tau Cancer Research Results

tau, tau: Click to Expand ⟱
Source:
Type:
In healthy neurons, tau binds to and stabilizes microtubules, which are essential for maintaining cell structure and facilitating axonal transport.

In AD, tau becomes abnormally hyperphosphorylated. This excessive phosphorylation reduces its affinity for microtubules, leading to destabilization of the cytoskeletal structure.
-Abnormal phosphorylated tau (p-tau) can be detected in cerebrospinal fluid (CSF) and blood plasma.
-Imaging techniques like tau PET scans can visualize tau deposits in the brain.
Natural Products targeting tau
-Curcumin                via GSK-3β inhibition
-Resveratrol             Activates SIRT1
-EGCG                    inhibits Tau, but BBB penetration is questionable
Scientific Papers found: Click to Expand⟱
3271- ALA,    Decrypting the potential role of α-lipoic acid in Alzheimer's disease
- Review, AD, NA
*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

3441- ALA,    α-Lipoic Acid Maintains Brain Glucose Metabolism via BDNF/TrkB/HIF-1α Signaling Pathway in P301S Mice
- in-vivo, AD, NA
*tau↓, α-lipoic acid (LA), which is a naturally occurring cofactor in mitochondrial, has been shown to have properties that can inhibit the tau pathology and neuronal damage in our previous research
*GlucoseCon↑, chronic LA administration significantly increased glucose availability by elevating glucose transporter 3 (GLUT3), GLUT4, vascular endothelial growth factor (VEGF) protein and mRNA level, and heme oxygenase-1 (HO-1) protein level in P301S mouse brain
*GLUT3↑,
*GLUT4↑,
*VEGF↑,
*HO-1↑,
*Glycolysis↑, LA also promoted glycolysis by directly upregulating hexokinase (HK) activity, indirectly by increasing proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and DNA repair enzymes (OGG1/2 and MTH1).
*HK1↑, Our results indicated that the activity of HK was significantly increased after 10 mg/kg LA treatment.
*PGC-1α↑,
*Hif1a↑, found the underlying mechanism of restored glucose metabolism might involve in the activation of brain-derived neurotrophic factor (BDNF)/tyrosine Kinase receptor B (TrkB)/hypoxia-inducible factor-1α (HIF-1α) signaling pathway by LA treatment.
*neuroP↑,

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

3687- Ash,    Role of Withaferin A and Its Derivatives in the Management of Alzheimer’s Disease: Recent Trends and Future Perspectives
- Review, AD, NA
*Aβ↓, neuroprotective potential of WA is mediated by reduction of beta-amyloid plaque aggregation, tau protein accumulation, regulation of heat shock proteins, and inhibition of oxidative and inflammatory constituents.
*tau↓,
*HSPs↝, WA inhibited Hsp90 [127] and induced Hsp 27 and Hsp70 expressions
*antiOx↑,
*ROS↓,
*Inflam↓,
*neuroP↑, confirming WA’s neuroprotective potency against AD.
*cognitive↑, In an AD model, cognitive defects induced by ibotenic acid that was significantly reversed by WA isolated from Ashwagandha root
*NF-kB↓, inhibited nuclear factor NF-κB activation
*HO-1↑, WA also increased the neuro-protective protein heme oxygenase-1, which is beneficial to AD prevention
*memory↑, WA additionally enhances memory [133], prevents Aβ production, reconstructs synapses, and regenerates axons
*AChE↓, WA Inhibits AChE and BuChE Activities
*BChE↓,
*ChAT↑, WA has an important role in AD by reversing the reduction in cholinergic markers such as choline acetyltransferase (ChAT) and acetylcholine
*Ach↑, WA increased the level of ACh, the amount of choline acetyltransferase (ChAT)

4303- Ash,    Ashwagandha (Withania somnifera)—Current Research on the Health-Promoting Activities: A Narrative Review
- Review, AD, NA
*neuroP↑, neuroprotective, sedative and adaptogenic effects and effects on sleep.
*Sleep↑,
*Inflam↓, anti-inflammatory, antimicrobial, cardioprotective and anti-diabetic properties
*cardioP↑,
*cognitive↑, Significant improvements in cognitive function were observed as a result of the inhibition of amyloid β-42, and a reduction in pro-inflammatory cytokines TNF-α, IL-1β, IL-6, and MCP-1, nitric oxide, and lipid peroxidation was also observed.
*Aβ↓,
*TNF-α↓,
*IL1β↓,
*IL6↓,
*MCP1↓,
*lipid-P↓,
*tau↓, reducing β-amyloid aggregation and inhibiting τ protein accumulation.
*ROS↓, withaferin A is responsible for inhibiting oxidative and pro-inflammatory chemicals and regulating heat shock proteins (HSPs), the expression of which increases when cells are exposed to stressors.
*BBB↑, ability of withanolide A to penetrate the blood-brain barrier (BBB) was demonstrated.
*AChE↓, potentially inhibiting acetylcholinesterase activity, which may have benefits in the treatment of canine cognitive dysfunction and Alzheimer’s disease
*GSH↑, increased glutathione concentration, increased glutathione S-transferase, glutathione reductase, glutathione peroxidase, superoxide dismutase and catalase activities,
*GSTs↑,
*GSR↑,
*GPx↑,
*SOD↑,
*Catalase↑,
ChemoSen↑, combination of Ashwagandha extract and intermittent fasting has potential as an effective breast cancer treatment that may be used in conjunction with cisplatin
*Strength↑, combination of Ashwagandha extract and intermittent fasting has potential as an effective breast cancer treatment that may be used in conjunction with cisplatin

4305- Ba,    Study on the Molecular Mechanism of Baicalin Phosphorylation of Tau Protein Content in a Cell Model of Intervention Cognitive Impairment
- in-vitro, NA, SH-SY5Y
*cognitive↑, In cell experiments, baicalein presented a positive impact on mild cognitive impairment by elevating P-AKT1 and P-GSK-3β levels while reducing the overall amount of P-tau.
*p‑Akt↑,
*p‑GSK‐3β↑,
*p‑tau↓,
*neuroP↑, baicalein demonstrates a neuroprotective by modulating pathways such as the NF-κB/MAPK signaling pathway and the AMPK/Nrf2 pathway.
*NF-kB↓,
*AMPK↑,
*NRF2↑,

4304- Ba,    Baicalein inhibits heparin-induced Tau aggregation by initializing non-toxic Tau oligomer formation
- in-vitro, AD, NA
*tau↓, Baicalein dissolved the preformed mature fibrils of Tau thereby possessing a dual target action
*Dose↝, 85% at 500 μM of Baicalein and 75% at 100 μM Baicalein
*BioAv↓, the potency of Baicalein to be a therapeutic is hampered by its poor water solubility and low bioavailability.

3682- BBR,    Berberine Improves Cognitive Impairment by Simultaneously Impacting Cerebral Blood Flow and β-Amyloid Accumulation in an APP/tau/PS1 Mouse Model of Alzheimer’s Disease
- in-vitro, AD, NA
*cognitive↑, results showed that BBR ameliorated cognitive deficits in 3×Tg AD mice, reduced the Aβ accumulation, inhibited the apoptosis of neurons
*Aβ↓,
*Apoptosis↓,
*CD31↑, promoted the formation of microvessels in the mouse brain by enhancing brain CD31, VEGF, N-cadherin, Ang-1.
*VEGF↑,
*N-cadherin↑,
*angioG↑,
*neuroP↑, berberine is effective to 3×Tg AD mice, has a neuroprotective effect,
*p‑tau↓, lowering Aβ levels, inhibiting the phosphorylation of Tau protein, anti-oxidation, inhibiting the activity of AchE and MAO, and regulating lipids, hypoglycemic.
*antiOx↑,
*AChE↓,
*MAOB↓,
*lipid-P↓,

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

4298- BBR,    Berberine mitigates cognitive decline in an Alzheimer’s Disease Mouse Model by targeting both tau hyperphosphorylation and autophagic clearance
- in-vivo, AD, NA
*cognitive↑, Berberine could improve 3×Tg AD mice’s cognitive function
*p‑tau↓, Berberine could attenuate the hyperphosphorylation of tau
*GSK‐3β↓, attenuated the hyperphosphorylation of tau. via modulating the activity of Akt/glycogen synthase kinase-3β and protein phosphatase 2A
*PP2A↑, inhibition of GSK3β or activation of PP2A attenuates tau hyperphosphorylation, thus, ameliorates cognitive impairment
*memory↑, Berberine-treated mice showed better performance in spatial learning and memory test
*Akt↑, Berberine decreases tau phosphorylation via activation of Akt and inhibition of GSK3β
*LC3II↑, both LC3-Ⅱ and Beclin-1 in the hippocampus of BBR-treated group were dramatically increased compared with the 3×Tg AD mice
*Beclin-1↑,

4299- BBR,    Berberine attenuates cognitive impairment and ameliorates tau hyperphosphorylation by limiting the self-perpetuating pathogenic cycle between NF-κB signaling, oxidative stress and neuroinflammation
- in-vivo, AD, NA
*memory↑, BBR improved learning and memory in APP/PS1 mice.
*p‑tau↓, BBR decreased the hyperphosphorylated tau protein in the hippocampus of APP/PS1 mice.
*NF-kB↓, BBR lowered the activity of NF-κB signaling in the hippocampus of AD mice.
*GSH↑, BBR-administration promoted the activity of glutathione (GSH) and inhibited lipid peroxidation in the hippocampus of AD mice.
*lipid-P↓,
*cognitive↑, BBR attenuated cognitive deficits and limited hyperphosphorylation of tau via inhibiting the activation of NF-κB
*ROS↓, by retarding oxidative stress and neuro-inflammation.
*Inflam↓,

5483- BM,    The Role of Bacopa monnieri in Alzheimer’s Disease: Mechanisms and Potential Clinical Use—A Review
- Review, AD, NA
*cognitive↑, Bacopa monnieri, also known as brahmi, which has gained particular popularity for its cognitive-function-enhancing properties and neuroprotective effects.
*neuroP↑,
*PI3K↑, figure 3
*Akt↑,
*GSK‐3β↓,
*tau↓,
*ROS↓,
*MMP3↓,
*Casp1↓,
*Casp3↓,
*NF-kB↓,
*TNF-α↓,
*IL6↓,

5474- BM,    Pharmacological attributes of Bacopa monnieri extract: Current updates and clinical manifestation
*memory↑, Bacopa monnieri has been used for centuries in Ayurvedic medicine, alone or in combination with other herbs, as a memory and learning enhancer, sedative, and anti-epileptic.
*neuroP↑, Brahmi as a lead formulation for treating neurological disorders and exerting cognitive-enhancing effects.
*cognitive↑,
*hepatoP↑, figure 1
*antiOx↑,
*AntiDiabetic↑,
*fatigue↓,
*GSK‐3β↓, figure 3
*PI3K↑,
*Akt↑,
*tau↓,
*ROS↓, The neuroprotective properties of these bioactive components include reduction of ROS, neuroinflammation, aggregation inhibition of amyloid-β and improvement of cognitive and learning behavior.
*Inflam↓,

3791- CA,    Caffeic Acid and Diseases—Mechanisms of Action
- Review, AD, NA
*memory↑, Feeding hyperinsulinemic rats with caffeic acid (30 mg/kg b.w./day) for 30 weeks significantly improved their memory and learning impairments caused by a high-fat diet
*cognitive↑, caffeic acid (100 mg/kg for two weeks) significantly improved learning deficits and increased cognitive function
*p‑tau↓, pretreatment with caffeic acid (10 μg/mL) decreased the level of phosphorylated tau protein
*ROS↓, Caffeic acid (100 mg/kg for two weeks) also suppressed oxidative stress, inflammation, NF-κB-p65 protein expression, and caspase-3 activity
*Inflam↓,
*NF-kB↓,
*Casp3↓,
*lipid-P↓, caffeic acid (50 mg/kg/day) improved cognitive functions and inhibited lipid peroxidation and nitric oxide formation in the brain
*AChE↓, Caffeic acid (12 μg/mL) inhibited acetylcholinesterase and butyrylcholinesterase activity in the brain of untreated rats in vitro
*BChE↓,
*GSK‐3β↓, improves cognitive functions, probably by inhibiting NF-κB and GSK3β signaling and acetylcholinesterase and butyrylcholinesterase activity (
*5LO↓, we consider the inhibitory effect of caffeic acid on 5-lipoxygenase as another factor in protecting the brain against damage
*BDNF↓, Caffeic acid also increased the expression of brain-derived neurotrophic factor (BDNF) in stressed mice; the effect was mediated by 5-lipoxygenase inhibition
VEGF↓, the primary way how caffeic acid affects hepatocellular carcinoma in vitro is inhibiting VEGF expression
HSP70/HSPA5↓, affeic acid (20 μM) also decreased the expression of mortalin(mitochondrial 70 kDa heat shock protein),

5756- CA,    Experimental Evidence of Caffeic Acid’s Neuroprotective Activity in Alzheimer’s Disease: In Vitro, In Vivo, and Delivery-Based Insights
- vitro+vivo, AD, NA
*neuroP↑, Caffeic acid (CA), a naturally occurring hydroxycinnamic acid, has emerged as a promising neuroprotective candidate due to its antioxidant, anti-inflammatory, and enzyme-inhibitory properties.
*antiOx↑,
*Inflam↓,
*AChE↓, CA modulates cholinergic activity by inhibiting AChE and BChE and exerting antioxidant and anti-amyloidogenic effects.
*BChE↓,
*cognitive↑, metabolic AD models have demonstrated improvements in cognitive function, reduction in oxidative stress, inflammation, and Aβ and tau pathologies following CA administration
*ROS↓,
*Aβ↓,
*tau↓,
eff↑, CA derivatives, including caffeic acid phenethyl ester and nitro-substituted analogs, exhibit improved pharmacokinetic and neuroprotective profiles.

5860- CAP,    Beneficial Effects of Capsaicin in Disorders of the Central Nervous System
- Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*neuroP↑, In Alzheimer’s disease, capsaicin reduces neurodegeneration and memory impairment.
*memory↑, dietary capsaicin (0.01% in a chow) improved memory in a mouse model of Alzheimer’s disease
*Pain↓, Additionally, this compound exerts pain-relieving effects in migraine and cluster headaches.
*TRPV1↑, capsaicin stimulates TRPV1 receptors
*Aβ↓, Alzheimer’s disease, that dietary capsaicin (0.01% in a chow) reduced beta-amyloid plaque formation and tau phosphorylation in different brain areas
*tau↓,
*cognitive↑, attenuated neurodegeneration and cognitive impairment
*Risk↓, In western regions of China, chili peppers are more often consumed and there is a smaller number of people with dementia than in other regions where dietary capsaicin intake is lower
*motorD↓, capsaicin reduced neurodegeneration and motor impairment in animal models of Parkinson’s disease
*ROS↓, this compound decreased the production of reactive oxygen species and proinflammatory cytokines (TNF-α and IL-β) by activated microglia
*TNF-α↓,
*IL1β↓,
*eff↑, Capsaicin exerts beneficial effects in stroke models not only by enhancing neuroprotection but also by influencing cerebral vasculature.
*Risk↓, Moreover, it was reported that dietary capsaicin (0.02% in a chow) delays the onset of stroke in stroke-prone rats with hypertension.

5854- CAP,    Pharmacological activity of capsaicin: Mechanisms and controversies (Review)
- Review, Var, NA - Review, AD, NA
Obesity↓, Capsaicin can also promote weight loss, making it potentially useful for treating obesity.
Half-Life↓, The clinical usefulness of capsaicin is limited by its short half-life.
antiOx↑, Capsaicin exerts analgesic, antioxidant, cardioprotective, anticancer and thermogenic effects, and it can promote weight loss
TRPV1↑, (TRPV1), to which capsaicin binds specifically.
STAT3↓, capsaicin may inhibit signal transducer and activator of transcription 3 (STAT3), but the minimal concentration needed to inhibit STAT3 (50 M) is substantially higher than the concentration required to stimulate TRPV1 (1–5 M)
Ca+2↑, mechanisms appear to involve accumulation of intracellular Ca2+, generation of reactive oxygen species, disruption of mitochondrial membrane potential and upregulation of the transcription factors NF-κB and STATS.
ROS↑,
MMP↓,
*neuroP↑, Capsaicin has demonstrated therapeutic potential in several animal models of Alzheimer's disease (AD).
*tau↓, capsaicin substantially ameliorated synaptic damage and tau hyperphosphorylation induced by cold water stress.
*Inflam↓, capsaicin appeared to activate TRPV1 in M1/M2 dopaminergic neurons, which may alleviate neuro-inflammation and oxidative stress from activated glia
*ROS?,

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

3855- CAP,    Capsaicin consumption reduces brain amyloid-beta generation and attenuates Alzheimer’s disease-type pathology and cognitive deficits in APP/PS1 mice
- in-vivo, AD, NA
*Risk↓, capsaicin-rich diet consumption was associated with better cognition and lower serum Amyloid-beta (Aβ) levels in people aged 40 years and over.
*Aβ↓, intake of capsaicin, the pungent ingredient in chili peppers, reduced brain Aβ burden and rescued cognitive decline in APP/PS1 mice
*p‑tau↓, capsaicin alleviated other AD-type pathologies, such as tau hyperphosphorylation, neuroinflammation and neurodegeneration.
*Inflam↓,
*neuroP↑,
*cognitive↑, Dietary capsaicin rescues cognition impairment in APP/PS1 mice
*ADAM10↑, capsaicin treatment increased the maturation of ADAM10 and thereby precluded Aβ generation
*PPARα↑, capsaicin also upregulated the levels of PPARα, which could activate ADAM10-mediated proteolysis of APP

5768- CAPE,    Neuroprotective Potential of Caffeic Acid Phenethyl Ester (CAPE) in CNS Disorders: Mechanistic and Therapeutic Insights
- Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*antiOx↑, it possesses antioxidant, anti-inflammatory, antimitogenic, and anti-cancer activities, as shown by preclinical studies.
*Inflam↑,
*AntiCan↑,
*NRF2↑, figure 1
*GSK‐3β↑,
*Akt↑,
*PI3K↑, directly activates the PI3/Akt signaling pathway as well as leads to increased phosphorylation of GSK-3β to yield it inactive
*ROS↓, decrease in the reactive oxygen species levels (ROS)
*SOD↑,
*GSH↑,
*MDA↓,
*tau↓, reduced hyperphosphorylation of Tau protein
*neuroP↑, Accorded neuroprotection through increased PI3K activity and eNOS mediated nitric oxide synthesis
*memory↑, CAPE treatment in the doses of 6 mg/kg for 28 days led to an improvement in spatial memory and reduction in the malondialdehyde (MDA),
*AChE↓, Other mechanisms which may contribute to its beneficial effect include the inhibition of acetylcholinesterase activity, which has also been reported by several authors
*other↝, Different studies have demonstrated the effectiveness of CAPE in stroke models through its anti-inflammatory and antioxidant properties.
*lipid-P↓, decreasing membrane fluidity, lipid peroxidation, release of cardiolipin, and Cyt c

6040- CGA,    Protective effect of chlorogenic acid on cognitive impairment in rats with early Alzheimer's disease via Wnt signaling pathway
- in-vivo, AD, NA
*neuroP↑, Chlorogenic acid (CGA) has neuroprotective properties associated with Alzheimer's disease (AD).
*Dose↝, gavage of CGA at a dose of 150 mg/kg/d
*GSK‐3β↓, decreased the expression of inflammatory factors, decreased the expression levels of GSK-3β, GFAP, and tau, and increased the expression levels of DVL2 and β-catenin.
*tau↓,
*β-catenin/ZEB1↑,
*Wnt↑, CGA can protect the cognitive impairment of early AD rats via Wnt signaling pathway. we hypothesized that activation of the Wnt signaling pathway can improve cognitive dysfunction in AD rats.
*memory↑, The results showed that CGA could improve the learning and memory ability and cognitive impairment of AD rats via Wnt signaling pathway
*cognitive↑, The result indicated that the CGA group could effectively improve the learning, memory and cognitive impairment of AD rats
*NRF2↑, CGA had a neuroprotective effect on the CI/R rats by regulating the oxidative stress-related Nrf2 pathway.
*ROS↓,

3889- Cin,    Orally administrated cinnamon extract reduces β-amyloid oligomerization and corrects cognitive impairment in Alzheimer's disease animal models
- in-vivo, AD, NA
*Aβ↓, cinnamon extract (CEppt), which markedly inhibits the formation of toxic Aβ oligomers and prevents the toxicity of Aβ on neuronal PC12 cells.
*cognitive↑, CEppt to an aggressive AD transgenic mice model led to marked decrease in 56 kDa Aβ oligomers, reduction of plaques and improvement in cognitive behavior.
*tau↓, cinnamon has an inhibitory effect on Tau aggregation related to AD

3894- Cin,    Interaction of cinnamaldehyde and epicatechin with tau: implications of beneficial effects in modulating Alzheimer's disease pathogenesis
- in-vitro, AD, NA
*tau↓, Previously we reported that an aqueous extract of cinnamon has the ability to inhibit tau aggregation in vitro
*ROS↓, Further, these compounds protected tau from oxidation caused by the reactive oxygen species, H2O2, and prevented subsequent formation of high molecular weight species that are considered to stimulate tangle formation.

3888- Cin,    Cinnamon, a promising prospect towards Alzheimer's disease
- NA, AD, NA
*tau↓, mild-to-moderate AD through the inhibition of tau protein aggregation and prevention of the formation and accumulation of amyloid-β peptides
*Aβ↓,
*neuroP↑, cinnamon possesses neuroprotective effects interfering multiple oxidative stress and pro-inflammatory pathways.
*ROS↓,
*Inflam↓,
*cardioP↑, figure 1
*antiOx↑,
*cognitive↑,
*BBB↑, cinnamon compounds may either cross the blood brain barrier (BBB) or probably pass through other peripheral routes
*p‑GSK‐3β↑, Cinnamon increased phosphorylated GSK3 (critical for choline metabolism), inhibited AChE activity and increased neuron number in hippocampus area of these animals
*AChE↓, In sum, cinnamon spp. and its biologically active compounds target every 3 AD hallmarks; inhibition of AChE activity, abeta formation/aggregation and tau phosphorylation

3893- Cin,    Cinnamon extract inhibits tau aggregation associated with Alzheimer's disease in vitro
- Review, AD, NA
*tau↓, Ceylon cinnamon (C. zeylanicum) is found to inhibit tau aggregation and filament formation, hallmarks of Alzheimer's disease (AD)
*toxicity↓, Cinnamon extract (CE) was not deleterious to the normal cellular function of tau, namely the assembly of free tubulin into microtubules.

3892- Cin,    Cinnamon from the selection of traditional applications to its novel effects on the inhibition of angiogenesis in cancer cells and prevention of Alzheimer's disease, and a series of functions such as antioxidant, anticholesterol, antidiabetes, antibacterial, antifungal, nematicidal, acaracidal, and repellent activities
- Review, AD, NA - Review, Var, NA
*antiOx↑, Cinnamon is known to have antioxidant, antibacterial, anti-inflammatory, and other therapeutic properties.
*Inflam↓,
*cardioP↑, natural remedy to treat serious diseases such as type 2 diabetes, chronic digestion problems, cardiovascular diseases, and even cancer and Alzheimer’s disease.
angioG↓, cinnamon extract (CE) displays anticancer activity5 and inhibits angiogenesis by blocking vascular endothelial growth factor (VEGF) 2 signaling
VEGF↓,
*LDL↓, , and low-density lipoprotein cholesterol (7–27%) for patients who consumed 1 g, 3 g, or 5 g of cinnamon for 40 days.
COX2↓, treatment of melanoma cell lines with CE also induced a decrease in Cox-2 and HIF-1α expression in the tumor tissues that mediate the potent antitumor activity of cinnamon
Hif1a↓,
*Aβ↓, A study found that Cinnamon (肉桂 ròu guì) extract (CEppt) inhibits the formation of toxic Aβ oligomers and prevents the toxicity of Aβ on neuronal PC12 cells.
*tau↓, he extract of the whole cinnamon effectively inhibited the aggregation of human tau in vitro, and this could be attributed to both proanthocyanidin timer and cinnamaldehyde in CE
*toxicity↓, In one study, the intake of up to 6 g/d of C. cassia for > 40 days did not show any adverse effects.

5798- CRMs,    Caloric restriction mimetics improve gut microbiota: a promising neurotherapeutics approach for managing age-related neurodegenerative disorders
- Review, Nor, NA - Review, AD, NA
*GutMicro↑, we have explored the beneficial effect of CRMs in extending lifespan by enhancing the beneficial bacteria and their effects on metabolite production
*neuroP↑, physiological conditions, and neurological dysfunctions including neurodegenerative disorders.
*eff↑, ‘Mediterranean diet’ composed of unsaturated fatty acids, fibers, and antioxidants has been shown to help in longevity by shifting the GM towards Bacteroides, Bifidobacterium, and Lactobacillus, with a reduction in the members of Pseudomonadota and B
*Dose↝, AD patients displayed fewer populations of Firmicutes, Proteobacteria, and Actinobacteria, and an increased abundance of Bacteroidetes.
*AMPK↑, major routes through which CRMs function include AMPK, Sirtuin1, mTOR, and Keap1-Nrf2 pathways which have been highlighted in Fig. 2.
*SIRT1↑, CRMs can function as activators of protein (de)acetylases, particularly, SIRT1
*mTOR↓,
*NRF2↑, Quercetin, a CRM led to the activation of Nrf2 and induced expression of antioxidant enzymes.
*p‑tau↓, metformin has shown its effect in reducing tau phosphorylation by inducing protein phosphatase 2A (PP2A) expression via the AMPK/mTOR pathway

3624- Cro,    Crocus Sativus L. (Saffron) in Alzheimer's Disease Treatment: Bioactive Effects on Cognitive Impairment
- Review, AD, NA
*AChE↓, aqueous and methanolic saffron extract presented a moderate activity as AChE inhibitor (up to 30%),
*memory↑, f 50-200 mg/kg of crocin enhanced memory impairment
*cognitive↑, crocin (30 mg/kg) for 3 weeks significantly improved cognitive impairment caused by intracerebroventricular injection of STZ,
*MDA↑, improved cognitive tasks and produced a significant decrease of malondialdehyde (MDA) levels and increase of total thiol content and glutathione peroxidase (GPx) activity in STZ-lesioned rats
*Thiols↑,
*GPx↑,
*antiOx↑, crocetin is only one and strong antioxidant, providing protection in rescuing cell viability, blocking reactive oxygen species (ROS) production and reducing caspase-3 activation
*ROS↓, crocin can prevent oxidative stress damage to hippocampus, memory and learning impairments
*Casp3↓,
*neuroP↑, neuroprotective effects of crocin against AD
*SOD↑, increase the levels of glutathione peroxidase, superoxide dismutase, acetylcholine and choline acetyltransferase,
*Ach↑,
*ChAT↑,
*BBB↑, shown that crocetin, able to pass through BBB, inhibits fibril Aβ formation,
*Aβ↓,
*tau↓, inhibitory effects of crocin on tau protein neurofibrillary tangles in AD.
*cognitive↑, (15 mg twice a day) or a capsule of placebo (two capsules a day) for 16 weeks. The results of this study indicated that saffron produces a significant improvement in cognitive performance
*Inflam↓, anticholinergic, anti-inflammatory and antioxidant features

3794- CUR,    Curcumin hybrid molecules for the treatment of Alzheimer's disease: Structure and pharmacological activities
- Review, AD, NA
*GSK‐3β↓, Firstly, curcumin can inhibit kinases, such as GSK-3β and Cyclin-Dependent Kinase 5 (Cdk5), that excessively phosphorylate Tau protein
*CDK5↓,
*p‑tau↓,
*IronCh↑, curcumin's metal ion chelating capability contributes to the reduction of free radicals
*ROS↓,
*HO-1↑, upregulating antioxidant enzymes including heme oxygenase 1 (HO-1), superoxide dismutase (SOD), catalase, and enzymes involved in the synthesis of endogenous antioxidants, specifically glutathione (GSH)
*SOD↑,
*Catalase↑,
*GSH↑,
*TNF-α↓, inhibiting the expression of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-12,
*IL6↓,
*IL12↓,
*NRF2↑, inducing the production of anti-inflammatory mediators including HO-1/NRF-2, PPARα-γ, and IL-4
*PPARγ↑,
*IL4↑,
*AChE↓, researchers have observed that curcumin can suppress AChE mRNA expression levels, effectively preventing the Cd-induced rise in AChE activity
*Dose↝, While curcumin directly interacts with AChE, its inhibitory activity remains weak (IC50 = 67.69 μM)
*GutMicro↑, curcumin's interaction with gut microbiota exhibits potential anti-AD properties.

3793- CUR,    Curcumin Downregulates GSK3 and Cdk5 in Scopolamine-Induced Alzheimer’s Disease Rats Abrogating Aβ40/42 and Tau Hyperphosphorylation
- in-vivo, AD, NA
*Aβ↓, We found that curcumin-treated AD rats markedly reduced the levels of Aβ40 and Aβ42 in the brain and in the plasma in comparison to untreated AD rats
*p‑tau↓, Moreover, the levels of phosphorylated tau at Ser396 (PHF13), Ser202/Thr205 (AT8), and Aβ40/42 (MOAB2) were decreased significantly in AD rats treated with curcumin.
*GSK‐3β↓, Phospho-GSK3β (Tyr216), the active form of GSK3β, and total GSK3β were significantly decreased in AD rats treated with curcumin.
*CDK5↓, Cdk5 and its activators p35 and p25 were significantly decreased in curcumin-treated AD rats.
*memory↑, Impaired spatial memory and locomotor activity in AD rats were partially reversed by curcumin.

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

3588- CUR,    The effect of curcumin on cognition in Alzheimer’s disease and healthy aging: A systematic review of pre-clinical and clinical studies
- Review, AD, NA
*cognitive↝, Clinical studies are mixed regarding curcumin’s effects on cognitive deficits.
*BioAv↑, Ways to improve curcumin’s bioavailability are required.
*Inflam↓, anti-inflammatory activity can be attributed to the suppression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) enzymes via down-regulation of nuclear factor kappa B (NF-κB)
*COX2↓,
*iNOS↓,
*NF-kB↓,
*TNF-α↓, nhibition of several inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-a) or interleukin (IL) -1, -2, -6, -8, and -12 (
*IL1↓,
*IL2↓,
*IL6↓,
*IL8↓,
*IL12↓,
*ROS↓, Curcumin’s ability to scavenge free radicals, such as reactive oxygen species (ROS) and reactive nitrogen species (RNS), provides its antioxidant capacity
*RNS↓,
*antiOx↑,
*BBB↑, Multiple studies in rodents and humans have shown that curcumin crosses the blood brain barrier (BBB)
*BioAv↓, drawback is the low bioavailability due to poor solubility, low absorption, rapid metabolism, and rapid excretion
*cognitive↑, The researchers detected a significant cognitive improvement at both doses compared to the untreated group, while a significant dose-response effect was found throughout time with higher doses of curcumin producing greater cognitive improvement
*memory↑, supplementation may improve memory and result in a number of biochemical alternations leading to suppressed tau aggregation
*tau↓,
*eff↑, Combined curcumin and piperine showed superiority, in a dose dependent manner,

3576- CUR,    Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer's Disease
- Review, AD, NA
*Inflam↓, known to have protective effects, including anti-inflammatory, antioxidant, anti-arthritis, pro-healing, and boosting memory cognitive functions.
*antiOx↑,
*memory↑,
*Aβ↓, curcumin prevents Aβ aggregation and crosses the blood-brain barrier,
*BBB↑,
*cognitive↑, curcumin ameliorates cognitive decline and improves synaptic functions in mouse models of AD
*tau↓, curcumin's effect on inhibition of A and tau,copper binding ability, cholesterol lowering ability, anti-inflammatory and modulation of microglia, acetylcholinesterase (AChE) inhibition, antioxidant properties,
*LDL↓,
*AChE↓,
*IL1β↓, Curcumin reduced the levels of oxidized proteins and IL1B in the brains of APP mice
*IronCh↑, Curcumin binds to redox-active metals, iron and copper
*neuroP↑, Curcumin, a neuroprotective agent, has poor brain bioavailability.
*BioAv↝,
*PI3K↑, They found that curcumin significantly upregulates phosphatidylinositol 3-kinase (PI3K), Akt, nuclear factor E2-related factor-2 (Nrf2), heme oxygenase 1, and ferritin expression
*Akt↑,
*NRF2↑,
*HO-1↑,
*Ferritin↑,
*HO-2↓, and that it significantly downregulates heme oxygenase 2, ROS, and A40/42 expression.
*ROS↓,
*Ach↑, significant increase in brain ACh, glutathione, paraoxenase, and BCL2 levels with respect to untreated group associated with significant decrease in brain AChE activity,
*GSH↑,
*Bcl-2↑,
*ChAT↑, nvestigation revealed that the selected treatments caused marked increase in ChAT positive cells.

6050- CUR,  SeNPs,    Efficacy of curcumin-selenium nanoemulsion in alleviating oxidative damage induced by aluminum chloride in a rat model of Alzheimer's disease
- in-vivo, AD, NA
*cognitive↑, Treatment with a curcumin-selenium nanoemulsion has been shown to enhance behavioural performance and mitigate degenerative changes induced by aluminium chloride (AlCl3)
*AChE↓, This nanoemulsion also reduced the activity of acetylcholinesterase (AChE) and lowered levels of key proteins, including Aβ, p53, tau, nuclear factor erythroid 2-related factor 2 (Nrf2), and tumour necrosis factor-alpha (TNF-α).
*Aβ↓,
*P53↓,
*tau↓,
*NRF2↓,
*TNF-α↓,
*NO↑, it significantly decreased nitric oxide (NO) levels in the brain while enhancing the activity of catalase (CAT) and superoxide dismutase (SOD).
*Catalase↑,
*antiOx↑, The study highlights the antioxidant and anti-inflammatory properties of the curcumin-selenium nanoemulsion, suggesting its potential as a therapeutic option for alleviating AD induced by AlCl3.
*Inflam↓,

3591- EGCG,    Epigallocatechin-3-Gallate Provides Protection Against Alzheimer's Disease-Induced Learning and Memory Impairments in Rats
- in-vivo, AD, NA
*p‑tau↓, EGCG decreased the hyperphosphorylation of Tau in hippocampus
*BACE↓, BACE1 expression and activity as well as the expression of Aβ1-42 were suppressed by EGCG.
*Aβ↓,
*Ach↑, Moreover, EGCG promoted Ach content by diminishing the activity of AchE.
*AChE↓,
*antiOx↑, to improve the antioxidant system and learning and memory function of rats with AD.
*memory↑,
*hepatoP↑, notable components found in coffee have been shown to exert anti-diabetic and hepatoprotective functions
*ROS↓, EGCG Improved the Antioxidant System and Scavenged Free Radicals in AD Rats
*GPx↑, Compared with the AD rats, GPx and T-SOD activities were enhanced in the AD rats with EGCG treatment, especially in the AD rats treated with 250 mg/kg EGCG.
*SOD↑,

3592- EGCG,    (-)-Epigallocatechin-3-gallate ameliorates memory impairment and rescues the abnormal synaptic protein levels in the frontal cortex and hippocampus in a mouse model of Alzheimer's disease
- in-vivo, AD, NA
*neuroP↑, mechanisms by which EGCG exerts its neuroprotective actions in Alzheimer's disease (AD) are presently lacking
*memory↑, long-term oral consumption of EGCG at a relatively high dose (15 mg/kg) improved memory function in SAMP8 mice in the Y-maze and Morris water maze
*p‑tau↓, EGCG treatment also prevented the hyperphosphorylation of tau

4290- EGCG,    EGCG impedes human Tau aggregation and interacts with Tau
- in-vitro, AD, NA
*tau↓, Epigallocatechin-3-gallate (EGCG) is an active phytochemical of green tea that has shown its potency against various diseases including aggregation inhibition of repeat Tau.
*Dose↝, The IC50 for Tau aggregation by EGCG was found to be 64.2 μM.
*neuroP↑, EGCG is a known neuroprotective and antioxidant molecule
*antiOx↑,

4291- EGCG,    Structure-based discovery of small molecules that disaggregate Alzheimer’s disease tissue derived tau fibrils in vitro
- in-vitro, AD, NA
*tau↓, EGCG, abundant in green tea, has long been known to disaggregate tau and other amyloid fibrils, but EGCG has poor drug-like properties, failing to fully penetrate the brain.
*BBB∅, EGCG itself is a poor therapeutic candidate owing to its polyphenolic molecular structure, which results in unfavorable drug-like properties and restricts brain penetration.

3830- EMD,    Traditional Chinese Medicine: Role in Reducing β-Amyloid, Apoptosis, Autophagy, Neuroinflammation, Oxidative Stress, and Mitochondrial Dysfunction of Alzheimer’s Disease
- Review, AD, NA
*neuroP↑, brain protection properties
*Aβ↓, Emodin suppresses Aβ deposition and tau phosphorylation.
*p‑tau↓,
*BACE↓, emodin downregulates the activity of β-site APP-cleaving enzyme 1 (BACE1) and increases protein phosphatase 2A levels

4071- FA,    Folate and Alzheimer: when time matters
- Review, AD, NA
*cognitive↑, olate deficiency is a risk factor for neural tube defects and late in life for cognitive decline and Alzheimer's dementia (AD).
*ROS↓, Deficiency induces several Alzheimer pathomechanisms like oxidative stress, Ca(++) influx, accumulation of hyperphosphorylated tau and β-amyloid
*Ca+2↓,
*p‑tau↓,
*Aβ↓,

3782- FA,    Ferulic acid ameliorates bisphenol A (BPA)-induced Alzheimer’s disease-like pathology through Akt-ERK crosstalk pathway in male rats
- in-vivo, AD, NA
*cognitive↑, Interestingly, the BPA + FA treated group showed a reversal in the cognitive impairments induced by BPA
*ERK↓, a significant decrease in brain inflammatory cytokines, ERK, and p-Akt levels
*p‑Akt↓,
*AChE↓, brain levels of AChE and BACE were substantially reduced in BPA + FA rats.
*BACE↓,
*neuroP↑, neuroprotective effect of FA was confirmed by restoring the normal architecture of brain tissue, which was associated with decreasing GFAP.
*ROS↓, FA was sufficient to trigger antioxidant capabilities and decrease intracellular reactive oxygen species (ROS
*MDA↓, BPA + FA revealed a substantial reduction in MDA levels compared to rats intoxicated with BPA
*GSH↑, BPA + FA revealed a significant increment of GSH associated with a significant decrease in GSSG
*GSSG↓,
*p‑tau↓, BPA + FA showed a significant decline in the brain level of pTau compared to intoxicated rats.
*lipid-P↓, inhibit lipid peroxidation
*Aβ↓, FA has significantly counteracted the deleterious effect of BPA by decreasing Aβ 1–42, as previously reported

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

4025- FulvicA,    Mumio (Shilajit) as a potential chemotherapeutic for the urinary bladder cancer treatment
- in-vitro, Bladder, T24/HTB-9 - Review, AD, NA
tumCV↓, Mumio affected the viability of both cell types in a time and concentration dependent manner
selectivity↑, We observed a selectivity of Mumio against cancer cells. Our results showed that Mumio was significantly more cytotoxic to urinary bladder cancer cells than to normal cells.
TumCCA↑, Cell cycle and apoptosis analysis showed that Mumio inhibited G0/G1 or S phase cell cycle, which in turn induced apoptosis.
other↝, Different names are used depending on where it is found such as: Mumijo, Mumie (Russia), Saljit, Shilajit (India), Kao-Tun (Birma), Arakul Dshabal (Kyrgyzstan) and many others
*neuroP↑, Mumio is considered to improve memory and to inhibit aging of the brain through its neuroprotective activity
*memory↑,
*tau↓, mechanism of action is based on fulvic acid-mediated prevention of Tau self-aggregation
*other↝, ain components of Mumio are humus (60–80%), benzoic acid, fatty acids, ichthyol, ellagic acid, resin, triterpenes, sterol, aromatic carboxylic acids, bioactive 3,4-benzokoumarins, amino acids, phenolic lipids and microelements.
*lipid-P↓, Ghosal et al. showed that these acids inhibit lipid peroxidation and possess the ability to recycle ascorbic acid and thereby exhibiting significant antioxidant activity
*VitC↑,
*antiOx↑,

4017- FulvicA,    Fulvic acid inhibits aggregation and promotes disassembly of tau fibrils associated with Alzheimer's disease
- NA, AD, NA
*cognitive↑, Fulvic acid, a humic substance, has several nutraceutical properties with potential activity to protect cognitive impairment.
*tau↓, In this work we provide evidence to show that the aggregation process of tau protein, forming paired helical filaments (PHFs) in vitro, is inhibited by fulvic acid affecting the length of fibrils and their morphology.

4016- FulvicA,    Shilajit: A Natural Phytocomplex with Potential Procognitive Activity
- Review, AD, NA
*tau↓, fulvic acid, the main active principle, blocks tau self-aggregation, opening an avenue toward the study of Alzheimer's therapy.
*AntiAge↑, Shilajit has been known and used for centuries by the Ayurvedic medicine, as a rejuvenator and as antiaging compound
*Strength↑, two important characteristics of a rasayana compound in the ancient Indian Ayurvedic medicine: that is, to increase physical strength and to promote human health
*Dose↝, health benefits of shilajit have been shown to differ from region to region, depending on the place from which it was extracted [3, 4].
*BioAv↑, Fulvic acid is soluble in water under different pH conditions, and because of its low molecular weight (around 2 kDa), it is well absorbed in the intestinal tract and eliminated within hours from the body
*antiOx↑, fulvic acid is known by its strong antioxidant actions [9] and likely has systemic effects as complement activator
*memory↑, figure 1 memory enhancer
*Inflam↓, fulvic acid, is known by its properties such as antioxidant, anti-inflammatory, and memory enhancer
*cognitive↑, Our laboratory has found evidence on the high activity of the Andean form of shilajit in improving cognitive disorders and as a stimulant of cognitive activity in humans
*neuroP↑, neuroprotective agent against cognitive disorders
*toxicity↝, Studies indicate the shilajit consumption without preliminary purification may lead to risks of intoxication given the presence of mycotoxin, heavy metal ions, polymeric quinones (oxidant agents), and free radicals, among others
*toxicity↑, recent studies indicate that several ayurvedic products including shilajit and other Indian manufactured products commercialized by the Internet may contain detectable heavy metals levels as lead, mercury, and arsenic

4020- FulvicA,    Natural products as a rich source of tau-targeting drugs for Alzheimer’s disease
- in-vitro, AD, NA
*tau↓, Fulvic acid standard I (35) (Suwannee River I 1S101F), was found to inhibit aggregation of tau fibrils in vitro with an IC50 value of 37 µM and promote the disassembly of tau fibrils with a DC50 value of 95 µM
*cognitive↑, shilajit, a tar-like substance reported to control aging-related cognitive disorders

4021- FulvicA,    Scaling the Andean Shilajit: A Novel Neuroprotective Agent for Alzheimer’s Disease
- in-vitro, AD, NA
*tau↓, The AnSh fractions inhibit tau self-aggregation after 10 days of treatment.
*neuroP↑, Additionally, they can promote an anti-aggregative effect and the disassembly of tangles and oligomers of tau protein, suggesting their potential for the treatment of neurodegenerative diseases such as AD.

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

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

4301- Gins,    Red Ginseng Inhibits Tau Aggregation and Promotes Tau Dissociation In Vitro
- in-vitro, AD, NA
*p‑tau↓, Panax ginseng reduced the hippocampal and cortical expression of phosphorylated tau in a rat model of AD
*eff↑, KRGE not only inhibited tau aggregation but also promoted the dissociation of tau aggregates.
*Inflam↓, main active components of RG, on AD-related pathology such as neuroinflammation [57, 58], mitochondrial dysfunction [59–62], and amyloidogenic mechanism [63–66] have previously been studied.


Showing Research Papers: 1 to 50 of 118
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 118

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Cell Death ⓘ

TRPV1↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↓, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

STAT3↓, 1,  

Migration ⓘ

Ca+2↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   eff↑, 1,   Half-Life↓, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

Obesity↓, 1,  
Total Targets: 19

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 18,   Catalase↑, 3,   GPx↑, 3,   GSH↑, 9,   GSR↑, 1,   GSSG↓, 1,   GSTs↑, 1,   HK1↑, 1,   HO-1↑, 6,   HO-2↓, 1,   lipid-P↓, 9,   MDA↓, 3,   MDA↑, 1,   MPO↓, 1,   NQO1↑, 1,   NRF2↓, 1,   NRF2↑, 10,   RNS↓, 1,   ROS?, 1,   ROS↓, 23,   SOD↓, 1,   SOD↑, 6,   Thiols↑, 1,   VitC↑, 1,  

Metal & Cofactor Biology ⓘ

Ferritin↑, 1,   IronCh↑, 3,  

Mitochondria & Bioenergetics ⓘ

PGC-1α↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 3,   CREB↑, 1,   GlucoseCon↑, 2,   Glycolysis↑, 1,   LDL↓, 3,   NADPH↓, 1,   PDH↑, 1,   PDKs↓, 1,   PPARα↑, 2,   PPARγ↓, 1,   PPARγ↑, 1,   SIRT1↑, 2,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 6,   p‑Akt↓, 1,   p‑Akt↑, 1,   Apoptosis↓, 2,   BAX↑, 1,   Bcl-2↑, 2,   Casp1↓, 1,   Casp3↓, 4,   iNOS↓, 2,   MAPK↓, 1,   MAPK↑, 1,   TRPV1↑, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 6,   other↝, 2,  

Protein Folding & ER Stress ⓘ

HSPs↝, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3II↑, 1,  

DNA Damage & Repair ⓘ

P53↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   ERK↑, 1,   GSK‐3β↓, 8,   GSK‐3β↑, 1,   p‑GSK‐3β↑, 2,   mTOR↓, 2,   PI3K↓, 1,   PI3K↑, 5,   Wnt↑, 1,  

Migration ⓘ

5LO↓, 1,   APP↓, 5,   Ca+2↓, 2,   CD31↑, 1,   CDK5↓, 3,   MMP-10↝, 1,   MMP3↓, 1,   N-cadherin↑, 1,   PKA↑, 1,   TXNIP↓, 1,   VCAM-1↓, 1,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↑, 1,   Hif1a↑, 2,   NO↓, 1,   NO↑, 1,   VEGF↑, 3,  

Barriers & Transport ⓘ

BBB↑, 6,   BBB∅, 1,   GLUT3↑, 2,   GLUT4↑, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IFN-γ↓, 1,   IL1↓, 1,   IL10↓, 1,   IL10↑, 1,   IL12↓, 2,   IL17↓, 1,   IL1β↓, 6,   IL1β↑, 1,   IL2↓, 1,   IL23↓, 1,   IL4↑, 1,   IL6↓, 5,   IL8↓, 1,   Inflam↓, 20,   Inflam↑, 1,   MCP1↓, 2,   NF-kB↓, 8,   TNF-α↓, 10,  

Synaptic & Neurotransmission ⓘ

5HT↑, 1,   AChE↓, 16,   ADAM10↑, 2,   BChE↓, 4,   BDNF↓, 1,   BDNF↑, 3,   ChAT↑, 4,   MAOA↓, 1,   tau↓, 28,   p‑tau↓, 22,  

Protein Aggregation ⓘ

Aβ↓, 24,   BACE↓, 6,   IDE↑, 1,   MAOB↓, 3,   NLRP3↓, 1,   PP2A↑, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 2,   BioAv↝, 1,   Dose↝, 7,   eff↑, 5,  

Clinical Biomarkers ⓘ

Ferritin↑, 1,   GutMicro↑, 2,   IL6↓, 5,  

Functional Outcomes ⓘ

AntiAge↑, 2,   AntiCan↑, 1,   AntiDiabetic↑, 1,   cardioP↑, 3,   cognitive↑, 31,   cognitive↝, 1,   fatigue↓, 1,   hepatoP↑, 3,   memory↑, 21,   motorD↓, 1,   motorD↑, 1,   neuroP↑, 30,   OS↑, 1,   Pain↓, 1,   Risk↓, 4,   Sleep↑, 1,   Strength↑, 2,   toxicity↓, 2,   toxicity↑, 1,   toxicity↝, 1,  
Total Targets: 152

Scientific Paper Hit Count for: tau, tau
9 Resveratrol
8 Urolithin
7 Curcumin
5 Cinnamon
5 Selenium NanoParticles
5 Shilajit/Fulvic Acid
5 Ginseng
4 Berberine
4 Capsaicin
4 EGCG (Epigallocatechin Gallate)
4 Hydrogen Gas
4 Luteolin
4 Quercetin
4 Vitamin B1/Thiamine
3 Thymoquinone
2 Alpha-Lipoic-Acid
2 Ashwagandha(Withaferin A)
2 Baicalein
2 Bacopa monnieri
2 Caffeic acid
2 Folic Acid, Vit B9
2 Ferulic acid
2 Magnetic Fields
2 Mushroom Lion’s Mane
2 Vitamin B3,Niacin
2 Rosmarinic acid
2 Sulforaphane (mainly Broccoli)
2 Vitamin K2
1 Aromatherapy
1 Caffeic Acid Phenethyl Ester (CAPE)
1 Chlorogenic acid
1 Calorie Restriction Mimetics
1 Crocetin
1 Emodin
1 Phosphatidylserine
1 Ginkgo biloba
1 Honokiol
1 Potassium
1 Lycopene
1 Methylene blue
1 Moringa oleifera
1 Methylsulfonylmethane
1 nicotinamide adenine dinucleotide
1 Phenylbutyrate
1 Piperine
1 Pterostilbene
1 chitosan
1 Rutin
1 S-adenosyl-L-methionine
1 Carvacrol
1 Shankhpushpi
1 Silymarin (Milk Thistle) silibinin
1 Ursolic acid
1 Vitamin A, Retinoic Acid
1 Vitamin B12
1 Vitamin B5,Pantothenic Acid
1 Vitamin D3
1 probiotics
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#:1231  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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