motorD Cancer Research Results

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3284- ALA,    Alpha-Lipoic Acid Mediates Clearance of Iron Accumulation by Regulating Iron Metabolism in a Parkinson's Disease Model Induced by 6-OHDA
- vitro+vivo, Park, NA
*antiOx↑, naturally occurring enzyme cofactor with antioxidant and iron chelator properties and has many known effects. ALA has neuroprotective effects on PD.
*IronCh↑,
*neuroP↑,
*ROS↓, decreasing the levels of intracellular reactive oxygen species and iron.
*Iron↓,
*BBB↑, ALA also provides neuroprotection against PD because it can penetrate the blood–brain barrier.
*motorD↑, ALA ameliorates motor behavior and prevents DA neuron loss in the SN of PD rat models.
*GSH↑, ALA Inhibits the Decrease in the Activity of SOD and GSH in the SN of a Rat Model of PD Induced by 6-OHDA

3443- ALA,    Molecular and Therapeutic Insights of Alpha-Lipoic Acid as a Potential Molecule for Disease Prevention
- Review, Var, NA - Review, AD, NA
*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 (

3547- ALA,    Potential Therapeutic Effects of Lipoic Acid on Memory Deficits Related to Aging and Neurodegeneration
- Review, AD, NA - Review, Park, NA
*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↑,

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

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

3821- Aroma,    Neuroprotective and Anti-Aging Potentials of Essential Oils from Aromatic and Medicinal Plants
- Review, AD, NA
*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.

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↑,

2731- BetA,    Betulinic Acid for Glioblastoma Treatment: Reality, Challenges and Perspectives
- Review, GBM, NA - Review, Park, NA - Review, AD, NA
BBB↑, Notably, its ability to cross the blood–brain barrier addresses a significant challenge in treating neurological pathologies.
*GSH↑, BA can also dramatically reduce catalepsy and stride length, while increasing the brain’s dopamine content, glutathione activity, and catalase activity in hemiparkinsonian rats
*Catalase↑,
*motorD↑,
*neuroP↑, in Alzheimer’s disease rat models, it can improve neurobehavioral impairments . BA has exhibited great neuroprotective properties.
*cognitive↑, BA improves cognitive ability and neurotransmitter levels, and protects from brain damage by lowering reactive oxygen species (ROS) levels
*ROS↓,
*antiOx↑, enhancing brain tissue’s antioxidant capacity, and preventing the release of inflammatory cytokines
*Inflam↓,
MMP↓, BA can decrease the mitochondrial outer membrane potential (MOMP)
STAT3↓, The compound can inhibit the signal transducer and activator of transcription (STAT) 3 signaling pathways, involved in differentiation, proliferation, apoptosis, metastasis formation, angiogenesis, and metabolism, and the NF-kB signaling pathway,
NF-kB↓,
Sp1/3/4↓, BA has shown an ability to control cancer growth through the modulation of Sp transcription factors, inhibit DNA topoisomerase
TOP1↓,
EMT↓, inhibit the epithelial-to-mesenchymal transition (EMT)
Hif1a↓, BA has also been associated with an antiangiogenic response under hypoxia conditions, through the STAT3/hypoxia-inducible factor (HIF)-1α/vascular endothelial growth factor (VEGF) signaling pathway
VEGF↓,
ChemoSen↑, BA has shown great potential as an adjuvant to therapy since its use combined with standard treatment of chemotherapy and irradiation can enhance their cytotoxic effect on cancer cells
RadioS↑,
BioAv↓, Despite having great potential as a therapeutic agent, it is hard for BA to fulfill the requirements for adequate water solubility, maintaining both significant cytotoxicity and selectivity for tumor cells.

3511- Bor,    Boron
- Review, NA, NA
*memory↑, In boron-deprived humans, boron supplementation improved mental alertness, attention, short-term memory, and motor speed and dexterity.
*motorD↑,
*neuroP↑,
Ca+2↓, human prostate cells, boric acid acts as a reversible noncompetitive inhibitor of cADPR leading to decreased endoplasmic reticulum Ca2+
ATF4↑, The decreased Ca2+ results in the E74 like ETS transcription factor 2α activating transcription factor 4 (ATF4) and nuclear factor erythroid 2 like 2 (Nrf2),
NRF2↑,
*Inflam↓, a dietary boron intake >0.4 mg/d may be useful for bone and brain health and in modulating inflammatory and oxidative stress
*ROS↓,

4265- CA,    Potential applications of nanomedicine for treating Parkinson's disease
- Review, Park, NA
*NRF2↑, Carnosic acid (CA) is defined as a natural product synthesized by plants of the Lamiaceae family, known for its potent Nrf2-ARE activating properties and neuroprotective role in early brain injury.
*ARE↑,
*neuroP↑,
*motorD↑, It enhances motor and cognitive function while modulating inflammatory markers in the central nervous system.
*cognitive↑,
*SOD↑, enhancement in the expression of superoxide dismutase, glutathione reductase, γ-glutamate-cysteine ligase modifier subunit, and γ-glutamate-cysteine ligase catalytic subunit, induction of caspase 3 cleavage
*GSR↑,
*NGF↑, Carnosic acid is a phenolic diterpene that promotes the synthesis of NGF in the glioblastoma cell lines and also enhances BDNF production in the dopaminergic neurons.
*BDNF↑,

5888- CAR,    Therapeutic application of carvacrol: A comprehensive review
- Review, Var, NA - Review, Stroke, NA - Review, Diabetic, NA - Review, Park, NA
*antiOx↑, demonstrated as anti‐oxidant, anticancer, diabetes prevention, cardioprotective, anti‐obesity, hepatoprotective and reproductive role, antiaging, antimicrobial, and immunomodulatory properties.
*AntiCan↑,
*AntiDiabetic↑,
*cardioP↑,
*Obesity↓,
*hepatoP↑,
*AntiAg↑,
*Bacteria↓,
*Imm↑,
MMP2↓, anticancer ability against malignant cells via decreasing the expressions of matrix metalloprotease 2 and 9, inducing apoptosis
MMP9↓,
Apoptosis↓,
MMP↓, disrupting mitochondrial membrane, suppressing extracellular signal‐regulated kinase 1/2 mitogen‐activated protein kinase signal transduction
ERK↓,
PI3K↓, decreasing the phosphoinositide 3‐kinase/protein kinase B.
ALAT↓, decreased the concentrations of alanine aminotransferase, alkaline phosphatase and aspartate aminotransferase,
*ROS↓, Essential oils found in plants are natural anti‐oxidants that reduce cell damage caused by reactive species and prevent mutagenic and carcinogenic processes.
*Catalase↑, Carvacrol has remarkably higher anti‐oxidative and hepatoprotective properties, which improves the activity of enzymatic anti‐oxidants (catalase, superoxide dismutase, and glutathione peroxidase)
*SOD↑,
*GPx↑,
*AST↓, Carvacrol decreased the level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactic acid dehydrogenase (LDH) and improved the status of inflammation, necrosis, and coagulation in the liver
*LDH↓,
*necrosis↓,
ROS↑, prostate cancer cells via lowering cell viability, increasing the rate of reactive oxygen species, and disrupting the mitochondrial membrane potential.
TumCCA↑, Carvacrol induced cell cycle arrest at G0/G1 that declined increased CDK inhibitor p21 expression and decreased cyclin‐dependent kinase 4 (CDK4), and cyclin D1 expressions.
CDK4↓,
cycD1/CCND1↓,
NOTCH↓, carvacrol inhibited Notch signaling in PC‐3 cells via downregulating Jagged‐1 and Notch‐1
IL6↓, human prostate cancer cell lines, which significantly reduced IL‐6
chemoP↑, Carvacrol has significant protective effects in reducing the side effects of chemotherapeutics such as irinotecan hydrochloride anticancer drugs that cause induction of intestinal mucositis.
*Pain↓, Pain management
*neuroP↑, The neuroprotective role of carvacrol was examined by Guan et al. in 2019 against ischemic stroke,
*TRPM7↓, downregulating TRPM7 channels
*motorD↑, improved catalepsy, akinesia, bradykinesia, locomotor activity, and motor coordination.
*NF-kB↓, Carvacrol reduced inflammatory biomarkers, such as nuclear factor κB and cyclooxygenase‐2, and levels of nitric oxides, malondialdehyde, and glutathione create oxidative stress.
*COX2↓,
*MDA↓,

5908- CAR,    Carvacrol improves neurological function by inhibiting TRPM7-mediated BBB disruption and hemorrhage after TBI
- in-vivo, Nor, NA
*TRPM7↓, carvacrol, a TRPM7 inhibitor
*BBB↑, Carvacrol treatment significantly attenuated BBB disruption and hemorrhage, preserved tight junction proteins
*motorD↑, Behaviorally, carvacrol improved neurological scores, motor performance, and cognitive function after TBI.
*cognitive↑, Carvacrol improves motor and cognitive function after TBI
*Dose↝, Carvacrol was administered at a dose of 50 mg/kg immediately and 8 h after TBI
MMPs↓, Carvacrol prevents loss of tight junction proteins by attenuating MMPs expression and activity after TBI

5927- CAR,    Neuroprotective Potential and Underlying Pharmacological Mechanism of Carvacrol for Alzheimer’s and Parkinson’s Diseases
- Review, AD, NA - Review, Park, NA
*memory↑, Carvacrol enhances memory and cognition by modulating the effects of oxidative stress, inflammation, and Aβ25-35-induced neurotoxicity in AD
*cognitive↑,
*ROS↓, reduces the production of reactive oxygen species and proinflammatory cytokine levels in PD
*Inflam↓,
*motorD↑, improves motor functions
*toxicity↓, in general, it is potentially safe for consumption
*TRPV3↑, Carvacrol is a potent agonist of transient receptor potential vanilloid 3 (TRPV3)
*other↓, mitigating oxidative stress (OS)/ADP-ribose (ADPR)-induced TRPM2 and GSK1016790A (GSK)-mediated TRPV4 activations
*antiOx↑, Essential oils, high in carvacrol, have powerful antioxidant properties [85-88] similar to vitamin E, ascorbic acid, and butyl hydroxyl toluene
*LDL↓, Low-density lipoprotein (LDL) is inhibited by carvacrol in vitro and mediates LDL oxidation within an incubation period of 12 h
*COX2↓, suppressing the expression level of cyclooxygenase-2 (COX-2),
*PPARα↑, triggering the peroxisome proliferator-activated receptors (PPAR) α and γ
*NO↓, inhibiting NO production
*AChE↓, Carvacrol's acetylcholinesterase inhibitory action is 10 times higher than thymol's, even though the two compounds have a relatively similar structure
*eff↑, carvacrol nanoemulsion treatment has shown more notable effects compared to carvacrol oil.
*SOD↑, increases superoxide dismutase (SOD) and catalase (CAT) activity
*Catalase↑,
*neuroP↑, neuroprotective effects of carvacrol against cognitive impairments and its potential in AD are shown in Fig. (2)
*BioAv↝, In rabbits, 1.5 g of orally administered carvacrol is progressively absorbed from the intestines, with approximately 30% of the whole dose remaining in the gastrointestinal system and 25% eliminated via urine after 22 h of administratio
*BBB↑, carvacrol in the brain tissues as it easily crosses the blood-brain barrier owing to its low molecular weight (150.2 g/mol) and higher lipophilicity
*BioAv↑, liposomal encapsulation [136], and solid lipid nanoparticles [137], were developed and found bioavailable on oral administration. These formulations exhibit improved solubility, stability, and bioavailability and enhance drug accumulation in the tiss

6041- CGA,    Effect of Chlorogenic Acid Intake on Cognitive Function in the Elderly: A Pilot Study
- Trial, AD, NA
*Dose↝, 6-month intake of a test beverage containing 330 mg of CGAs just before bedtime(dissolved in 100 mL of water)caffeine level of the test beverage was below the limit of quantification (<1 mg/100 g)
*memory↑, A 6-month intake of CGAs may improve attentional, executive, and memory functions in the elderly with complaints of subjective memory loss.
*Risk↓, High intake of fruits, vegetables, fish, nuts, and legumes and low intake of meat, high fat dairy, and sweets have been shown to delay aging-related cognitive impairment and reduce the risk of Alzheimer's disease (AD)
*cognitive↑, Improved cognitive function as a result of drinking coffee is thought to be mediated by caffeine and chlorogenic acids (CGAs).
*Aβ↓, CGAs protect neurons and suppress the aggregation of Aβ through antioxidative effects [12, 13].
*antiOx↓,
*motorD↑, Motor speed 92.5 ± 5.2 98.4 ± 7.7

6036- CGA,    Effect of Chlorogenic Acids on Cognitive Function: A Randomized, Double-Blind, Placebo-Controlled Trial
- Trial, Nor, NA
*motorD↑, The CGA group showed significant increase in the Cognitrax domain scores for motor speed, psychomotor speed, and executive function compared with the placebo group,
*cognitive↑, These results suggest that CGAs may improve some cognitive functions, which would help in the efficient performance of complex tasks.
*eff↑, Therefore, early intervention for maintaining normal cognitive function is one of the important factors for successful aging

4237- H2,    Hydrogen-Rich Saline Protects Against Spinal Cord Injury in Rats
- in-vitro, NA, NA
*Apoptosis↓, administration of hydrogen-rich saline decreased the number of apoptotic cells, suppressed oxidative stress, and improved locomotor functions.
*ROS↓,
*motorD↑,
*BDNF↑, Hydrogen-rich saline increased the release of BDNF.

4238- HNK,    Neuropharmacological potential of honokiol and its derivatives from Chinese herb Magnolia species: understandings from therapeutic viewpoint
- Review, AD, NA - NA, Park, NA
*BDNF↑, honokiol treatment led to an improvement in plasma BDNF levels.
*hepatoP↑, prevented liver damage by reducing transaminase levels (ALT and AST), liver OS, and TNF-α activity in mice challenged with LPS.
*ALAT↓,
*AST↓,
*TNF-α↓,
*SIRT3↑, 0.5, 1, 2, 5, 10 and 20 μM Enhanced SIRT3 expression, reduced Aβ levels
*Aβ↓,
*Apoptosis↓, Honokiol exhibited a dose-dependent reduction in hippocampal neural apoptosis, ROS generation, and decline in the membrane potential of mitochondria caused by AβO
*ROS↓,
*MMP↑,
*Ca+2↓, Dose-dependent reduction of ROS, suppression of intracellular Ca elevation, and inhibition of caspase-3 activity
*Casp3↓,
*Ach↑, Increased extracellular acetylcholine release to 165.5 ± 5.78% of the basal level
*PPARγ↑, Increased the expression of PPARγ and PGC1α
*PGC-1α↑,
*motorD↑, Improvement of motor dysfunction due to reversal of nigrostriatal dopaminergic neuronal loss
*TNF-α↓, Attenuated the levels of ROS, TNF-α, and IL-1β in both the in vivo and in vitro
*IL1β↓,

2872- HNK,    Honokiol alleviated neurodegeneration by reducing oxidative stress and improving mitochondrial function in mutant SOD1 cellular and mouse models of amyotrophic lateral sclerosis
- in-vivo, ALS, NA - NA, Stroke, NA - NA, AD, NA - NA, Park, NA
*eff↑, Honokiol (HNK) has been reported to exert therapeutic effects in several neurologic disease models including ischemia stroke, Alzheimer's disease and Parkinson's disease
*ROS↓, honokiol alleviated cellular oxidative stress by enhancing glutathione (GSH) synthesis and activating the nuclear factor erythroid 2-related factor 2 (NRF2)-antioxidant response element (ARE) pathway.
*GSH↑,
*NRF2↑,
*motorD↑, Importantly, honokiol extended the lifespan of the SOD1-G93A transgenic mice and improved the motor function
*OS↑,
*neuroP↑, honokiol exerted neuroprotection in ALS models.
*BBB↑, due to its strong lipophilic property, honokiol can readily permeate the blood–brain barrier and blood–cerebrospinal fluid barrier.
*cognitive↑, honokiol was shown a beneficial effect on the cognitive impairment in APP/PS1 via ameliorating the mitochondrial dysfunction
*eff↑, Furthermore, honokiol was applied for patent (200310121303.0) for ischemic stroke treatment, and the clinical trials would be started soon in China
*antiOx↑, Honokiol showed strong antioxidant capacity in vitro and protected the yeast against H2O2 induced oxidative damage
*Cyt‑c↑, cytoplasmic release of cytochrome c was markedly decreased
*PGC-1α↑, 10 μmol/L and significantly upregulated the PGC-1α, NRF1, and TFAM protein

2869- HNK,    Nature's neuroprotector: Honokiol and its promise for Alzheimer's and Parkinson's
- Review, AD, NA - Review, Park, NA
*neuroP↑, neuroprotective, anti-oxidant, anti-apoptotic, neuromodulating, anti-inflammatory, and many more qualities, honokiol,
*Inflam↓,
*motorD↑, degradation of dopaminergic neurons in Parkinson's disease and improving motor function.
*Aβ↓, Alzheimer's disease, honokiol showed promise in lowering the production of amyloid-beta (Aβ) plaques, phosphorylating tau, and enhancing cognitive performance
*p‑tau↓,
*cognitive↑,
*memory↑, prevented Acetylcholinesterase activity from elevation as well as improved acetylcholine levels, and improved learning, and memory deficits via increased ERK1/2 and Akt phosphorylation
*ERK↑,
*p‑Akt↑,
*PPARγ↑, honokiol has been reported to elevate PPARγ levels in APPswe/PS1dE9 mice as PPARγ is related to ani-inflammatory
*PGC-1α↑, honokiol boosted the expression of PGC1α and PPARγ
*MMP↑, as well as reduced elevated mitochondrial membrane potential and mitochondrial ROS
*mt-ROS↓,
*SIRT3↑, Honokiol has been found as a dual SIRT-3 activator and PPAR-γ agonist that reduced oxidative stress markers within cells and changed the AMPK pathway
*IL1β↓, honokiol prevented restraint stress-induced cognitive dysfunction by reducing the hippocampus's production of IL-1β, TNF-α, glucose-regulated protein (GRP78), and C/EBP homologous protein (CHOP)
*TNF-α↓,
*GRP78/BiP↓,
*CHOP↓,
*NF-kB↓, Additionally, the neuroprotective benefits of honokiol in mice with Aβ-induced learning and memory impairment have been attributed to the inactivation of NF-κB
*GSK‐3β↓, Treatment of honokiol in PC12 cells resulted in reduced GSK-3β and induced β-catenin which effectively showed the neuroprotective and anti-oxidant effect in AD therapy
*β-catenin/ZEB1↑,
*Ca+2↓, , anti-apoptotic effect via reduced caspase 3 levels, and protected membrane injury by reduced calcium level has been investigated in PC12 cells of AD models
*AChE↓, protective effects by serving as an antioxidant, reduced AchE levels, repaired neurofibrillary tangles, reduced NF-kB which downregulates Aβ plaque
*SOD↑, fig1
*Catalase↑,
*GPx↑,

4233- LEC,    Lecithinized brain-derived neurotrophic factor promotes the differentiation of embryonic stem cells in vitro and in vivo
- in-vitro, Nor, NA
*BDNF↑, In the current study, we show that lecithinized BDNF (PC-BDNF) has a higher affinity than BDNF for neural precursor cells.
*motorD↑, PC-BDNF-treated cells was more effective than BDNF-treated cells at improving impaired motor function caused by spinal cord injury.
*Diff↑, PC-BDNF has a better potential than BDNF for promoting neural differentiation, partly due to a higher cellular affinity.

2253- MF,    Low-frequency pulsed electromagnetic field promotes functional recovery, reduces inflammation and oxidative stress, and enhances HSP70 expression following spinal cord injury
- in-vivo, Nor, NA
*Inflam↓, LPEMFs decreased the expression of inflammatory factors, including tumor necrosis factor-α, interleukin-1β and nuclear factor-κB.
*TNF-α↓, after 2 weeks of LPEMF treatment, the expression of TNF-α and IL-1β were decreased in comparison with the SCI group
*IL1β↓,
*NF-kB↓, administration of LPEMFs significantly reduced the immunoreactivity of NF-κB in SCI rats
*iNOS↓, Additionally, LPEMFs exposure reduced the levels of inducible nitric oxide synthase and reactive oxygen species, and upregulated the expression of catalase and superoxide dismutase.
*ROS↓, LPEMFs can alleviate the oxidative stress by reducing ROS production following SCI
Catalase↑,
*SOD↑,
*HSP70/HSPA5↑, Furthermore, treatment with LPEMFs significantly enhanced the expression of HSP70 in spinal cord-injured rats
*neuroP↑, LPEMFs exhibit strong neuroprotective effects in the nervous system
*motorD↑, LPEMF exposure can promote locomotor recovery in SCI rats
*antiOx↑, protective effect of LPEMFs on oxidative stress may be attributed to the upregulation of antioxidant enzymes.

4097- MF,    Theta Frequency Electromagnetic Stimulation Enhances Functional Recovery After Stroke
- Trial, Stroke, NA
*motorD↑, ELF-EMF (5 Hz) effectively enhances functional recovery in a reach-to-grasp task, whereas neither gamma-frequency (40 Hz) nor combination frequency (5–16-40 Hz) ELF-EMFs induce a significant effect
*eff↑, gamma-band oscillations in general, and 40 Hz in specific, are important for learning and memory and for setting how the brain will form new connections as it develops.
*Dose↝, 56-turn Helmholtz coils (42 cm radius), capable of generating 1–100 Hz EMFs at intensities of 0.3 to 10G

4095- MF,    Frequency-tuned electromagnetic field therapy improves post-stroke motor function: A pilot randomized controlled trial
- Trial, Stroke, NA
*Dose↝, ENTF therapy (1–100 Hz, < 1 G). Participants received 40 min of active ENTF or sham treatment 5 days/week for 8 weeks;
*motorD↑, ENTF stimulation in subacute ischemic stroke patients was associated with improved UE motor function and reduced overall disability, and results support its safe use in the indicated population.

4119- MF,    Therapeutic potential and mechanisms of repetitive transcranial magnetic stimulation in Alzheimer’s disease: a literature review
- Review, AD, NA
*cognitive↑, Recent clinical evidence demonstrates that rTMS can significantly improve cognitive function, memory, language abilities, and motor performance in AD patients, particularly when administered with optimized parameters targeting key brain regions, such
*memory↑,
*motorD↑,
*eff↑, Meta-analyses indicate that high-frequency protocols (particularly 20 Hz) delivered over at least 3 weeks with a minimum of 20 sessions produce the most significant cognitive improvements
*eff↑, high-frequency stimulation at 20 Hz, with stimulation durations of 1–2 s and intervals of 20–30 s between stimulations
*Dose↝, The common scheme of intermittent θ burst is 2 s burst, 8 s off, and repeated in turn
*Dose↝, After half an hour of transcranial magnetic stimulation treatment with 1.5 T
*Dose↝, rTMS to the left dorsolateral prefrontal cortex (DLPFC) at 120% of motor threshold, using 10 Hz frequency for 4-s durations, with 26-s intervals between train deliveries, totaling 75 trains (37.5 min per session).
*BDNF↑, repetitive transcranial magnetic stimulation reverses hippocampal depletion of nerve growth factor and brain-derived neurotrophic factor (BDNF)
*Aβ↓, reduces β-amyloid (Aβ) aggregation—mechanisms that collectively improve cognitive function.
*eff↑, Studies have identified 3 Hz as the optimal stimulation frequency for achieving maximal therapeutic benefit in addressing swallowing disorders

4101- MF,    Benign Effect of Extremely Low-Frequency Electromagnetic Field on Brain Plasticity Assessed by Nitric Oxide Metabolism during Poststroke Rehabilitation
- Human, Stroke, NA
*motorD↑, ELF-EMF treatments improved functional and mental status
*cognitive↑,
*eff↑, We conclude that ELF-EMF therapy is capable of promoting recovery in poststroke patients.
*NO↑, evidence that application of extremely low-frequency electromagnetic field increases nitric oxide generation and its metabolism, as well as improving the effectiveness of poststroke ischemic patients' treatments.
*other↝, Due to its vasodilating and proangiogenic effects, NO serves as a protective function during cerebral ischemia
*neuroP↑, In conclusion, ELF-EMF therapy increases the metabolism and generation of NO, which has both neuroprotective and cytotoxic properties.

3566- MF,    Positive and Negative Effects of Administering a Magnetic Field to Patients with Rheumatoid Arthritis (RA)
- Study, Arthritis, NA
*Inflam↓, Magnetotherapy applied to patients with rheumatoid arthritis (RA) produces anti-inflammatory, analgesic and antioedema effects.
*QoL↑, findings show improved functional status by 0.26 points on average (p = 0.0166) measured with the Health Assessment Questionnaire (HAQ-20),
*Pain↓, reduced pain by 2.2 points on average (p = 0.0000) on the Visual Analogue Scale (VAS)
*motorD↑, decreased duration of morning stiffness by 23.2 min on average (p = 0.0010) and reduced severity of morning stiffness by 15.2 points on average. entire group showed an increase in the range of motion in the joints of the dominant hand by 1.9 mm on av
*toxicity↓, Magnetotherapy, being a non-thermal method, is safe and rarely causes negative effects
*Cartilage↑, it slows down degenerative processes in the porcine articular cartilage.
*Inflam↓, Conversely, in the PEMF group, the hand volume decreased by as much as 19.5 mm3 on average and the change was statistically significant.

3568- MF,    The Efficacy of Pulsed Electromagnetic Fields on Pain, Stiffness, and Physical Function in Osteoarthritis: A Systematic Review and Meta-Analysis
- Review, Arthritis, NA
*eff↑, Compared with the control groups, the PEMF treatment yielded a more favorable output.
*Pain↓, PEMF alleviated pain (standardized mean differences [SMD] = 0.71, 95% confidence interval [CI]: 0.08–1.34, p = 0.03),
*motorD↑, improved stiffness (SMD = 1.34, 95% CI: 0.45–2.23,p=0.003), and restored physical function (SMD = 1.52, 95% CI: 0.49–2.55,p=0.004).

3569- MF,    Current Evidence Using Pulsed Electromagnetic Fields in Osteoarthritis: A Systematic Review
- Review, Arthritis, NA
*Pain↓, Pain reduction, assessed through VAS and WOMAC scores, showed significant improvement (60% decrease in VAS, 42% improvement in WOMAC). The treatment duration varied (15 to 90 days), with diverse PEMF devices used
*QoL↑, Secondary outcomes included improvements in quality of life, reduced medication usage, and enhanced physical function.
*motorD↑,

3489- MFrot,  MF,    Rotating magnetic field inhibits Aβ protein aggregation and alleviates cognitive impairment in Alzheimer's disease mice.
- in-vivo, AD, NA
*Aβ↓, RMF directly inhibited Aβ amyloid fibril formation and reduced Aβ-induced cytotoxicity in neural cells .
*motorD↑, RMF restored motor abilities to healthy control levels and significantly alleviated cognitive impairments, including exploration and spatial and non-spatial memory abilities.
*cognitive↑,
*memory↑,
*ROS↓, reduced oxidative stress in the APP/PS1 mouse brain.

212- MFrot,  MF,    Rotating magnetic field inhibits Aβ protein aggregation and alleviates cognitive impairment in Alzheimer’s disease mice
- in-vivo, AD, SH-SY5Y
*β-Amyloid↓, Aβ amyloid fibril formation
*cognitive↑,
*motorD↑, RMF improves motor and exploration abilities in APP/PS1 mice
*ROS↓, RMF reduces oxidative stress in APP/PS1 mouse brains and lipid deposition in the liver
*memory↑, RMF significantly alleviates spatial memory impairments in APP/PS1 mice
*Aβ?, 0.4 T RMF inhibits Aβ amyloid fibril formation in vitro

3806- mushLions,    Dietary Supplementation of Lion's Mane Medicinal Mushroom, Hericium erinaceus (Agaricomycetes), and Spatial Memory in Wild-Type Mice
- in-vitro, NA, NA
*motorD↑, H. erinaceus increased general locomotor activity but had no effect on spatial memory.
*memory↑, oral supplementation with H. erinaceus yields specific and selective improvements in recognition memory without altering spatial working memory, which supports the hypothesis that recognition memory can be modeled as a dual process.

4036- NAD,  VitB3,    NAD+ supplementation normalizes key Alzheimer’s features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency
- in-vivo, AD, NA
*Inflam↓, NAD+ supplementation with nicotinamide riboside significantly normalized neuroinflammation, synaptic transmission, phosphorylated Tau, and DNA damage as well as improved learning and memory and motor function.
*p‑tau↓, NR Decreases Tau Phosphorylation but Not Aβ Accumulation in AD and AD/Polβ Mice.
*DNAdam↓,
*memory↑,
*motorD↑,
*cognitive↑, NR improved cognitive function in multiple behavioral tests and restored hippocampal synaptic plasticity in 3xTgAD mice and 3xTgAD/Polβ+/− mice.
*BBB↑, NR enters the brain and boosts cellular NAD+ levels when administered orally.
IL1β↓, AD/Polβ mice had elevated levels of proinflammatory cytokines and chemokines, including IL-1α, TNFα, MCP-1, IL-1β, MIP-1α, and RANTES, and decreased levels of antiinflammatory cytokines such as IL-10 (Fig. 3G and Fig. S4A). NR treatment normalized
*TNF-α↓,
*MCP1↓,
*RANTES↓,
*ROS↓, NR treatment of AD fibroblasts resulted in decreased levels of mitochondrial ROS compared with vehicle-treated cells
*SIRT3↑, NR Treatment Decreases DNA Damage and Apoptosis Through SIRT3 and SIRT6.
*SIRT6↑,

4223- NarG,    Effect of 2-Week Naringin Supplementation on Neurogenesis and BDNF Levels in Ischemia–Reperfusion Model of Rats
- in-vivo, Stroke, NA
*neuroG↑, 2 weeks of naringin supplementation may have protective effects on impaired neurogenesis and BDNF levels after brain ischemia and reperfusion in rats
*BDNF↑,
*motorD↑, Naringin Improved Motor Function After Ischemia/Reperfusion

4225- NarG,    Naringin treatment improves functional recovery by increasing BDNF and VEGF expression, inhibiting neuronal apoptosis after spinal cord injury
- in-vivo, NA, NA
*motorD↑, naringin-treated animals had significantly better locomotor function recovery, less myelin loss, and higher expression of BDNF and VEGF.
*BDNF↑,
*VEGF↑,
*Bax:Bcl2↓, naringin treatment significantly increased in Bcl-2:Bax ratio, reduced the enzyme activity of caspase-3 and decreased the number of apoptotic cells after SCI.
*Casp3↓,
*Apoptosis↓,
*eff↑, findings suggest that naringin treatment starting 1 day after SCI can significantly improve locomotor recovery, and this neuroprotective effect may be related to the upregulation of BDNF and VEGF and the inhibition of neural apoptosis.

3249- PBG,    Can Propolis Be a Useful Adjuvant in Brain and Neurological Disorders and Injuries? A Systematic Scoping Review of the Latest Experimental Evidence
- Review, Var, NA
*Inflam↓, ropolis was consistently demonstrated to reduce the expression of inflammatory and oxidative markers such as malonaldehyde (MDA), tumor necrosis factor-α (TNF-α), nitric oxide (NO), and inducible nitric oxide synthase (iNOS)
*ROS↓,
*MDA↓,
*TNF-α↓,
*NO↓,
*iNOS↓,
*SOD↑, while increasing and maintaining antioxidant parameters, namely superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH)
*GPx↑,
*GSR↓,
*GSH↑,
*neuroP↑, neuroprotective effect of propolis was also demonstrated in terms of alleviating symptoms associated with aneurysm, ischemia, ischemia-reperfusion and traumatic brain injuries.
*IL6↓, Propolis reduced the expression of interleukin-6 (IL-6), TNF-α, matrix metalloproteinase-2 (MMP-2), MMP-9, monocyte chemotactic protein-1 (MCP-1), and iNOS
*MMP2↓,
*MMP9↓,
*MCP1↓,
*HSP70/HSPA5↑, while increasing the expression of protective proteins such as heat shock protein-70 (hsp70)
*motorD↑, significantly ameliorate the impairment of sensory–motor and other physical indices in animals subjected to these injuries
*Pain↓, Unsurprisingly, propolis was shown to be effective in attenuating symptoms of neuroinflammation, pain, and oxidative stress.
*VCAM-1↓, consistently shown to reduce inflammation markers such as vascular cell adhesion molecule-1 (VCAM-1), nuclear factor kappa B (NF-kB), mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK)-
*NF-kB↓,
*MAPK↓,
*JNK↓,
*IL1β↓, It also reduced the expression of reactive oxygen species (ROS) and pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α
*AChE↓, propolis inhibited the activity of both acetylcholinesterase and butyrylcholinesterase in a dose-dependent manner
*toxicity∅, Kalia et al. (2014) observed no cytotoxicity in organs, including the brain of normal mice fed up to 1000 mg propolis extract/ kg body weight.
cognitive↑, figure 4

3587- PI,    Piperine: A review of its biological effects
- Review, Park, NA - Review, AD, NA
*hepatoP↑, piperine has also been documented for its hepatoprotective, anti-allergic, anti-inflammatory, and neuroprotective properties
*Inflam↓,
*neuroP↑,
*antiOx↑, antiangiogenesis, antioxidant, antidiabetic, antiobesity, cardioprotective,
*angioG↑,
*cardioP↑,
*BioAv↑, nano-encapsulation and resulting piperine-loaded nanoparticles enhance the bioavailability of piperine via oral administration
*P450↓, piperine inactivates cytochrome P450 (CYP) 3A (CYP3A), which plays a critical role in drug metabolism
*eff↑, enhances the anti-inflammatory effects when combined with resvera- trol
*BioAv↑, piperine increases the bioavailability of various compounds such as ciprofloxacin, norfloxacin, metronidazole, oxytetracycline, nimesulide, pentobarbitone, phenytoin, resveratrol, beta-carotene, curcumin, gallic acid, tiferron, nevirapine, and sparte
E-cadherin↓, Downregulates the E-cadherin (E-cad), estrogen receptor (ER), matrix metalloproteinase 2 (MMP-2), matrix metalloproteinase 9 (MMP- 9), vascular endothelial growth factor (VEGF) levels, and c-Myc.
ER(estro)↓,
MMP2↓,
MMP9↓,
VEGF↓,
cMyc↓,
BAX↑, Increases the expressions of Bax and p53.
P53↑,
TumCG↓, Lowers the tumor growth and elevates survival time
OS↑,
*cognitive↑, piperine ameliorated the neuro-chemical, neuroinflammatory, and cognitive alterations caused by chronic exposure to galactose
*GSK‐3β↓, piperine reversed D-Gal-induced GSK-3β activation through modulating PKC and PI3K/AKT pathways, s
*GSH↑, Piperine stimulates glutathione levels in rats' striatum, reduced caspase-3 and 9 activation, and diminished release of cytochrome-c from mitochondria along with a reduction in lipid peroxidation
*Casp3↓,
*Casp9↓,
*Cyt‑c↓,
*lipid-P↓,
*motorD↑, piperine also caused improvement in motor coordination and balance behavior along with reduction in contralateral rotations.
*AChE↓, significantly amended impaired memory and hippo-campus neurodegeneration and lowered lipid peroxidation and acetylcholinesterase enzyme
*memory↑,
*cardioP↑,
*ROS↓, fig 6
*PPARγ↑,
*ALAT↓, piperine lowers alanine aminotransferase (ALT), AST, and ALP levels in sera of cholesterol-fed albino mice
*AST↓,
*ALP↓,
*AMPK↑, reversed the downregulation of AMPK signaling molecules, which are responsible for fatty acid oxidation, insulin signaling, and lipogenesis in mouse liver.
*5HT↑, t causes a significant decrease in serotonin (5-HT) and brain-derived neurotrophic factor (BDNF) contents in the hippocampus and frontal cortex.
*SIRT1↑, , it may enhance the SIRT1 expression in cells and SIRT1 activity enhancing its potential to prevent SIRT1-mediated disease
*eff↑, combination ther- apy of resveratrol and piperine as an approach to enhance the biologi- cal effects with respect to cerebral blood flow and improved cognitive functions

3606- QC,    The Effect of Quercetin on Inflammatory Factors and Clinical Symptoms in Women with Rheumatoid Arthritis: A Double-Blind, Randomized Controlled Trial
- Trial, Arthritis, NA
*motorD↑, Quercetin supplementation for 8 weeks significantly reduced EMS, morning pain, and after-activity pain
*Pain↓,
*TNF-α↓, Plasma hs-TNFα level was significantly reduced in the quercetin group compared to placebo
*IL8↓, Other studies showed that 30 mM quercetin decreased gene expression and production of IL-8, 1L-6, IL-1b, and TNFa, which are the major inflammatory cytokines i
*IL6↓,
*IL1β↓,
*NF-kB↓, also inhibited the activity of NF-kB and P38-kinase protein
*p38↓,

3367- QC,    Targeting Nrf2 signaling pathway by quercetin in the prevention and treatment of neurological disorders: An overview and update on new developments
- Review, Stroke, NA - Review, AD, NA
*NRF2↑, Que enhanced the expression of Nrf2 and inhibited alterations in the shape and death of neurons in the hippocampus.
*neuroP↑,
*motorD↑, Que protected the blood-brain barrier via stimulating Nrf2 in animal stroke, which alleviated ischemic reperfusion and motor dysfunction.
*Inflam↓, (2) By triggering the Nrf2 pathway, Que reduced the neuroinflammation and oxidative damage brought on by TBI in the cortex
*cognitive↑, (3) In an experimental model of AD, Que enhanced cognitive function by decreasing A1-4, antioxidant activity, and Nrf2 levels in the brain.

5781- RES,    Resveratrol improves health and survival of mice on a high-calorie diet
- in-vivo, Nor, NA
*AntiAge↑, Resveratrol produces changes associated with longer lifespan, including increased insulin sensitivity, reduced insulin-like growth factor-1 (IGF-I) levels, increased AMP-activated protein kinase (AMPK)
*IGF-1↓,
*AMPK↑,
*CRM↑, resveratrol opposed the effects of the high-calorie diet in 144 out of 153 significantly altered pathways.
*PGC-1α↑, activated receptor- γ coactivator 1α (PGC-1α) activity, increased mitochondrial number, and improved motor function.
*mtDam↓,
*motorD↑, Surprisingly, the resveratrol-fed HC mice steadily improved their motor skills as they aged
*hepatoP↑, At 18 months of age it was apparent that the high-calorie diet greatly increased the size and weight of livers and that resveratrol prevented these changes
*Dose↝, this study shows that an orally available small molecule at doses achievable in humans can safely reduce many of the negative consequences of excess caloric intake, with an overall improvement in health and survival.

2566- RES,    A comprehensive review on the neuroprotective potential of resveratrol in ischemic stroke
- Review, Stroke, NA
*neuroP↑, comprehensive overview of resveratrol's neuroprotective role in IS
*NRF2↑, Findings from previous studies suggest that Nrf2 activation can significantly reduce brain injury following IS and lead to better outcomes
*SIRT1↑, neuroprotective effects by activating nuclear factor erythroid 2-related factor 2 (NRF2) and sirtuin 1 (SIRT1) pathways.
*PGC-1α↑, IRT1 activation by resveratrol triggers the deacetylation and activation of downstream targets like peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α) and forkhead box protein O (FOXO)
*FOXO↑,
*HO-1↑, ctivation of NRF2 through resveratrol enhances the expression of antioxidant enzymes, like heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1), which neutralize reactive oxygen species and mitigate oxidative stress in the ischemic bra
*NQO1↑,
*ROS↓,
*BP↓, Multiple studies have demonstrated that resveratrol presented protective effects in IS, it can mediate blood pressure and lipid profiles which are the main key factors in managing and preventing stroke
*BioAv↓, The residual quantity of resveratrol undergoes metabolism, with the maximum reported concentration of free resveratrol being 1.7–1.9 %
*Half-Life↝, The levels of resveratrol peak 60 min following ingestion. Another study found that within 6 h, there was a further rise in resveratrol levels. This increase can be attributed to intestinal recirculation of metabolites
*AMPK↑, Resveratrol also increases AMPK and inhibits GSK-3β (glycogen synthase kinase 3 beta) activity in astrocytes, which release energy, makes ATP available to neurons and reduces ROS
*GSK‐3β↓,
*eff↑, Furthermore, oligodendrocyte survival is boosted by resveratrol, which may help to preserve brain homeostasis following a stroke
*AntiAg↑, resveratrol may suppress platelet activation and aggregation caused by collagen, adenosine diphosphate, and thrombin
*BBB↓, Although resveratrol is a highly hydrophobic molecule, it is exceedingly difficult to penetrate a membrane like the BBB. However, an alternate administration is through the nasal cavity in the olfactory area, which results in a more pleasant route
*Inflam↓, Resveratrol's anti-inflammatory effects have been demonstrated in many studies
*MPO↓, Resveratrol dramatically lowered the amounts of cerebral infarcts, neuronal damage, MPO activity, and evans blue (EB) content in addition to neurological impairment scores.
*TLR4↓, TLR4, NF-κB p65, COX-2, MMP-9, TNF-α, and IL-1β all had greater levels of expression after cerebral ischemia, whereas resveratrol decreased these amounts
*NF-kB↓,
*p65↓,
*MMP9↓,
*TNF-α↓,
*IL1β↓,
*PPARγ↑, Previous studies have shown that resveratrol activates the PPAR -γ coactivator 1α (PGC-1 α), which has free radical scavenging properties
*MMP↑, Resveratrol can prevent mitochondrial membrane depolarization, preserve adenosine triphosphate (ATP) production, and inhibit the release of cytochrome c
*ATP↑,
*Cyt‑c∅,
*mt-lipid-P↓, mitochondrial lipid peroxidation (LPO), protein carbonyl, and intracellular hydrogen peroxide (H2O2) content were significantly reduced in the resveratrol treatment group, while the expression of HSP70 and metallothionein were restored
*H2O2↓,
*HSP70/HSPA5↝,
*Mets↝,
*eff↑, Shin et al. showed that 5 mg/kg intravenous (IV) resveratrol reduced infarction volume by 36 % in an MCAO mouse model.
*eff↑, This study indicates that resveratrol holds the potential to improve stroke outcomes before ischemia as a pre-treatment strategy
*motorD↑, resveratrol treatment significantly reduced infarct volume and prevented motor impairment, increased glutathione, and decreased MDA levels compared to the control group,
*MDA↓,
*NADH:NAD↑, Resveratrol treatment significantly enhanced the intracellular NAD+/NADH ratio
eff↑, Pretreatment with resveratrol (20 or 40 mg/kg) significantly lowered the cerebral edema, infarct volume, lipid peroxidation products, and inflammatory markers
eff↑, Intraperitoneal administration of resveratrol at a dose of 50 mg/kg reduced cerebral ischemia reperfusion damage, brain edema, and BBB malfunction

3617- RosA,  Aroma,    Effect of aromatherapy on patients with Alzheimer's disease
- in-vivo, AD, NA
*other↝, Aromatherapy consisted of the use of rosemary and lemon essential oils in the morning, and lavender and orange in the evening
*cognitive↑, All patients showed significant improvement in personal orientation related to cognitive function on both the GBSS-J and TDAS after therapy.
*motorD↑, In addition, some improvement in movement was noted

2358- SK,    SIRT1 improves lactate homeostasis in the brain to alleviate parkinsonism via deacetylation and inhibition of PKM2
- in-vivo, Park, NA
*eff↑, inhibition of PKM2 by shikonin or PKM2-IN-1 alleviates parkinsonism in mice
*PKM2↓,
*motorD↑, Behavioral tests showed that shikonin treatment improved the performance on rotarod, tail suspension, and olfaction (Figure 7B).
*lactateProd↓, Lactate in the CSF was reduced in shikonin-treated A30P mice

2138- TQ,    Thymoquinone has a synergistic effect with PHD inhibitors to ameliorate ischemic brain damage in mice
- in-vivo, Nor, NA
*Hif1a↑, TQ can activate the HIF-1α pathway and its downstream genes such as VEGF, TrkB, and PI3K, which in turn enhance angiogenesis and neurogenesis.
*VEGF↑,
*TrkB↑,
*PI3K↑,
*angioG↑, which in turn enhance angiogenesis and neurogenesis.
*neuroG↑,
*motorD↑, TQ has the same effect as DMOG to activate HIF-1 α and can improve motor dysfunction after ischemic stroke

2139- TQ,    Thymoquinone regulates microglial M1/M2 polarization after cerebral ischemia-reperfusion injury via the TLR4 signaling pathway
- in-vivo, Nor, NA
*TLR4↓, TQ inhibits the TLR4 / NF-κB pathway to regulate microglia polarization.
*NF-kB↓,
*Inflam↓, TQ attenuates inflammation in brain I/R by affecting microglia polarization.
*Hif1a↑, TQ can activate Hif-1α to counter-regulate the TLR4 / NF-κB pathway.
*motorD↑, TQ could improve the motor deficits caused by I/R.

4869- Uro,    Urolithin A in Central Nervous System Disorders: Therapeutic Applications and Challenges
- Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*MitoP↑, key biological effects of UA, including its promotion of mitophagy and mitochondrial homeostasis, as well as its anti-inflammatory, antioxidant, anti-senescence, and anti-apoptotic properties
*Inflam↓,
*antiOx↑,
*Risk↓, UA’s therapeutic potential in CNS disorders, such as Alzheimer’s disease, Parkinson’s disease, and stroke.
*Aβ↓, UA enhances microglial phagocytosis of Aβ plaques, suppresses neuroinflammation, and reduces tau hyperphosphorylation by restoring mitophagy to eliminate abnormal mitochondria
*p‑tau↓,
*p62↓, In doxorubicin-induced cardiomyopathy mice, UA upregulates p62, LC3-II, PINK1, and Parkin expression, restoring impaired mitophagy, mitigating membrane potential loss and ROS accumulation,
*PARK2↑,
*MMP↑,
*ROS↓,
*Strength↑, Randomized controlled trials in healthy middle-aged and older adults show that oral supplementation with 500–1000 mg of UA significantly improves skeletal muscle endurance and mitochondrial efficiency, reduces plasma inflammatory markers (such as C-r
*CRP↓,
*IL1β↓, UA activates sirtuin 1 (SIRT1)-mediated deacetylation of NF-κB p65, suppressing glial cell activation and the production of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α)
*IL6↓,
*TNF-α↓,
*AMPK↑, UA enhances brain adenosine 5′-monophosphate-activated protein kinase (AMPK) activation, attenuating NF-κB and MAPK activity, mitigating neuroinflammation, and supporting synaptic recovery
*NF-kB↓,
*MAPK↓,
*p62↑, In a renal ischemia-reperfusion injury model, UA activates the p62—kelch-like ECH-associated protein 1 (Keap1)—nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, boosting superoxide dismutase and catalase activity while lowering ROS levels
*NRF2↑,
*SOD↑,
*Catalase↑,
*HO-1↑, UA upregulates the Keap1-Nrf2/heme oxygenase 1 (HO-1) pathway to inhibit ferroptosis and reduce lipid peroxide accumulation in lung tissue
*Ferroptosis↓,
*lipid-P↓,
*Cartilage↑, reducing cartilage degradation and synovial inflammation
*PI3K↓, UA suppresses the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) and Akt/IκB kinase (IKK)/NF-κB signaling pathways, reducing neuronal apoptosis while enhancing BBB integrity and neurological outcomes
*Akt↓,
*mTOR↓,
*Apoptosis↓,
*neuroP↑,
*Bcl-2↓, cerebral artery occlusion model, UA treatment lowers Bcl-2 expression and elevates Bcl-2 associated X protein (Bax) and caspase-3 levels
*BAX↑,
*Casp3↑,
*ATP↑, UA restores mitochondrial membrane potential and ATP production in cardiomyocytes, balancing carnitine palmitoyltransferase1-dependent fatty acid oxidation to reduce apoptosis
*eff↑, in humanized homozygous amyloid beta knockin mice modeling late-onset AD, UA combined with green tea extract (Epigallocatechin gallate) more effectively reduces brain Aβ40 and Aβ42 levels compared to UA alone [106].
*motorD↑, UA administration elevated striatal dopamine levels and enhanced motor coordination, accompanied by suppression of NLRP3 inflammasome activation
*NLRP3↓,
*radioP↑, In a radiation-induced primary astrocyte model, UA activated the PINK1/Parkin-mediated mitophagy pathway, significantly reducing ROS levels in both cells and mitochondria,
*BBB↑, preclinical studies showing that UA primarily crosses the mouse BBB

4861- Uro,    Urolithin A improves Alzheimer's disease cognition and restores mitophagy and lysosomal functions
- in-vivo, AD, NA
*memory↑, Long‐term UA treatment significantly improved learning, memory, and olfactory function in different AD transgenic mice.
*Aβ↓, UA also reduced amyloid beta (Aβ) and tau pathologies and enhanced long‐term potentiation
*toxicity↓, A phase I clinical study confirmed that UA was safe in healthy, sedentary older adults, and that activation of mitochondrial biomarkers in muscle and plasma was observed
*BBB↑, may play a therapeutic role in the brain as it crosses the blood–brain barrier.
*p‑tau↓, UA decreased Aβ accumulation and tau phosphorylation in AD mice
*eff↓, and that the effects disappeared if UA treatment was suspended for 1 month.
*IL1α↓, several proinflammatory cytokines were increased in AD mice and decreased after UA treatment, including Interleukin 1 alpha (IL‐1α), monocyte chemoattractant protein‐1 (MCP‐1)
*MCP1↓,
*MIP‑1α↓, macrophage inflammatory protein‐1 alpha (MIP‐1α), tumor necrosis factor (TNFα), Interleukin 2 (IL‐2)
*TNF-α↓,
*IL2↓,
*SIRT1↓, UA induced sirtuin expression, mitophagy, and decreased DNA damage
*DNAdam↓,
*Dose↝, UA at doses from 250 to 2000 mg in humans 25 and 1–450 mg/kg in mice 80 has been reported to be safe.
*Strength↑, UA increased muscle strength and physical performance in a 6‐min walk test in elderly humans after 4 months of supplementation.
*motorD↑, Other studies reported that UA improved motor activity in the rotarod test and increased total distance traveled and average speed in the open field test in young C57BL/6J mice 82 and 3xTg AD mice
*CTSZ↓, Ctsz was highly expressed in multiple AD transgenic mouse models, and its expression was normalized by UA treatment

4874- Uro,  EGCG,    A Combination Therapy of Urolithin A+EGCG Has Stronger Protective Effects than Single Drug Urolithin A in a Humanized Amyloid Beta Knockin Mice for Late-Onset Alzheimer's Disease
- in-vivo, AD, NA
*motorD↑, increased positive effects of urolithin A and a combination treatment of urolithin A+EGCG in hAbKI mice for phenotypic behavioral changes including motor coordination, locomotion/exploratory activity, spatial learning and working memory
*memory↑,
*MitoP↑, mitophagy and autophagy genes were upregulated
*Aβ↓, The levels of amyloid beta (Aβ) 40 and Aβ42 are reduced in both treatments, however, the reduction is higher for combined treatment
*mitResp↑, Mitochondrial respiration is stronger for urolithin A compared to EGCG, indicating that mitophagy enhancer, urolithin A is a better and more promising molecule to enhance mitophagy activity.
*Nrf1↑, table4
*PINK1↑,
*PARK2↑,
*ATG5↑,
*Bcl-2↑,
*H2O2↓, we found hydrogen peroxide levels were reduced in urolithin A (p = 0.0008) and urolithin A+EGCG (p = 0.0004) treated hAbKI mice relative to untreated mice.
*ROS↓, urolithin A and EGCG act as free radical scavengers in hAbKI mice
*lipid-P↓, (lipid peroxidation) were also significantly reduced in urolithin A (p = 0.0003) and urolithin A+EGCG (p = 0.0002) treated hAbKI mice relative to untreated hAbKI mice
*mt-ATP↑, mitochondrial ATP levels were increased in urolithin A (p = 0.007) and urolithin A+EGCG (p = 0.0002) treated hAbKI mice relative to hAbKI untreated mice.

4334- VitB5,    Pantethine treatment is effective in recovering the disease phenotype induced by ketogenic diet in a pantothenate kinase-associated neurodegeneration mouse model
- in-vivo, AD, NA
*neuroP↑, pantethine administration can prevent the onset of the neuromuscular phenotype in mice suggesting the possibility of experimental treatment in patients with pantothenate kinase-associated neurodegeneration.
*motorD↑, Motor performance evaluation
*MMP↑, Pantethine restores mitochondrial membrane potential of Pank2−/− neurons
*OCR↑, pantethine was able to significantly increase oxygen consumption rate


Showing Research Papers: 1 to 48 of 48

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 48

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↑, 1,   NRF2↑, 1,   ROS↓, 1,   ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 2,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   cMyc↓, 1,   Glycolysis↓, 1,   PDH↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↓, 1,   BAX↑, 1,   p27↑, 1,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   ERK↓, 1,   NOTCH↓, 1,   PI3K↓, 1,   STAT3↓, 1,   TOP1↓, 1,   TumCG↓, 1,  

Migration ⓘ

Ca+2↓, 1,   E-cadherin↓, 1,   MMP2↓, 2,   MMP9↓, 2,   MMPs↓, 1,  

Angiogenesis & Vasculature ⓘ

ATF4↑, 1,   EGFR↓, 1,   Hif1a↓, 1,   VEGF↓, 2,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   IL6↓, 1,   NF-kB↓, 2,  

Hormonal & Nuclear Receptors ⓘ

ER(estro)↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 1,   eff↑, 2,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   EGFR↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoP↑, 1,   cognitive↑, 1,   OS↑, 1,  
Total Targets: 51

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 11,   ARE↑, 1,   Catalase↑, 6,   Ferroptosis↓, 1,   GPx↑, 4,   GSH↑, 6,   GSR↓, 1,   GSR↑, 1,   H2O2↓, 2,   HO-1↑, 4,   Iron↓, 1,   lipid-P↓, 4,   mt-lipid-P↓, 1,   MDA↓, 3,   Mets↝, 1,   MPO↓, 1,   NQO1↑, 2,   Nrf1↑, 1,   NRF2↑, 6,   PARK2↑, 2,   ROS↓, 21,   mt-ROS↓, 1,   SIRT3↑, 3,   SOD↑, 8,   VitC↑, 1,   VitE↑, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 3,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 2,   mt-ATP↑, 1,   mitResp↑, 1,   MMP↑, 5,   mtDam↓, 1,   OCR↑, 1,   PGC-1α↑, 5,   PINK1↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 2,   AMPK↑, 4,   CREB↑, 1,   CRM↑, 1,   GlucoseCon↑, 1,   lactateProd↓, 1,   LDH↓, 1,   LDL↓, 1,   NADH:NAD↑, 1,   PKM2↓, 1,   PPARα↑, 1,   PPARγ↑, 5,   SIRT1↓, 1,   SIRT1↑, 2,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↑, 2,   Apoptosis↓, 5,   BAX↑, 1,   Bax:Bcl2↓, 1,   Bcl-2↓, 1,   Bcl-2↑, 1,   Casp3↓, 3,   Casp3↑, 1,   Casp9↓, 1,   Cyt‑c↓, 1,   Cyt‑c↑, 1,   Cyt‑c∅, 1,   Ferroptosis↓, 1,   iNOS↓, 2,   JNK↓, 1,   MAPK↓, 2,   necrosis↓, 1,   p38↓, 1,  

Kinase & Signal Transduction ⓘ

TRPV3↑, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,   other↓, 6,   other↝, 2,  

Protein Folding & ER Stress ⓘ

CHOP↓, 1,   GRP78/BiP↓, 1,   HSP70/HSPA5↑, 2,   HSP70/HSPA5↝, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   MitoP↑, 2,   p62↓, 1,   p62↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 2,   SIRT6↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,   ERK↑, 1,   p‑ERK↑, 1,   FOXO↑, 1,   GSK‐3β↓, 3,   IGF-1↓, 1,   IGF-1↑, 1,   mTOR↓, 1,   neuroG↑, 2,   PI3K↓, 1,   PI3K↑, 1,   TRPM7↓, 2,  

Migration ⓘ

AntiAg↑, 2,   APP↓, 1,   Ca+2↓, 2,   Cartilage↑, 2,   MMP2↓, 1,   MMP9↓, 2,   VCAM-1↓, 1,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature ⓘ

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

Barriers & Transport ⓘ

BBB↓, 1,   BBB↑, 9,   GLUT3↑, 1,   GLUT4↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   CRP↓, 1,   CTSZ↓, 1,   IL1α↓, 1,   IL1β↓, 8,   IL2↓, 1,   IL6↓, 3,   IL8↓, 1,   Imm↑, 1,   Inflam↓, 18,   MCP1↓, 3,   MIP‑1α↓, 1,   NF-kB↓, 9,   p65↓, 1,   RANTES↓, 1,   TLR4↓, 2,   TNF-α↓, 11,  

Synaptic & Neurotransmission ⓘ

5HT↑, 3,   AChE↓, 6,   BChE↓, 1,   BDNF↑, 9,   ChAT↑, 1,   NGF↑, 1,   tau↓, 1,   p‑tau↓, 4,   TrkB↑, 1,  

Protein Aggregation ⓘ

Aβ?, 1,   Aβ↓, 10,   BACE↓, 1,   NLRP3↓, 1,   β-Amyloid↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 4,   BioAv↝, 3,   Dose↝, 10,   eff↓, 1,   eff↑, 19,   Half-Life↓, 1,   Half-Life↝, 1,   P450↓, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 2,   ALP↓, 1,   AST↓, 3,   BP↓, 1,   CRP↓, 1,   GutMicro↑, 1,   IL6↓, 3,   LDH↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 2,   AntiCan↑, 1,   AntiDiabetic↑, 1,   cardioP↓, 1,   cardioP↑, 3,   cognitive↑, 22,   hepatoP↑, 4,   memory↑, 16,   Mood↑, 2,   motorD↑, 48,   neuroP↑, 18,   Obesity↓, 1,   OS↑, 1,   Pain↓, 6,   QoL↑, 2,   radioP↑, 1,   Risk↓, 2,   Strength↑, 2,   toxicity↓, 3,   toxicity∅, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 181

Scientific Paper Hit Count for: motorD, motor function
10 Magnetic Fields
3 Alpha-Lipoic-Acid
3 Aromatherapy
3 Carvacrol
3 Honokiol
3 Urolithin
2 Chlorogenic acid
2 Magnetic Field Rotating
2 Naringin
2 Quercetin
2 Resveratrol
2 Thymoquinone
1 Apigenin (mainly Parsley)
1 Berberine
1 Betulinic acid
1 Boron
1 Carnosic acid
1 Hydrogen Gas
1 Lecithin
1 Mushroom Lion’s Mane
1 nicotinamide adenine dinucleotide
1 Vitamin B3,Niacin
1 Propolis -bee glue
1 Piperine
1 Rosmarinic acid
1 Shikonin
1 EGCG (Epigallocatechin Gallate)
1 Vitamin B5,Pantothenic Acid
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#:1256  State#:%  Dir#:2
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