p = 0.009) and word list recall (p = 0.04).
*Mood↑, In addition, there were trends suggesting reduced depressive symptoms (p = 0.08) and lower glucose levels (p = 0.10)
*glucose↓,
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*cardioP↑, Epidemiological studies associate regular, moderate intake of blueberries and/or anthocyanins with reduced risk of cardiovascular disease, death, and type 2 diabetes, and with improved weight maintenance and neuroprotection.
*neuroP↑,
*Inflam↓, Among the more important healthful aspects of blueberries are their anti-inflammatory and antioxidant actions and their beneficial effects on vascular and glucoregulatory function
*antiOx↓,
*GutMicro↑, Blueberry phytochemicals may affect gastrointestinal microflora and contribute to host health
*Half-Life↑, However, >50% of the 13C still remained in the body after 48 h
*LDL↓, controlled study of 58 diabetic patients, blueberry intake led to a decline in LDL cholesterol, triglycerides, and adiponectin and an increase in HDL cholesterol
*adiP↓,
*HDL↑,
*CRP↓, reduction was documented in inflammatory markers, including serum high-sensitivity C-reactive protein, soluble vascular adhesion molecule-1, and plasma IL-1β
*IL1β↓,
*Risk↓, lower Parkinson disease risk was associated with the highest quintile of anthocyanin (RR: 0.76) and berry (RR: 0.77) intake
*Risk↓, Nurse's Health Study, greater intake of blueberries and strawberries was associated with slower rates of cognitive decline in older adults, with an estimated delay in decline of about 2.5 y
*cognitive↑, Cognitive performance in elderly adults improved after 12 wk of daily intake of blueberry (94) or Concord grape (95) juice.
*memory↑, Better task switching and reduced interference in memory was found in healthy older adults after 90 d of blueberry supplementation
*other↑, After 12 wk of blueberry consumption, greater brain activity was detected using magnetic resonance imaging in healthy older adults during a cognitive challenge.
*BOLD↑, Similarly, during a memory test, regional blood oxygen level-dependent activity detected by MRI (99) was enhanced in the subjects taking blueberry, but not in those taking placebo.
*NO↓, 50–200 mg/d bilberry showed a dose-dependent decrease in neurotoxic NO and malondialdehyde, combined with an increase in neuroprotective antioxidant capacity due to glutathione, vitamin C, superoxide dismutase, and glutathione peroxidase
*MDA↓,
*GSH↑,
*VitC↑,
*SOD↑,
*GPx↑,
*eff↓, The percentage loss of blueberry anthocyanins during −18°C storage was 12% after 10 mo of storage
*eff↓, Freeze-dried blueberry powder loses anthocyanins in a temperature-dependent manner with a half-life of 139, 39, and 12 d when stored at 25, 42, and 60°C, respectively
*eff↓, Blueberries are low in ascorbic acid and high in anthocyanins (187), and notably anthocyanins are readily degraded by ascorbic acid
*eff↝, Shelf-stable blueberry products like jam (196), juice (197), and extracts (198) can lose polyphenolic compounds when stored at ambient temperature whereas refrigeration mitigates losses.
*Risk↓, It can be safely stated that daily moderate intake (50 mg anthocyanins, one-third cup of blueberries) can mitigate the risk of diseases and conditions of major socioeconomic importance in the Western world.
*memory↑, Improvements in verbal fluency (p = 0.014), short-term memory (p = 0.014) and long-term memory (p ≤ 0.001) were found in the cherry juice group.
*BP↓, A significant reduction in systolic (p = 0.038) blood pressure and a trend for diastolic (p = 0.160) blood pressure reduction was evident in the intervention group.
*cognitive↑, This study found that daily consumption of a feasible serving of anthocyanin-rich cherry juice for 12 weeks improved cognitive performance across almost all tasks in older adults with mild-to-moderate dementia
*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↓, 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↓,
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.
*BioAv↑, another key property of allicin is its hydrophobicity, which allows it to be absorbed easily through the cell membrane without causing any physical or chemical damage to the phospholipid bilayer, thereby allowing its rapid metabolism to produce pharm
*cardioP↑, Allicin exhibits protective effects in multiple organ systems, including the brain, intestines, lungs, liver, kidneys, prostate, and heart.
*hepatoP↑,
*RenoP↑,
*Half-Life↝, half-life (t1/2)of allicin was 227 min–260 min. Because allicin is eliminated from the body by the respiratory tract, the concentration of allicin in lung tissue is significantly lower than that in the blood
*BioAv↓, We believe that the bioavailability of allicin is relatively low for the following reasons: At first, allicin is characterized by a distinctive garlic odor and chemical instability. It can be easily degraded under room temperature.
*neuroP↑, Neuroprotective activity
*cognitive↑, On the other hand, allicin improves cognitive deficits via Protein kinase R-like endoplasmic reticulum kinase (PERK)/Nuclear factor erythroid-2-related factor 2 (NRF2) signaling pathway and c-Jun N-terminal kinase (JNK) signaling pathways
*ROS↓, They found that allicin suppressed ROS generation and decreased lipid peroxidation in 6-hydroxydopamine (6-OHDA)-induced Pheochromocytoma 12 (PC12) cells
*lipid-P↓,
*DNArepair↑, Allicin not only directly protects DNA, but also indirectly protects DNA through antioxidant activity and regulation of oxidizing enzymes
*ChemoSen↑, Allicin combined with other chemotherapy drugs showed a better anti-cancer effect
*AntiCan↑, Allicin has shown anticancer, antimicrobial, antioxidant properties and also serves as an efficient therapeutic agent against cardiovascular diseases
*antiOx↑,
*cardioP↑,
*neuroP↑, present review describes allicin as an antioxidant, and neuroprotective molecule
cognitive↑, that can ameliorate the cognitive abilities in case of neurodegenerative and neuropsychological disorders.
*ROS↓, As an antioxidant, allicin fights the reactive oxygen species (ROS) by downregulation of NOX (NADPH oxidizing) enzymes, it can directly interact to reduce the cellular levels of different types of ROS produced by a variety of peroxidases.
*NOX↓,
*TLR4↓, inhibition of TLR4/MyD88/NF-κB, P38 and JNK pathways.
*NF-kB↓,
*JNK↓,
*AntiAg↑, A low concentration of allicin (0.4 mM) can inhibit the platelet aggregation up to 90%, the impact is significantly higher than of similar concentration of aspirin.
*H2S↑, Allicin decomposes rapidly and undergoes a series of reactions with glutathione resulting in the production of hydrogen sulphide (H2S).
*BP↓, H2S is a gaseous signalling molecule involved in the regulation of blood pressure.
Telomerase↓, Allicin inhibits the activity of telomerase in a dose dependent manner subsequently inhibiting the proliferation in the cancer cells
*Insulin↑, Studies have shown a significant increase in the blood insulin levels after treatment with allicin
BioAv↝, optimum temperature for the activity of alliinase is 33 °C, it operates best at pH 6.5, the enzyme is sensitive to acids [42,43] (Figure 3), enteric-coated formulations of garlic supplements are therefore recommended
*GSH↑, It helps to lower the hyperglycaemic conditions and improves the glutathione and catalase biosynthesis [37,38]
*Catalase↑,
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*Inflam↓, allicin integrate a broad spectrum of properties (e.g., anti-inflammatory, immunomodulatory, antibiotic, antifungal, antiparasitic, antioxidant, nephroprotective, neuroprotective, cardioprotective, and anti-tumoral activities, among others).
*antiOx↑, improving the antioxidant system
*neuroP↑,
*cardioP↑,
*AntiTum↑,
*mtDam↑, Indeed, the current evidence suggests that allicin improves mitochondrial function by enhancing the expression of HSP70 and NRF2, decreasing RAAS activation, and promoting mitochondrial fusion processes.
*HSP70/HSPA5↑, llicin improves mitochondrial function by enhancing the expression of HSP70 and decreasing RAAS activation
*NRF2↑,
*RAAS↓,
*cognitive↑, Allicin enhances the cognitive function of APP (amyloid precursor protein)/PS1 (presenilin 1) double transgenic mice by decreasing the expression levels of Aβ, oxidative stress, and improving mitochondrial function.
*SOD↑, positive effects on cognition in an AD mouse model by administrating a preventive dose of allicin. These effects might be mediated by an increase of SOD and reduction of ROS
*ROS↓,
*NRF2↑, Chronic treatment with allicin increased the expression of NRF2 and targeted downstream of NRF2, such as NADPH, quinone oxidoreductase 1 (NQO1), and γ-glutamyl cysteine synthetase (γ-GCS), in the hippocampus of aged mice
*ER Stress↓, protective effects of 16 weeks of allicin treatment in a rat model of endoplasmic reticulum stress-related cognitive deficits.
*neuroP↑, allicin was able to ameliorate depressive-like behaviors by decreasing neuroinflammation, oxidative stress iron
aberrant accumulation,
*memory↑, allicin improved lead acetate-caused learning and memory deficits and decreased the ROS level
*TBARS↓, Oral administration of allicin was able to reduce thiobarbituric reactive substances (TBARS) and
myeloperoxidase (MPO) levels, and concurrently increased (SOD) activity, glutathione S-transferase (GST) and glutathione (GSH) levels in a rat model of
*MPO↓,
*SOD↑,
*GSH↑,
*iNOS↓, decreasing the expression of iNOS and increased the phosphorylation of endothelial NOS (eNOS)
*p‑eNOS↑,
*HO-1↑, OSCs upregulate the endogenous antioxidant NRF2 and heme oxygenase-1 (HO-1)
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*Inflam↓, It showed neuroprotective effects, exhibited anti-inflammatory properties, demonstrated anticancer activity, acted as an antioxidant, provided cardioprotection, exerted antidiabetic effects, and offered hepatoprotection.
AntiCan↑,
*antiOx↑,
*cardioP↑, This vasodilatory effect helps protect against cardiovascular diseases by reducing the risk of hypertension and atherosclerosis.
*hepatoP↑,
*BBB↑, This allows allicin to easily traverse phospholipid bilayers and the blood-brain barrier
*Half-Life↝, biological half-life of allicin is estimated to be approximately one year at 4°C. However, it should be noted that its half-life may differ when it is dissolved in different solvents, such as vegetable oil
*H2S↑, allicin undergoes metabolism in the body, leading to the release of hydrogen sulfide (H2S)
*BP↓, H2S acts as a vasodilator, meaning it relaxes and widens blood vessels, promoting blood flow and reducing blood pressure.
*neuroP↑, It acts as a neuromodulator, regulating synaptic transmission and neuronal excitability.
*cognitive↑, Studies have suggested that H2S may enhance cognitive function and protect against neurodegenerative diseases like Alzheimer's and Parkinson's by promoting neuronal survival and reducing oxidative stress.
*neuroP↑, various research studies suggest that the neuroprotective mechanisms of allicin can be attributed to its antioxidant and anti-inflammatory properties
*ROS↓,
*GutMicro↑, may contribute to the overall health of the gut microbiota.
*LDH↓, Liu et al. found that allicin treatment led to a significant decrease in the release of lactate dehydrogenase (LDH),
*ROS↓, allicin's capacity to lower the production of reactive oxygen species (ROS), decrease lipid peroxidation, and maintain the activities of antioxidant enzymes
*lipid-P↓,
*antiOx↑,
*other↑, allicin was found to enhance the expression of sphingosine kinases 2 (Sphk2), which is considered a neuroprotective mechanism in ischemic stroke
*PI3K↓, allicin downregulated the PI3K/Akt/nuclear factor-kappa B (NF-κB) pathway, inhibiting the overproduction of NO, iNOS, prostaglandin E2, cyclooxygenase-2, interleukin-6, and tumor necrosis factor-alpha induced by interleukin-1 (IL-1)
*Akt↓,
*NF-kB↓,
*NO↓,
*iNOS↓,
*PGE2↓,
*COX2↓,
*IL6↓,
*TNF-α↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
*MPO↓, Furthermore, allicin significantly decreased tumor necrosis factor-alpha (TNF-α) levels and myeloperoxidase (MPO) activity, indicating its neuroprotective effect against brain ischemia via an anti-inflammatory pathway
*eff↑, Allicin, in combination with melatonin, demonstrated a marked reduction in the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2), Kelch-like ECH-associated protein 1 (Keap-1), and NF-κB genes in rats with brain damage induced by acryl
*NRF2↑, Allicin treatment decreased oxidative stress by upregulating Nrf2 protein and downregulating Keap-1 expression.
*Keap1↓,
*TBARS↓, It significantly reduced myeloperoxidase (MPO) and thiobarbituric acid reactive substances (TBARS) levels,
*creat↓, and decreased blood urea nitrogen (BUN), creatinine, LDH, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA) levels.
*LDH↓,
*AST↓,
*ALAT↓,
*MDA↓,
*SOD↑, Allicin also increased the activity of superoxide dismutase (SOD) as well as the levels of glutathione S-transferase (GST) and glutathione (GSH) in the liver, kidneys, and brain
*GSH↑,
*GSTs↑,
*memory↑, Allicin has demonstrated its ability to improve learning and memory deficits caused by lead acetate injury by promoting hippocampal astrocyte differentiation.
chemoP↑, Allicin safeguards mitochondria from damage, prevents the release of cytochrome c, and decreases the expression of pro-apoptotic factors (Bax, cleaved caspase-9, cleaved caspase-3, and p53) typically activated by cisplatin
IL8↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
Cyt‑c↑, In addition, allicin was reported to induce cytochrome c, increase expression of caspase 3 [86], caspase 8, 9 [82,87], caspase 12 [80] along with enhanced p38 protein expression levels [81], Fas expression levels [82].
Casp3↑,
Casp8↑,
Casp9↑,
Casp12↑,
p38↑,
Fas↑,
P53↑, Also, significantly increased p53, p21, and CHK1 expression levels decreased cyclin B after allicin treatment.
P21↑,
CHK1↓,
CycB/CCNB1↓,
GSH↓, Depletion of GSH and alterations in intracellular redox status have been found to trigger activation of the mitochondrial apoptotic pathway was the antiproliferative function of allicin
ROS↑, Hepatocellular carcinoma (HCC) cells were sensitised by allicin to the mitochondrial ROS-mediated apoptosis induced by 5-fluorouracil
TumCCA↑, According to research findings, allicin has been shown to decrease the percentage of cells in the G0/G1 and S phases [87], while causing cell cycle arrest at the G2/M phase
Hif1a↓, Allicin treatment was found to effectively reduce HIF-1α protein levels, leading to decreased expression of Bcl-2 and VEGF, and suppressing the colony formation capacity and cell migration rate of cancer cells
Bcl-2↓,
VEGF↓,
TumCMig↓,
STAT3↓, antitumor properties of allicin have been attributed to various mechanisms, including promotion of apoptosis, inhibition of STAT3 signaling
VEGFR2↓, suppression of VEGFR2 and FAK phosphorylation
p‑FAK↓,
GSH↓, allicin reacts with GSH
Bacteria↓, Antimicrobial
LDL↓, reduction without altering HDL
ROS↑, antioxidant at low doses
NRF2↑,
cognitive↑, by activating the Nrf2-system
memory↑, by activating the Nrf2-system
BP↓, via H2S generation
RNS↓,
*AChE↓, ALA activated AChE and increased glucose uptake, thus providing more acetyl-CoA to generate acetylcholine (ACh). (note activated AChE in this review likely should say inhibited!!!)
*GlucoseCon↑,
*ACC↑,
*GSH↑, ALA increased intracellular GSH levels by chelating redox-active transition metals, thus inhibiting the formation of hydroxyl radicals and Aβ aggregation.
*Aβ↓,
*Catalase↑, Levels of several antioxidant enzymes including catalase, GR, glutathione-S-transferase (GST), NADPH, and quinone oxidoreductase-1 (NQO1) were enhanced by ALA
*GSR↑,
*GSTs↑,
*NADPH↑,
*NQO1↑,
*iNOS↓, LA prevented the induction of iNOS, inhibited TNFα-induced activation of NF-κB [42], levels of which are
increased in AD.
*NF-kB↓,
*lipid-P↓, ALA reduced the levels of lipid peroxidation products
*BBB↑, ALA could
easily cross the blood–brain barrier (BBB)
*memory↑, ALA treatment significantly improved the spatial memory and cognition capacity of the mice in the Morris
water maze and novel object recognition test.
*cognitive↑,
*antiOx↑, antioxidant and anti-inflammatory activities of ALA
*Inflam↓,
*cognitive↑, led to a stabilization of cognitive functions in the study group
*other↝, In patients with mild dementia (ADAScog < 15), the disease progressed extremely slowly (ADAScog: +1.2 points/year, MMSE: -0.6 points/year), in patients with moderate dementia at approximately twice the rate.
*neuroP↑, alpha-lipoic acid might be a successful 'neuroprotective' therapy option for AD
*IronCh↑, a-Lipoic acid chelates redox-active transition metals, thus inhibiting the formation of hydroxyl radicals and also scavenges reactive oxygen species (ROS), thereby increasing the levels of reduced glutathione
*ROS↓,
*GSH↑,
*antiOx↑, Alpha-lipoic acid (α-LA), a natural antioxidant
*memory↑, multiple preclinical studies indicating beneficial effects of α-LA in memory functioning, and pointing to its neuroprotective effects
*neuroP↑, α-LA could be considered neuroprotective
*Inflam↓, α-LA shows antioxidant, antiapoptotic, anti-inflammatory, glioprotective, metal chelating properties in both in vivo and in vitro studies.
*IronCh↑, α-LA leads to a marked downregulation in iron absorption and active iron reserve inside the neuron
*NRF2↑, α-LA induces the activity of the nuclear factor erythroid-2-related factor (Nrf2), a transcription factor.
*BBB↑, capable of penetrating the BBB
*GlucoseCon↑, Fig 2, α-LA mediated regulation of glucose uptake
*Ach↑, α-LA may show its action on the activity of the ChAT enzyme, which is an essential enzyme in
acetylcholine metabolism
*ROS↓,
*p‑tau↓, decreased degree of tau phosphorylation following treatment with α-LA
*Aβ↓, α-LA possibly induce the solubilization of Aß plaques in the frontal cortex
*cognitive↑, cognitive reservation of α-LA served AD model was markedly upgraded in additional review
*Hif1a↑, α-LA treatment efficaciously induces the translocation and activity of hypoxia-inducible factor-1α (HIF-1α),
*Ca+2↓, research found that α-LA therapy remarkably declines Ca2+ concentration and calpain signaling
*GLUT3↑, inducing the downstream target genes expression, such as GLUT3, GLUT4, HO-1, and VEGF.
*GLUT4↑,
*HO-1↑,
*VEGF↑,
*PDKs↓, α-LA also ameliorates survival in mutant mice of Huntington's disease [150–151], possibly due to the inhibition of the activity of pyruvate dehydrogenase kinase
*PDH↑, α-LA administration enhances PDH expression in mitochondrial hepatocytes by inhibiting the pyruvate dehydrogenase kinase (PDK),
*VCAM-1↓, α-LA inhibits
the expression of cell-cell adhesion molecule-1 and VCAM-1 in spinal cords and TNF-α induced neuronal endothelial cells injury
*GSH↑, α-LA may enhance glutathione production in old-aged models
*NRF2↑, activation of the Nrf2 signaling by α-LA
*hepatoP↑, α-LA also protected the liver against oxidative stress-mediated hepatotoxicity
*ChAT↑, α-LA in mice models may prevent neuronal injury possibly due to an increase in ChAT in the hippocampus of animal models
*antiOx↑, LA has long been touted as an antioxidant,
*glucose↑, improve glucose and ascorbate handling,
*eNOS↑, increase eNOS activity, activate Phase II detoxification via the transcription factor Nrf2, and lower expression of MMP-9 and VCAM-1 through repression of NF-kappa-B.
*NRF2↑,
*MMP9↓,
*VCAM-1↓,
*NF-kB↓,
*cardioP↑, used to improve age-associated cardiovascular, cognitive, and neuromuscular deficits,
*cognitive↑,
*eff↓, The efficiency of LA uptake was also lowered by its administration in food,
*BBB↑, LA has been shown to cross the blood-brain barrier in a limited number of studies;
*IronCh↑, LA preferentially binds to Cu2+, Zn2+ and Pb2+, but cannot chelate Fe3+, while DHLA forms complexes with Cu2+, Zn2+, Pb2+, Hg2+ and Fe3+
*GSH↑, LA markedly increases intracellular glutathione
(GSH),
*PKCδ↑, PKCδ, LA activates Erk1/2 [92,93], p38 MAPK [94], PI3 kinase [94], and Akt
*ERK↑,
*p38↑,
*MAPK↑,
*PI3K↑,
*Akt↑,
*PTEN↓, LA decreases the activities of Protein Tyrosine Phosphatase 1B [99], Protein Phosphatase 2A [95], and the phosphatase and tensin homolog PTEN [95],
*AMPK↑, LA activates peripheral AMPK
*GLUT4↑, stimulate GLUT4 translocation
*GLUT1↑, LA-stimulated translocation of GLUT1 and GLUT4.
*Inflam↓, LA as an anti-inflammatory agent
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*antiOx↑, Both of alpha lipoic acid and its reduced form have been shown to possess anti-oxidant, cardiovascular, cognitive, anti-ageing, detoxifying, anti-inflammatory, anti-cancer, and neuroprotective pharmacological properties
*cardioP↑,
*cognitive↑, Alpha lipoic acid has the ability to decrease cognitive impairment and may be a successful therapy for Alzheimer’s disease and any disease related dementias
*AntiAge↑,
*Inflam↓,
*AntiCan↑,
*neuroP↑, ALA has neuroprotective effects in experimental brain injury caused by trauma and subarachnoid hemorrhage
*IronCh↑, Also, the ability of ALA to chelate metals can produce an antioxidant effect
*ROS↑, DHLA can exert a pro-oxidant effect of donating its electrons for the reduction of iron, which can then break down peroxide to the prooxidant hydroxyl radical via the Fenton reaction [10]. So, ALA and its reduced form DHLA, can promote antioxidant pr
*Weight↓, α-lipoic acid supplementation at a dose of 300 mg/day might help to could help to promote weight loss and fat mass reduction in healthy overweight/obese women following an energy-restricted balanced diet
*Ach↑, Alpha lipoic acid increases the production of Acetylcholine (Ach) via activating choline acetyl transferase and increases glucose uptake, hence, supplying more acetyl-CoA for the production of Ach of each
*ROS↓, also scavenges
reactive oxygen species, thereby increasing the concentration levels
of reduced Glutathione (GSH).
*GSH↑,
*lipid-P↓, Alpha lipoic acid can scavenge lipid peroxidation products as hydroxynonenal and
acrolein.
*memory↑, learning and memory in the passive avoidance test partially
through its antioxidant activity.
*NRF2↑, α-LA treatment has been shown to increase Nrf2 nuclear localization
*ChAT↑, Alpha lipoic acid increases the production of Acetylcholine (Ach) via activating choline acetyl transferase and increases glucose uptake, hence, supplying more acetyl-CoA for the production of Ach of each
*GlucoseCon↑,
*Acetyl-CoA↑,
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*antiOx↑, antioxidant potential and free radical scavenging activity.
*ROS↓,
*IronCh↑, Lipoic acid acts as a chelating agent for metal ions, a quenching agent for reactive oxygen species, and a reducing agent for the oxidized form of glutathione and vitamins C and E.
*cognitive↑, α-Lipoic acid enantiomers and its reduced form have antioxidant, cognitive, cardiovascular, detoxifying, anti-aging, dietary supplement, anti-cancer, neuroprotective, antimicrobial, and anti-inflammatory properties.
*cardioP↓,
AntiCan↑,
*neuroP↑,
*Inflam↓, α-Lipoic acid can reduce inflammatory markers in patients with heart disease
*BioAv↓, bioavailability in its pure form is low (approximately 30%).
*AntiAge↑, As a dietary supplements α-lipoic acid has become a common ingredient in regular products like anti-aging supplements and multivitamin formulations
*Half-Life↓, it has a half-life (t1/2) of 30 min to 1 h.
*BioAv↝, It should be stored in a cool, dark, and dry environment, at 0 °C for short-term storage (few days to weeks) and at − 20 °C for long-term storage (few months to years).
other↝, Remarkably, neither α-lipoic acid nor dihydrolipoic acid can scavenge hydrogen peroxide, possibly the most abundant second messenger ROS, in the absence of enzymatic catalysis.
EGFR↓, α-Lipoic acid inhibits cell proliferation via the epidermal growth factor receptor (EGFR) and the protein kinase B (PKB), also known as the Akt signaling, and induces apoptosis in human breast cancer cells
Akt↓,
ROS↓, α-Lipoic acid tramps the ROS followed by arrest in the G1 phase of the cell cycle and activates p27 (kip1)-dependent cell cycle arrest via changing of the ratio of the apoptotic-related protein Bax/Bcl-2
TumCCA↑,
p27↑,
PDH↑, α-Lipoic acid drives pyruvate dehydrogenase by downregulating aerobic glycolysis and activation of apoptosis in breast cancer cells, lactate production
Glycolysis↓,
ROS↑, HT-29 human colon cancer cells; It was concluded that α-lipoic acid induces apoptosis by a pro-oxidant mechanism triggered by an escalated uptake of mitochondrial substrates in oxidizable form
*eff↑, Several studies have found that combining α-lipoic acid and omega-3 fatty acids has a synergistic effect in slowing functional and cognitive decline in Alzheimer’s disease
*memory↑, α-lipoic acid inhibits brain weight loss, downregulates oxidative tissue damage resulting in neuronal cell loss, repairs memory and motor function,
*motorD↑,
*GutMicro↑, modulates the gut microbiota without reducing the microbial diversity (
*BBB↑, ALA's ability to cross the blood-brain barrier and its dual solubility in both water and lipid environments position it as a promising compound in the realm of cognitive enhancement and neurological health
*cognitive↑,
*neuroP↑, Alpha-lipoic acid demonstrates robust neuroprotective and cognitive-enhancing effects through its potent antioxidant properties
*antiOx↑,
*ATP↑, Incubation with ALA showed a significant increase in ATP levels in both SH-SY5Y-APP695 and SH-SY5Y-MOCK cells.
*MMP↑, MMP levels were elevated in SH-SY5Y-MOCK cells, treatment with rotenone showed a reduction in MMP, which could be partly alleviated after incubation with ALA in SH-SY5Y-MOCK cells.
*ROS↓, ROS levels were significantly lower in both cell lines treated with ALA.
*GlucoseCon↑, benefits to diabetic neuropathy and impaired glucose uptake, and the regeneration of glutathione (GSH) and vitamins C and E
*GSH↑,
*neuroP↑, ALA seems to have a positive effect on neurodegenerative diseases such as AD
*cognitive↑, ALA improves cognitive performance and could be considered as a promising bioactive substance for AD by affecting multiple mechanisms such as:
*Ach↑, (1) impaired acetylcholine production;
*Inflam↓, (2) hydroxyl radical formation, ROS production, and neuroinflammation;
*Aβ↓, (3) impaired amyloid plaque formation;
OXPHOS↓, ALA has also been shown to restore the expression of OXPHOS complexes in HepG2 cells, ranging in a concentration between 0.5–2 mM
*cognitive↑, ALA improves cognitive function in ageing mice.
*Apoptosis↓, ALA downregulates apoptosis, and neuroinflammatory associated proteins in ageing mice.
*Inflam↓,
*antiOx↑, Alpha lipoic acid (ALA), a powerful antioxidant, has the potential to relieve age-related cognitive impairment and neurodegenerative disease.
*BioAv↝, Alpha lipoic acid (ALA) is a sulfur-containing and both water-soluble and lipid-soluble coenzyme involved in the energy metabolism of carbohydrates, proteins and lipids
*neuroP↑, neuroprotective action of alpha lipoic acid has been demonstrated in a number of cellular or animal models of Parkinson's disease (PD), AD and amyotrophic lateral sclerosis (ALS) due to its antioxidative and anti-inflammatory properties
*ROS↓, scavenges free radicals, chelates metals, and restores intracellular glutathione levels which otherwise decline with age.
*IronCh↑, LA preferentially binds to Cu2+, Zn2+ and Pb2+, but cannot chelate Fe3+, while DHLA forms complexes with Cu2+, Zn2+, Pb2+, Hg2+ and Fe3+
*GSH↑,
*antiOx↑, LA has long been touted as an antioxidant
*NRF2↑, activate Phase II detoxification via the transcription factor Nrf2
*MMP9↓, lower expression of MMP-9 and VCAM-1 through repression of NF-kappa-B.
*VCAM-1↓,
*NF-kB↓,
*cognitive↑, it has been used to improve age-associated cardiovascular, cognitive, and neuromuscular deficits, and has been implicated as a modulator of various inflammatory signaling pathways
*Inflam↓,
*BioAv↝, LA bioavailability may be dependent on multiple carrier proteins.
*BioAv↝, observed that approximately 20-40% was absorbed [
*BBB↑, LA has been shown to cross the blood-brain barrier in a limited number of studies
*H2O2∅, Neither species is active against hydrogen peroxide
*neuroP↑, chelation of iron and copper in the brain had a positive effect in the pathobiology of Alzheimer’s Disease by lowering free radical damage
*PKCδ↑, In addition to PKCδ, LA activates Erk1/2 [92, 93], p38 MAPK [94], PI3 kinase [94], and Akt [94-97].
*ERK↑,
*MAPK↑,
*PI3K↑,
*Akt↑,
*PTEN↓, LA decreases the activities of Protein Tyrosine Phosphatase 1B [99], Protein Phosphatase 2A [95], and the phosphatase and tensin homolog PTEN
*AMPK↑, LA activates peripheral AMPK
*GLUT4↑, In skeletal muscle, LA is proposed to recruit GLUT4 from its storage site in the Golgi to the sarcolemma, so that glucose uptake is stimulated by the local increase in transporter abundance.
*GlucoseCon↑,
*BP↝, Feeding LA to hypertensive rats normalized systolic blood pressure and cytosolic free Ca2+
*eff↑, Clinically, LA administration (in combination with acetyl-L-carnitine) showed some promise as an antihypertensive therapy by decreasing systolic pressure in high blood pressure patients and subjects with the metabolic syndrome
*ICAM-1↓, decreased demyelination and spinal cord expression of adhesion molecules (ICAM-1 and VCAM-1)
*VCAM-1↓,
*Dose↝, Considering the transient cellular accumulation of LA following an oral dose, which does not exceed low micromolar levels, it is entirely possible that some of the cellular effects of LA when given at supraphysiological concentrations may be not be c
*cognitive↑, Our study suggests that ALA therapy could be effective in slowing cognitive decline in patients with AD and IR.
*antiOx↑, Alpha-lipoic acid (ALA) is a naturally occurring disulfide molecule with antioxidant and anti-inflammatory properties.
*Inflam↓,
*neuroP↑, ALA plays many different roles in pathogenic pathways of dementia, acting as a neuroprotective agent.
*Ach↑, It increases acetylcholine production, inhibits hydroxyl radical production, and increases the process of getting rid of reactive oxygen species.
*ROS↓,
*GlucoseCon↑, (ii) increased glucose uptake, supplying more acetyl-CoA for the production of Ach;
*lipid-P↓, (v) scavenging lipid peroxidation products;
*GSH↑, (vi) inducing enzymes of glutathione synthesis
*Acetyl-CoA↑,
*NO↓, ALA reduced NO without a corresponding reduction of iNOS.
*cognitive↑, select microglial immune functions by ALA and LA could be one of the mechanisms underlying the observed link between certain dietary patterns and AD, such as reduced risk of cognitive decline and dementia associated with the Mediterranean diet.
*antiOx↑, antioxidant and anti-inflammatory properties
*Inflam↓,
*PGE2↓, α-LA has mechanisms of epigenetic regulation in genes related to the expression of various inflammatory mediators, such PGE2, COX-2, iNOS, TNF-α, IL-1β, and IL-6
*COX2↓,
*iNOS↓,
*TNF-α↓,
*IL1β↓,
*IL6↓,
*BioAv↓, α-LA has rapid uptake and low bioavailability and the metabolism is primarily hepatic
*Ach↑, α-LA increases the production of acetylcholine [30], inhibits the production of free radicals [31], and promotes the downregulation of inflammatory processes
*ROS↓,
*cognitive↑, Studies have shown that patients with mild AD who were treated with α-LA showed a slower progression of cognitive impairment
*neuroP↑, α-LA is classified as an ideal neuroprotective antioxidant because of its ability to cross the blood-brain barrier and its uniform uptake profile throughout the central and peripheral nervous systems
*BBB↑,
*Half-Life↓, α-LA presented a mean time to reach the maximum plasma concentration (tmax) of 15 minutes and a mean plasma half-life (t1/2) of 14 minutes
*BioAv↑, LA consumption is recommended 30 minutes before or 2 hours after food intake
*Casp3↓, α-LA had an effect on caspases-3 and -9, reducing the activity of these apoptosis-promoting molecules to basal levels
*Casp9↓,
*ChAT↑, α-LA increased the expression of M2 muscarinic receptors in the hippocampus and M1 and M2 in the amygdala, in addition to ChaT expression in both regions.
*cognitive↑, α-LA acts on these apoptotic signalling pathways, leading to improved cognitive function and attenuation of neurodegeneration.
*eff↑, Based on their results, the authors suggest that treatment with α-LA would be a successful neuroprotective option in AD, at least as an adjuvant to standard treatment with acetylcholinesterase inhibitors.
*cAMP↑, The increase of cAMP caused by α-LA inhibits the release of proinflammatory cytokines, such as IL-2, IFN-γ, and TNF-α.
*IL2↓,
*INF-γ↓,
*TNF-α↓,
*SIRT1↑, Protein expression encoded by SIRT1 showed higher levels after α-LA treatment, especially in liver cells.
*SOD↑, antioxidant enzymes (SOD and GSH-Px) and malondialdehyde (MDA) were analysed by ELISA after 24 h of MCAO, which showed that the enzymatic activities were recovered and MDA was reduced in the α-LA-treated groups i
*GPx↑,
*MDA↓,
*NRF2↑, The ratio of nucleus/cytoplasmic Nrf2 was higher in the α-LA group 40 mg/kg, indicating that the activation of this factor also occurred in a dose-dependent manner
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*memory↑, a number of preclinical studies showing beneficial effects of LA in memory functioning, and pointing to its neuroprotective potential effect
*neuroP↑,
*motorD↑, Improved motor dysfunction
*VitC↑, elevates the activities of antioxidants such as ascorbate (vitamin C), α-tocoferol (vitamin E) (Arivazhagan and Panneerselvam, 2000), glutathione (GSH)
*VitE↑,
*GSH↑,
*SOD↑, superoxide dismutase (SOD) activity (Arivazhagan et al., 2002; Cui et al., 2006; Militao et al., 2010), catalase (CAT) (Arivazhagan et al., 2002; Militao et al., 2010), glutathione peroxidase (GSH-Px)
*Catalase↑,
*GPx↑,
*5HT↑, ↑levels of neurotransmitters (dopamine, serotonin and norepinephrine) in various brain regions
*lipid-P↓, ↓ level of lipid peroxidation,
*IronCh↑, ↓cerebral iron levels,
*AChE↓, ↓ AChE activity, ↓ inflammation
*Inflam↓,
*GlucoseCon↑, ↑brain glucose uptake; ↑ in the total GLUT3 and GLUT4 in the old mice;
*GLUT3↑,
*GLUT4↑,
NF-kB↓, authors showed that LA inhibited the stimulation of nuclear factor-κB (NF-κB)
*IGF-1↑, LA restored the parameters of total homocysteine (tHcy), insulin, insulin like growth factor-1 (IGF-1), interlukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Mahboob et al. (2016), analyzed the effects of LA in AlCl3- model of neurodegeneration,
*IL1β↓,
*TNF-α↓, Suppression of NF-κβ p65 translocation and production of proinflammatory cytokines (IL-6 and TNF-α) followed inhibition of cleaved caspase-3
*cognitive↑, demonstrating its capacity in ameliorating cognitive functions and enhancing cholinergic system functions
*ChAT↑, LA treatment increased the expression of muscarinic receptor genes M1, M2 and choline acetyltransferase (ChaT) relative to AlCl3-treated group.
*HO-1↑, R-LA and S-LA also enhanced expression of genes related to anti-oxidative response such as heme oxygenase-1 (HO-1) and phase II detoxification enzymes such as NAD(P)H:Quinone Oxidoreductase 1 (NQO1).
*NQO1↑,
*neuroP↑, potential therapeutic effects for the prevention or treatment of neurodegenerative disease
*Inflam↓, ALA is able to regulate inflammatory cell infiltration into the central nervous system and to down-regulate VCAM-1 and human monocyte adhesion to epithelial cells
*VCAM-1↓, down-regulate vascular cell adhesion molecule-1 (VCAM-1) and the human monocyte adhesion to epithelial cells
*5HT↑, ALA is able to improve the function of the dopamine, serotonin and norepinephrine neurotransmitters
*memory↑, scientific evidence shows that ALA possesses the ability to improve memory capacity in a number of experimental neurodegenerative disease models and in age-related cognitive decline in rodents
*BioAv↝, Between 27 and 34% of the oral intake is available for tissue absorption; the liver is one of the main clearance organs on account of its high absorption and storage capacity
*Half-Life↓, The plasma half-life of ALA is approximately 30 minutes. Peak urinary excretion occurs 3-6 hours after intake.
*NF-kB↓, As an inhibitor of NF-κβ, ALA has been studied in cytokine-mediated inflammation
*antiOx↑, In addition to the direct antioxidant properties of ALA, some studies have shown that both ALA and DHLA and a great capacity to chelate redox-active metals, such as copper, free iron,
zinc and magnesium, albeit in different ways (
*IronCh↑, ALA is able to chelate transition metal ions and, therefore, modulate the iron- and copper-mediated oxidative stress in Alzheimer’s plaques
*ROS↓, iron and copper chelation with DHLA may explain the low level of free radical damage in the brain and the improvement in the pathobiology of Alzheimer’s Disease
*ATP↑, ALA may increase the mitochondrial synthesis of ATP in the brain of elderly rats, thereby increasing the activity of the mitochondrial enzymes
*ChAT↑, ALA may also play a role in the activation of the choline acetyltransferase enzyme (ChAT), which is essential in the anabolism of acetylcholine
*Ach↑,
*cognitive↑, One experimental study has shown that in rats that had been administered ALA there was an inversion in the cognitive dysfunction with an increase in ChAT activity in the hippocampus
*lipid-P↓, administration of ALA reduces lipid peroxidation in different areas of the brain and increases the activity of antioxidants such as ascorbate (vitamin C), α-tocopherol (vitamin E), glutathione,
*VitC↑,
*VitE↑,
*GSH↑,
*SOD↑, and also the activity of superoxide dismutase, catalase, glutathione-peroxidase, glutathione-reductase, glucose-6-P-dehydrogenase
*Catalase↑,
*GPx↑,
*Aβ↓, Both ALA and DHLA have been seen to inhibit the formation of Aβ fibrils
*antiOx↑, ALA is a low molecular weight antioxidant, readily absorbed from the diet or an oral dose, and crosses the blood brain barrier
*BBB↑,
*VitC↑, DHLA regenerates through redox cycling other antioxidants like vitamin C and E and raises levels of intracellular glutathione, an important thiol antioxidant
*VitE↑,
*GSH↑,
*IronCh↑, ALA al-
so chelates certain metals, forming stable complexes with copper,
manganese and zinc (Sigel 1978)
*neuroP↑, ALA would seem an ideal candidate as an antioxidant agent in neurodegenerative diseases.
*NO↓, ALA also modulates nitric oxide levels in brain and neural tissue, which may have effects in neurodegeneration, learning, cognition, and aging (Gross 1995)
*cognitive↑, elderly patients with dementia were given ALA. Findings suggested a stabilization of cognitive functions in the study group,
*AntiAge↑,
*memory↑, ALA has gained considerable attention following studies demonstrating partial reversal of memory loss in aged rats.
*ROS↓, scavenging hy-
droxyl or superoxide radicals (Suzuki 1991) and by scavenging per-
oxyl radicals (
*Dose↝, n a 2003 meta-analysis of 21 clinical trials, a total of 1,204 adults with mild cognitive impairment or mild Alzheimer’s disease took supplements containing 1.5 to 3.0 g/day acetyl-L-carnitine or placebo for 3 to 12 months.
*cognitive↑, Clinical and psychometric assessment scores were better, and improvements determined by clinicians were greater in supplement users than in the placebo groups [30].
*cognitive↑, beneficial effects were seen on both the clinical scales and the psychometric tests.
*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↑,
*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
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*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
*BChE↓, Essential oils (EOs) from Salvia leriifolia Benth. exhibited high BChE inhibitory.
*AChE↓, Volatile oil from Marlierea racemosa Vell. (Myrtaceae) demonstrated concentration‐dependent inhibition of AChE
*other↓, EOs from the leaves and flowers of Polygonum hydropiper L., 28 sandalwood oil and its chief constituent α‐santalol were reported the AChE, BChE inhibitory efficacy.
*other?, The extract of Rosmarinus officinalis L. leaf led to improved long‐term memory in scopolamine‐induced rats, which can be partially explained by its inhibition of AChE activity in rat brain
*Ach?, It was observed in APP/PS1 mice that 4 weeks of Lemon essential oil treatment could significantly decrease hippocampal AChE, and thus increased ACh levels
*eff↑, Most studies have found that terpenoids in aromatic plant extracts are the main anticholinesterase active components
*antiOx↑, aromatic plant extracts for their potent antioxident and free radical scavenging properties
*ROS↓, Several compounds like safranal, linalool, and SHXW essential oil have been found to decrease ROS levels induced by Aβ in rats or mouse
*cognitive↑, aromatic plant extracts can improve cognitive function, reduce agitation, and improve sleep quality in AD patients.
*Mood↑,
*Sleep↑,
*cognitive↑, Inhaled aromatherapy improves cognitive function in patients with cognitive impairment.
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*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
*cognitive↑, EOs were effective on several pathological targets and have improved cognitive performance in animal models and human subjects.
*AChE↓, Recently, Ayaz et al. (2015) reported the AChE, BChE inhibitory and free radicals scavenging efficacy of EOs from the leaves and flowers of Polygonum hydropiper.
*BChE↓,
*ROS↓,
*other↓, , Ahmad et al. (2016) reported the anti-cholinesterase and antiradicals potentials of EO from Rumex hastatus D. Don. GC-MS analysis of EO revealed the presence of 123 compounds. I
*other↓, (Ahmad et al., 2016). Okello et al. (2008) reported the in vitro AChE, BChE inhibitory activity of flower oil from Narcissus poeticus L. belonging to family Amaryllidaceae.
*other↓, The EO from Marlierea racemosa Vell. (Myrtaceae) were evaluated by Souza et al. (2009) against AChE enzyme.
*other↓, C. salvifolius exhibited AChE inhibitory activity with IC50 value of 58.1 μg/ml. Whereas, C. libanotis, C. creticus and C. salvifolius showed significant inhibitory activities against BChE with IC50 values of 23.7, 29.1 and 34.2 μg/ml respectively.
*other↓, Rosemary EO also possess moderate AChE inhibitory activity and can synergistically act with 2-pinene and 1,8-cineole.
*memory↑, Owing to the memory enhancing capabilities of Salvia lavandulifolia Vahl (Spanish sage),
*BACE↓, EOs can inhibit the activity of BACE1 to hamper the Aβ load.
*Mood↑, Lavandula angustifolia Mill. and Melissa officinalis L. belonging to Lamiaceae for the management of agitation in individuals with severe dementia. The sedative and calming effect of both EOs is already established which can contribute in consolidati
*motorD↑, lavender EO: locomotor activity and motor functions were improved in animal models.
*cognitive↑, Aromatherapy may have some potential for improving cognitive function, especially in AD patients.
*other↑, Lavandula angustifolia Mill, Salvia rosmarinus and lemon citrus:potential for improving cognitive function, especially in AD patients.
*other↓, Rosmarinus officinalis: improving cognitive function by inhaled administration
*BioAv↑, There is no doubt that components from EOs are often absorbed through the skin, enter into the circulation then
cross the BBB.
*BBB?,
*cognitive↑, The most notable cognitive and mood effects were improved memory performance and increased 'calmness' at all postdose time points for the highest (1600 mg) dose.
*memory↑,
*AChE∅, However, no cholinesterase inhibitory properties were detected
*Mood↑,
*eff↝, The results also suggest that different preparations derived from the same plant species may exhibit different properties depending on the process used for the sample preparation.
*Inflam↓, Artemisinin has potent anti-inflammatory and immune activities.
*neuroP↑, Artemisinin inhibited neuroinflammation and exerted neuroprotective effects by regulating the Toll-like receptor 4 (TLR4)/Nuclear factor-kappa B (NF-κB) signaling pathway.
*TLR4↓,
*NF-kB↓,
*memory↑, reversing spatial learning and memory deficits.
*ROS↓, Artemisinin Decreased the Production of ROS and iNOS in BV2 Cells
*iNOS↓,
*COX2↓, Artemisinin treatment decreased the expression of COX2 and iNOS
*cognitive↑, Artemisinin Improved the Cognitive Impairment of AD Model Mice
*cognitive↑, artemisinin administration significantly improved LPS-induced cognitive impairments assessed in Morris water maze and Y maze tests
*neuroP↑, attenuated neuronal damage and microglial activation in the hippocampus.
*TNF-α↓, artemisinin (40 μΜ) significantly reduced the production of proinflammatory cytokines (i.e., TNF-α, IL-6)
*IL6↓,
*NF-kB↓, artemisinin significantly suppressed the nuclear translocation of NF-κB and the expression of proinflammatory cytokines by activating the AMPKα1 pathway;
*AMPK↑,
*ROS↓, artemisinin protects neuronal HT-22 cells from oxidative injury by activating the Akt pathway
*Akt↑,
*MCP1↓, artemisinin reversed the LPS-induced increases in the chemokines MCP-1 and MIP-2
*MIP2↓,
*TGF-β↑, Artemisinin also significantly increased the mRNA and protein expression of TGF-β
*Inflam↓, The AMPKα1 pathway is involved in the anti-inflammatory effect of artemisinin
*cognitive↑, Cognition Promoting Effect
*Inflam↓, anti-inflammatory and anti-arthritic
*Strength↑, swimming time was approximately doubled after Withania somnifera (WS) treatment
*VitC↑, Withania somnifera treatment prevents, decrease of adrenal cortisol and ascorbic acid which occurs due to swimming stress.
*memory↑, It is useful for different types of diseases like Parkinson, dementia, memory loss, stress induced diseases, malignoma and others.
Showing Research Papers: 1 to 50 of 453
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 453
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
GSH↓, 2, NRF2↑, 1, OXPHOS↓, 1, RNS↓, 1, ROS↓, 1, ROS↑, 3,
Core Metabolism/Glycolysis ⓘ
Glycolysis↓, 1, LDL↓, 1, PDH↑, 1,
Cell Death ⓘ
Akt↓, 1, Bcl-2↓, 1, Casp12↑, 1, Casp3↑, 1, Casp8↑, 1, Casp9↑, 1, Cyt‑c↑, 1, Fas↑, 1, p27↑, 1, p38↑, 1, Telomerase↓, 1,
Transcription & Epigenetics ⓘ
other↝, 1,
DNA Damage & Repair ⓘ
CHK1↓, 1, P53↑, 1,
Cell Cycle & Senescence ⓘ
CycB/CCNB1↓, 1, P21↑, 1, TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
STAT3↓, 1,
Migration ⓘ
p‑FAK↓, 1, TumCMig↓, 1,
Angiogenesis & Vasculature ⓘ
EGFR↓, 1, Hif1a↓, 1, VEGF↓, 1, VEGFR2↓, 1,
Immune & Inflammatory Signaling ⓘ
IL8↓, 1, NF-kB↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↝, 1,
Clinical Biomarkers ⓘ
BP↓, 1, EGFR↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 2, chemoP↑, 1, cognitive↑, 2, memory↑, 2,
Infection & Microbiome ⓘ
Bacteria↓, 1,
Total Targets: 43
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 1, antiOx↑, 22, Catalase↑, 5, GPx↑, 5, GSH↑, 15, GSR↑, 1, GSTs↑, 2, H2O2∅, 1, HDL↑, 1, HO-1↑, 4, Keap1↓, 1, lipid-P↓, 7, MDA↓, 3, MPO↓, 2, NQO1↑, 2, NRF2↑, 10, ROS↓, 24, ROS↑, 1, SOD↑, 8, TBARS↓, 2, VitC↑, 5, VitE↑, 3,
Metal & Cofactor Biology ⓘ
IronCh↑, 9,
Mitochondria & Bioenergetics ⓘ
ATP↑, 3, Insulin↑, 1, MMP↑, 1, mtDam↑, 1,
Core Metabolism/Glycolysis ⓘ
ACC↑, 1, Acetyl-CoA↑, 2, adiP↓, 1, ALAT↓, 1, AMPK↑, 3, cAMP↑, 1, CREB↑, 1, glucose↓, 1, glucose↑, 1, GlucoseCon↑, 7, H2S↑, 2, LDH↓, 3, LDL↓, 1, NADPH↑, 1, PDH↑, 1, PDKs↓, 1, PPARγ↑, 1, SIRT1↑, 1,
Cell Death ⓘ
Akt↓, 1, Akt↑, 4, Apoptosis↓, 1, Casp3↓, 1, Casp9↓, 1, iNOS↓, 6, JNK↓, 1, MAPK↓, 1, MAPK↑, 2, p38↑, 1,
Transcription & Epigenetics ⓘ
Ach?, 1, Ach↑, 8, other?, 1, other↓, 8, other↑, 4, other⇅, 1, other↝, 3,
Protein Folding & ER Stress ⓘ
ER Stress↓, 1, HSP70/HSPA5↑, 1,
DNA Damage & Repair ⓘ
DNArepair↑, 1,
Proliferation, Differentiation & Cell State ⓘ
ERK↑, 2, GSK‐3β↓, 1, IGF-1↑, 1, PI3K↓, 1, PI3K↑, 3, PTEN↓, 2,
Migration ⓘ
AntiAg↑, 1, APP↓, 1, Ca+2↓, 2, MMP9↓, 2, PKCδ↑, 2, TGF-β↑, 1, VCAM-1↓, 5,
Angiogenesis & Vasculature ⓘ
eNOS↑, 1, p‑eNOS↑, 1, Hif1a↑, 1, NO↓, 4, VEGF↑, 1,
Barriers & Transport ⓘ
BBB?, 1, BBB↑, 12, GLUT1↑, 1, GLUT3↑, 2, GLUT4↑, 4,
Immune & Inflammatory Signaling ⓘ
COX2↓, 4, CRP↓, 1, ICAM-1↓, 1, IL1β↓, 4, IL2↓, 1, IL6↓, 3, INF-γ↓, 1, Inflam↓, 22, MCP1↓, 1, MIP2↓, 1, NF-kB↓, 8, p‑NF-kB↓, 1, PGE2↓, 3, TLR4↓, 3, TNF-α↓, 7,
Cellular Microenvironment ⓘ
NOX↓, 1,
Synaptic & Neurotransmission ⓘ
5HT↑, 6, AChE↓, 5, AChE∅, 1, BChE↓, 2, BDNF↑, 5, ChAT↑, 5, GABA↑, 1, MAOA↓, 1, tau↓, 1, p‑tau↓, 1, TrkB↑, 1,
Protein Aggregation ⓘ
Aβ↓, 7, BACE↓, 2, NLRP3↓, 1,
Hormonal & Nuclear Receptors ⓘ
RAAS↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 3, BioAv↑, 3, BioAv↝, 5, ChemoSen↑, 1, Dose↝, 5, eff↓, 4, eff↑, 7, eff↝, 2, Half-Life↓, 3, Half-Life↑, 1, Half-Life↝, 2,
Clinical Biomarkers ⓘ
ALAT↓, 1, AST↓, 1, BP↓, 3, BP↝, 1, creat↓, 1, CRP↓, 1, GutMicro↑, 3, IL6↓, 3, LDH↓, 3,
Functional Outcomes ⓘ
AntiAge↑, 3, AntiCan↑, 2, AntiTum↑, 1, BOLD↑, 1, cardioP↓, 1, cardioP↑, 7, cognitive↑, 49, hepatoP↑, 3, memory↑, 20, Mood↑, 7, motorD↑, 5, neuroP↑, 27, RenoP↑, 1, Risk↓, 4, Sleep↑, 1, Strength↑, 1, Weight↓, 1,
Total Targets: 156
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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:557 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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