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

AD, Alzheimer's Disease: Click to Expand ⟱

Brain Energy Systems Matrix (AD)

Tier 1–2 as “core metabolic cofactors / redox pools”
Tier 4 as “alternative fuels / bypass strategies”
Tier 5–6 as “capacity + delivery constraints” (often explains why supplements don’t translate)

Tier	Rank	Node / Lever	What it Supports (Bioenergetic Role)	Key Enzymes / Targets	AD-Relevant Mechanism	TSF	Evidence	Common Constraints / Gotchas
1	1	Thiamine (B1) / TPP	Glucose → acetyl-CoA entry + TCA throughput + NADPH support	PDH, α-KGDH, Transketolase (PPP)	Addresses cerebral glucose hypometabolism; improves mitochondrial flux; PPP→NADPH supports redox	R, G	Mechanistic + small clinical	Benefit strongest if low status; standard thiamine vs lipophilic derivatives differ
1	2	Benfotiamine	Higher-bioavailability B1 strategy	Transketolase ↑; glycation axis ↓	AGE/RAGE burden reduction + metabolic support (model/trial dependent)	G	Small clinical + mechanistic	Not a “rapid” effect; mostly longer-term metabolic/toxicity load reduction
1	3	Riboflavin (B2) / FAD, FMN	ETC redox enzymes + mitochondrial dehydrogenases	Complex I/II flavoproteins; many oxidoreductases	Supports electron handling; can be limiting in mitochondrial enzyme insufficiency	R, G	Mechanistic	Direct AD cognitive trial support limited; “helps” mostly when deficient or enzyme-limited
1	4	Niacin forms (B3) → NAD pool	NAD+/NADH redox + signaling + repair	NAD salvage; sirtuins; PARP substrate	NAD decline is an aging/inflammation theme; supports mitochondrial redox capacity	R, G	Emerging human + mechanistic	Different forms behave differently; NAD raising ≠ guaranteed clinical cognition benefit
1	5	Pantothenic acid (B5) → CoA	Acetyl-CoA formation; lipid metabolism; TCA entry	CoA biosynthesis; acetylation capacity	Foundational for fuel oxidation and acetylation balance	G	Mechanistic	Often overlooked; deficiency uncommon but suboptimal intake can matter in frailty
1	6	Magnesium	ATP handling (Mg-ATP) + enzyme kinetics	ATP-dependent enzymes; synaptic function	Supports neuronal energy usage + plasticity; deficiency can worsen excitotoxic vulnerability	R, G	Supportive human + mechanistic	Form/absorption variability; renal constraints for supplementation in some patients
2	1	NAD+ precursors (NR/NMN/NA/NAM)	Restores NAD+ availability for redox + signaling	NAMPT salvage; sirtuins; PARPs; CD38	Supports mitochondrial function; may improve resilience under oxidative/repair load	R, G	Animal > human (emerging)	NAD “sinks” (CD38/PARP) can dominate; response varies by inflammation/age
2	2	Alpha-lipoic acid (ALA)	Mitochondrial redox cofactor + antioxidant recycling	PDH/α-KGDH cofactor; GSH recycling support	Improves redox tone and mitochondrial efficiency (signals strongest in metabolic/oxidative phenotypes)	R, G	Small AD trials + mechanistic	“Antioxidant” framing can be misleading—main value is mitochondrial/redox coupling support
2	3	Glutathione system support	Detox + peroxide handling	GSH, GPx, GR, NADPH supply (PPP)	Reduces oxidative damage load that impairs mitochondria/synapses	R, G	Mechanistic	GSH depends on substrates + NADPH; pushing one component may not fix system
2	4	Selenium (GPx capacity)	Peroxide detox via selenoenzymes	Glutathione peroxidases	Supports antioxidant enzyme capacity (context-dependent)	G	Mixed human	Narrower safety margin; avoid “more is better” mindset
3	1	CoQ10 (ubiquinone)	ETC electron carrier (I/II→III) + membrane redox	Complex I/II→III transfer	Supports OXPHOS efficiency; may reduce electron leak under some conditions	R, G	Limited AD-specific	Bioavailability/formulation matters; AD cognition data not robust
3	2	Cardiolipin / mitochondrial membranes (support axis)	ETC supercomplex stability; cristae integrity	Inner mitochondrial membrane architecture	Membrane integrity affects ETC efficiency and ROS leak	G	Mechanistic	Hard to “target” nutritionally in a clean way; effects indirect
3	3	Iron / copper homeostasis (burden control)	Prevents metal-catalyzed oxidative damage	Fenton chemistry burden; metal transport/storage	Metal dyshomeostasis can amplify ROS and mitochondrial injury	R, G	Mechanistic + mixed human	“Chelation” is not casually safe; needs careful framing and evidence
4	1	Ketone utilization (BHB/acetoacetate axis)	Alternative brain fuel bypassing glucose bottlenecks	MCT1/2 transport; ketolysis enzymes	Addresses brain glucose hypometabolism by providing alternate substrate	R, G	Moderate (human MCI/AD signals exist)	GI tolerance and adherence; response varies by genotype/metabolic status
4	2	Creatine / phosphocreatine shuttle	ATP buffering and rapid energy stabilization	Creatine kinase system	May stabilize energy during stress; supports muscle/functional reserve that impacts cognition indirectly	G	Limited AD	CNS benefit uncertain; stronger for muscle/functional outcomes
4	3	Acetyl-L-carnitine (ALCAR)	Fatty acid oxidation support + acetyl group handling	Carnitine shuttle; acetyl-CoA support	May support mitochondrial energy and neuronal function (mixed clinical results)	R, G	Mixed human	Benefits heterogeneous; not a universal cognitive improver
4	4	Medium-chain triglycerides (MCT oil → ketones)	Rapid ketone support strategy	Hepatic ketogenesis; brain ketone uptake	Practical ketone-raising approach for some phenotypes	R, G	Moderate human	GI effects; calorie load; titration matters
5	1	AMPK → PGC-1α biogenesis axis	Mitochondrial number/quality regulation	AMPK, PGC-1α, SIRT1	Supports long-term mitochondrial capacity and stress resistance	G	Mechanistic	Most effects are slow; many “activators” are indirect and context-dependent
5	2	Mitophagy / autophagy quality control	Removes damaged mitochondria	PINK1/Parkin axis; autophagy machinery	Damaged mitochondria drive ROS and energy failure; quality control is protective in theory	G	Mechanistic	Autophagy modulation is double-edged; oversimplified “more autophagy = good” is risky
5	3	Exercise signaling (the “master cofactor”)	Improves vascular + mitochondrial + neurotrophic tone	BDNF; insulin sensitivity; AMPK/PGC-1α	Most evidence-backed multi-pathway energy intervention for aging brain	R, G	Strong (human)	Adherence/ability constraints; must be individualized
6	1	Cerebral perfusion / vascular health	Fuel + oxygen delivery and waste clearance support	Neurovascular unit; endothelial function	Vascular dysfunction worsens hypometabolism and inflammation	R, G	Strong (human)	Often upstream of “supplement” efficacy; if delivery is poor, cofactors underperform
6	2	Sleep / glymphatic clearance	Waste clearance & metabolic recovery	Glymphatic system; circadian regulation	Supports clearance of metabolic byproducts; indirectly supports energy balance	G	Strong (human)	Often neglected; impacts cognition and inflammation strongly
6	3	Oxygen utilization context (respiratory capacity)	Oxidative metabolism support	OXPHOS dependence	If oxygen delivery/usage is limited, pushing mitochondrial cofactors won’t fully translate	R, G	Supportive	More about system constraints than a “node to supplement”

TSF (Time-Scale Flag): P = 0–30 min, R = 30 min–3 hr, G = >3 hr (adaptation/phenotype). Evidence: "Strong (human)" = consistent clinical/epidemiologic support; "Moderate" = mixed but plausible human signals; "Emerging" = early-stage human; "Mechanistic" = preclinical/biochemical rationale.

Scientific Papers found: Click to Expand⟱

3271-

ALA,

Decrypting the potential role of α-lipoic acid in Alzheimer's disease

Review,

AD,

*antiOx↑, *memory↑, *neuroP↑, *Inflam↓, *IronCh↑, *NRF2↑, *BBB↑, *GlucoseCon↑, *Ach↑, *ROS↓, *p‑tau↓, *Aβ↓, *cognitive↑, *Hif1a↑, *Ca+2↓, *GLUT3↑, *GLUT4↑, *HO-1↑, *VEGF↑, *PDKs↓, *PDH↑, *VCAM-1↓, *GSH↑, *NRF2↑, *hepatoP↑, *ChAT↑,

3441-

ALA,

α-Lipoic Acid Maintains Brain Glucose Metabolism via BDNF/TrkB/HIF-1α Signaling Pathway in P301S Mice

in-vivo,

AD,

mice

*tau↓, *GlucoseCon↑, *GLUT3↑, *GLUT4↑, *VEGF↑, *HO-1↑, *Glycolysis↑, *HK1↑, *PGC-1α↑, *Hif1a↑, *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,

in-vitro,

AD,

mice

*cognitive↑, *Dose↝, *Aβ↓, *tau↓, *BDNF↑, *motorD↑,

3687-

Ash,

Role of Withaferin A and Its Derivatives in the Management of Alzheimer’s Disease: Recent Trends and Future Perspectives

Review,

AD,

*Aβ↓, *tau↓, *HSPs↝, *antiOx↑, *ROS↓, *Inflam↓, *neuroP↑, *cognitive↑, *NF-kB↓, *HO-1↑, *memory↑, *AChE↓, *BChE↓, *ChAT↑, *Ach↑,

4303-

Ash,

Ashwagandha (Withania somnifera)—Current Research on the Health-Promoting Activities: A Narrative Review

Review,

AD,

*neuroP↑, *Sleep↑, *Inflam↓, *cardioP↑, *cognitive↑, *Aβ↓, *TNF-α↓, *IL1β↓, *IL6↓, *MCP1↓, *lipid-P↓, *tau↓, *ROS↓, *BBB↑, *AChE↓, *GSH↑, *GSTs↑, *GSR↑, *GPx↑, *SOD↑, *Catalase↑, ChemoSen↑, *Strength↑,

4304-

Ba,

Baicalein inhibits heparin-induced Tau aggregation by initializing non-toxic Tau oligomer formation

in-vitro,

AD,

27.8 μM

 IC50 of 27.8 μM for inhibition of Tau

*tau↓, *Dose↝, *BioAv↓,

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,

mouse

*cognitive↑, *Aβ↓, *Apoptosis↓, *CD31↑, *VEGF↑, *N-cadherin↑, *angioG↑, *neuroP↑, *p‑tau↓, *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,

*Inflam↓, *antiOx↓, *AChE↓, *BChE↓, *MAOA↓, *MAOB↓, *lipid-P↓, *GSH↑, *ROS↓, *APP↓, *BACE↓, *p‑tau↓, *NF-kB↓, *TNF-α↓, *IL1β↓, *MAPK↓, *PI3K↓, *Akt↓, *neuroP↑, *memory↑,

4298-

BBR,

Berberine mitigates cognitive decline in an Alzheimer’s Disease Mouse Model by targeting both tau hyperphosphorylation and autophagic clearance

in-vivo,

AD,

in drinking water at 100 mg/kg/day, and lasted four months

3×Tg AD mice

*cognitive↑, *p‑tau↓, *GSK‐3β↓, *PP2A↑, *memory↑, *Akt↑, *LC3II↑, *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,

AD mice

*memory↑, *p‑tau↓, *NF-kB↓, *GSH↑, *lipid-P↓, *cognitive↑, *ROS↓, *Inflam↓,

5483-

BM,

The Role of Bacopa monnieri in Alzheimer’s Disease: Mechanisms and Potential Clinical Use—A Review

Review,

AD,

*cognitive↑, *neuroP↑, *PI3K↑, *Akt↑, *GSK‐3β↓, *tau↓, *ROS↓, *MMP3↓, *Casp1↓, *Casp3↓, *NF-kB↓, *TNF-α↓, *IL6↓,

3791-

CA,

Caffeic Acid and Diseases—Mechanisms of Action

Review,

AD,

*memory↑, *cognitive↑, *p‑tau↓, *ROS↓, *Inflam↓, *NF-kB↓, *Casp3↓, *lipid-P↓, *AChE↓, *BChE↓, *GSK‐3β↓, *5LO↓, *BDNF↓, VEGF↓, HSP70/HSPA5↓,

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,

*neuroP↑, *antiOx↑, *Inflam↓, *AChE↓, *BChE↓, *cognitive↑, *ROS↓, *Aβ↓, *tau↓, eff↑,

5860-

CAP,

Beneficial Effects of Capsaicin in Disorders of the Central Nervous System

Review,

AD,

Review,

Park,

Review,

Stroke,

*neuroP↑, *memory↑, *Pain↓, *TRPV1↑, *Aβ↓, *tau↓, *cognitive↑, *Risk↓, *motorD↓, *ROS↓, *TNF-α↓, *IL1β↓, *eff↑, *Risk↓,

5854-

CAP,

Pharmacological activity of capsaicin: Mechanisms and controversies (Review)

Review,

Var,

Review,

AD,

Obesity↓, Half-Life↓, antiOx↑, TRPV1↑, STAT3↓, Ca+2↑, ROS↑, MMP↓, *neuroP↑, *tau↓, *Inflam↓, *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,

mice

*Aβ↓, *cognitive↑, *APP↓, *MMP-10↝, *p‑tau↓, *Inflam↓, *neuroP↑, *Risk↓, *TNF-α↓, *IFN-γ↓, *IL6↓, *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,

30 mg/kg

APP/PS1 mice

*Risk↓, *Aβ↓, *p‑tau↓, *Inflam↓, *neuroP↑, *cognitive↑, *ADAM10↑, *PPARα↑,

5768-

CAPE,

Neuroprotective Potential of Caffeic Acid Phenethyl Ester (CAPE) in CNS Disorders: Mechanistic and Therapeutic Insights

Review,

AD,

Review,

Park,

Review,

Stroke,

*antiOx↑, *Inflam↑, *AntiCan↑, *NRF2↑, *GSK‐3β↑, *Akt↑, *PI3K↑, *ROS↓, *SOD↑, *GSH↑, *MDA↓, *tau↓, *neuroP↑, *memory↑, *AChE↓, *other↝, *lipid-P↓,

6040-

CGA,

Protective effect of chlorogenic acid on cognitive impairment in rats with early Alzheimer's disease via Wnt signaling pathway

in-vivo,

AD,

Forty male rats

*neuroP↑, *Dose↝, *GSK‐3β↓, *tau↓, *β-catenin/ZEB1↑, *Wnt↑, *memory↑, *cognitive↑, *NRF2↑, *ROS↓,

3889-

Cin,

Orally administrated cinnamon extract reduces β-amyloid oligomerization and corrects cognitive impairment in Alzheimer's disease animal models

in-vivo,

AD,

*Aβ↓, *cognitive↑, *tau↓,

3894-

Cin,

Interaction of cinnamaldehyde and epicatechin with tau: implications of beneficial effects in modulating Alzheimer's disease pathogenesis

in-vitro,

AD,

*tau↓, *ROS↓,

3888-

Cin,

Cinnamon, a promising prospect towards Alzheimer's disease

NA,

AD,

*tau↓, *Aβ↓, *neuroP↑, *ROS↓, *Inflam↓, *cardioP↑, *antiOx↑, *cognitive↑, *BBB↑, *p‑GSK‐3β↑, *AChE↓,

3893-

Cin,

Cinnamon extract inhibits tau aggregation associated with Alzheimer's disease in vitro

Review,

AD,

*tau↓, *toxicity↓,

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,

Review,

Var,

*antiOx↑, *Inflam↓, *cardioP↑, angioG↓, VEGF↓, *LDL↓, COX2↓, Hif1a↓, *Aβ↓, *tau↓, *toxicity↓,

5798-

CRMs,

Caloric restriction mimetics improve gut microbiota: a promising neurotherapeutics approach for managing age-related neurodegenerative disorders

Review,

Nor,

Review,

AD,

*GutMicro↑, *neuroP↑, *eff↑, *Dose↝, *AMPK↑, *SIRT1↑, *mTOR↓, *NRF2↑, *p‑tau↓,

3624-

Cro,

Crocus Sativus L. (Saffron) in Alzheimer's Disease Treatment: Bioactive Effects on Cognitive Impairment

Review,

AD,

*AChE↓, *memory↑, *cognitive↑, *MDA↑, *Thiols↑, *GPx↑, *antiOx↑, *ROS↓, *Casp3↓, *neuroP↑, *SOD↑, *Ach↑, *ChAT↑, *BBB↑, *Aβ↓, *tau↓, *cognitive↑, *Inflam↓,

3794-

CUR,

Curcumin hybrid molecules for the treatment of Alzheimer's disease: Structure and pharmacological activities

Review,

AD,

*GSK‐3β↓, *CDK5↓, *p‑tau↓, *IronCh↑, *ROS↓, *HO-1↑, *SOD↑, *Catalase↑, *GSH↑, *TNF-α↓, *IL6↓, *IL12↓, *NRF2↑, *PPARγ↑, *IL4↑, *AChE↓, *Dose↝, *GutMicro↑,

3793-

CUR,

Curcumin Downregulates GSK3 and Cdk5 in Scopolamine-Induced Alzheimer’s Disease Rats Abrogating Aβ40/42 and Tau Hyperphosphorylation

in-vivo,

AD,

Rats

*Aβ↓, *p‑tau↓, *GSK‐3β↓, *CDK5↓, *memory↑,

3795-

CUR,

Curcumin: A Golden Approach to Healthy Aging: A Systematic Review of the Evidence

Review,

AD,

*antiOx↑, *Inflam↓, *AntiAge↑, *AMPK↑, *SIRT1↑, *NF-kB↓, *mTOR↓, *NLRP3↓, *NADPH↓, *ROS↓, *COX2↓, *MCP1↓, *IL1β↓, *IL17↓, *IL23↓, *TNF-α↓, *MPO↓, *IL10↑, *lipid-P↓, *SOD↑, *Aβ↓, *p‑tau↓, *GSK‐3β↓, *CDK5↓, *TXNIP↓, *NRF2↑, *NQO1↑, *HO-1↑, *OS↑, *memory↑, *BDNF↑, *neuroP↑, *BACE↓, *AChE↓, *LDL↓,

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,

*cognitive↝, *BioAv↑, *Inflam↓, *COX2↓, *iNOS↓, *NF-kB↓, *TNF-α↓, *IL1↓, *IL2↓, *IL6↓, *IL8↓, *IL12↓, *ROS↓, *RNS↓, *antiOx↑, *BBB↑, *BioAv↓, *cognitive↑, *memory↑, *tau↓, *eff↑,

3576-

CUR,

Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer's Disease

Review,

AD,

*Inflam↓, *antiOx↑, *memory↑, *Aβ↓, *BBB↑, *cognitive↑, *tau↓, *LDL↓, *AChE↓, *IL1β↓, *IronCh↑, *neuroP↑, *BioAv↝, *PI3K↑, *Akt↑, *NRF2↑, *HO-1↑, *Ferritin↑, *HO-2↓, *ROS↓, *Ach↑, *GSH↑, *Bcl-2↑, *ChAT↑,

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,

rat

*cognitive↑, *AChE↓, *Aβ↓, *P53↓, *tau↓, *NRF2↓, *TNF-α↓, *NO↑, *Catalase↑, *antiOx↑, *Inflam↓,

3591-

EGCG,

Epigallocatechin-3-Gallate Provides Protection Against Alzheimer's Disease-Induced Learning and Memory Impairments in Rats

in-vivo,

AD,

Rats

*p‑tau↓, *BACE↓, *Aβ↓, *Ach↑, *AChE↓, *antiOx↑, *memory↑, *hepatoP↑, *ROS↓, *GPx↑, *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,

mouse

*neuroP↑, *memory↑, *p‑tau↓,

4290-

EGCG,

EGCG impedes human Tau aggregation and interacts with Tau

in-vitro,

AD,

 64.2 μM.

*tau↓, *Dose↝, *neuroP↑, *antiOx↑,

4291-

EGCG,

Structure-based discovery of small molecules that disaggregate Alzheimer’s disease tissue derived tau fibrils in vitro

in-vitro,

AD,

*tau↓, *BBB∅,

3830-

EMD,

Traditional Chinese Medicine: Role in Reducing β-Amyloid, Apoptosis, Autophagy, Neuroinflammation, Oxidative Stress, and Mitochondrial Dysfunction of Alzheimer’s Disease

Review,

AD,

*neuroP↑, *Aβ↓, *p‑tau↓, *BACE↓,

4071-

FA,

Folate and Alzheimer: when time matters

Review,

AD,

*cognitive↑, *ROS↓, *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,

Rats

*cognitive↑, *ERK↓, *p‑Akt↓, *AChE↓, *BACE↓, *neuroP↑, *ROS↓, *MDA↓, *GSH↑, *GSSG↓, *p‑tau↓, *lipid-P↓, *Aβ↓,

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,

APPswe/PS1dE9 transgenic mice

*cognitive↑, *IL1β↓, *Ach↑, *Aβ↓, *p‑tau↓, *BDNF↑, *APP↓,

4025-

FulvicA,

Mumio (Shilajit) as a potential chemotherapeutic for the urinary bladder cancer treatment

in-vitro,

Bladder,

T24/HTB-9

Review,

AD,

tumCV↓, selectivity↑, TumCCA↑, other↝, *neuroP↑, *memory↑, *tau↓, *other↝, *lipid-P↓, *VitC↑, *antiOx↑,

4017-

FulvicA,

Fulvic acid inhibits aggregation and promotes disassembly of tau fibrils associated with Alzheimer's disease

NA,

AD,

*cognitive↑, *tau↓,

4016-

FulvicA,

Shilajit: A Natural Phytocomplex with Potential Procognitive Activity

Review,

AD,

*tau↓, *AntiAge↑, *Strength↑, *Dose↝, *BioAv↑, *antiOx↑, *memory↑, *Inflam↓, *cognitive↑, *neuroP↑, *toxicity↝, *toxicity↑,

4020-

FulvicA,

Natural products as a rich source of tau-targeting drugs for Alzheimer’s disease

in-vitro,

AD,

*tau↓, *cognitive↑,

4021-

FulvicA,

Scaling the Andean Shilajit: A Novel Neuroprotective Agent for Alzheimer’s Disease

in-vitro,

AD,

Primary cultures of rat hippocampal neurons and mouse neuroblastoma cells

*tau↓, *neuroP↑,

3723-

Gb,

Can We Use Ginkgo biloba Extract to Treat Alzheimer’s Disease? Lessons from Preclinical and Clinical Studies

Review,

AD,

*memory↑, *antiOx↑, *Casp3↓, *APP↓, *AChE↓, *Aβ↓, *5HT↑, *SOD↓, *MDA↓, *NO↓, *GSH↑, *Bcl-2↑, *BAX↑, *TNF-α↓, *IL1β↑, *iNOS↓, *IL10↓, *p‑tau↓, *ROS↓, *MAOB↓, *cognitive↑, *neuroP↑, *Apoptosis↓,

4302-

Gins,

Panax ginseng: A modulator of amyloid, tau pathology, and cognitive function in Alzheimer's disease

Review,

AD,

*neuroP↑, *Aβ↓, *p‑tau↓, *cognitive↑, *eff↑, *PKA↑, *CREB↑, *BACE↓, *ADAM10↑, *MAPK↑, *ERK↑, *PI3K↑, *Akt↑, *NRF2↑, *PPARγ↓, *IDE↑, *APP↓, *PP2A↑, *memory↑,

4301-

Gins,

Red Ginseng Inhibits Tau Aggregation and Promotes Tau Dissociation In Vitro

in-vitro,

AD,

*p‑tau↓, *eff↑, *Inflam↓,

4243-

Gins,

Effects of Ginseng on Neurological Disorders

Review,

Stroke,

Review,

AD,

Review,

Park,

*BDNF↑, *TrkB↑, *neuroP↑, *VEGF↑, *p‑tau↓, *memory↑,

3829-

Gins,

Traditional Chinese Medicine: Role in Reducing β-Amyloid, Apoptosis, Autophagy, Neuroinflammation, Oxidative Stress, and Mitochondrial Dysfunction of Alzheimer’s Disease

Review,

AD,

*cognitive↑, *neuroP↑, *Aβ↓, *tau↓, *PI3K↑, *Akt↑, *memory↑,

Showing Research Papers: 1 to 50 of 108
Page 1 of 3 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 108

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes ⓘ

Obesity↓, 1,
Total Targets: 19

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↓, 1, antiOx↑, 17, 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↑, 9, RNS↓, 1, ROS?, 1, ROS↓, 22, SOD↓, 1, SOD↑, 6, Thiols↑, 1, VitC↑, 1,

Metal & Cofactor Biology ⓘ

Ferritin↑, 1, IronCh↑, 3,

Mitochondria & Bioenergetics ⓘ

PGC-1α↑, 1,

Core Metabolism/Glycolysis ⓘ

AMPK↑, 2, 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, 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↓, 7, GSK‐3β↑, 1, p‑GSK‐3β↑, 1, 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↑, 4,

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↓, 19, Inflam↑, 1, MCP1↓, 2, NF-kB↓, 7, TNF-α↓, 10,

Synaptic & Neurotransmission ⓘ

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

Protein Aggregation ⓘ

Aβ↓, 25, 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, cardioP↑, 3, cognitive↑, 30, cognitive↝, 1, hepatoP↑, 2, memory↑, 22, motorD↓, 1, motorD↑, 1, neuroP↑, 30, OS↑, 1, Pain↓, 1, Risk↓, 4, Sleep↑, 1, Strength↑, 2, toxicity↓, 2, toxicity↑, 1, toxicity↝, 1,
Total Targets: 150

Scientific Paper Hit Count for: tau, tau

9 Resveratrol
8 Urolithin
7 Curcumin
5 Cinnamon
5 Selenium NanoParticles
5 Shilajit/Fulvic Acid
4 Berberine
4 Capsaicin
4 EGCG (Epigallocatechin Gallate)
4 Ginseng
4 Hydrogen Gas
4 Quercetin
4 Vitamin B1/Thiamine
2 Alpha-Lipoic-Acid
2 Ashwagandha(Withaferin A)
2 Caffeic acid
2 Folic Acid, Vit B9
2 Ferulic acid
2 Luteolin
2 Magnetic Fields
2 Vitamin B3,Niacin
2 Sulforaphane (mainly Broccoli)
2 Thymoquinone
1 Aromatherapy
1 Baicalein
1 Bacopa monnieri
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 Moringa oleifera
1 Methylsulfonylmethane
1 Mushroom Lion’s Mane
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 Rosmarinic acid
1 Vitamin A, Retinoic Acid
1 Vitamin B12
1 Vitamin B5,Pantothenic Acid
1 Vitamin D3
1 Vitamin K2
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:38  Cells:%  prod#:%  Target#:1231  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

tau Cancer Research Results

Brain Energy Systems Matrix (AD)

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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