Salvia officinalis / CREB Cancer Research Results

Sage, Salvia officinalis: Click to Expand ⟱
Features:
Salvia officinalis(common sage) has been studied for its potential therapeutic effects in Alzheimer's disease (AD) and cancer due to its antioxidant, anti-inflammatory, neuroprotective, and anticancer properties.

Salvia officinalis — AD relevance: Sage has human clinical signals for cognition/AD, plausibly via cholinesterase inhibition plus anti-inflammatory/antioxidant support. Essential-oil chemotype matters for safety (thujone exposure).

Primary mechanisms (conceptual rank):
1) ↑ Cholinergic tone (AChE/BChE inhibition; symptomatic cognitive support)AChE ↓ → ACh ↑ (symptomatic cognitive enhancement)
2) ↓ Neuroinflammation (NF-κB/cytokine tone; model-supported)
3) ↓ Oxidative stress (↓ ROS/lipid peroxidation; stress-defense support)
4) Secondary network/synaptic efficiency effects (chronic adaptation)

Bioavailability / PK relevance: Oral leaf extracts used in trials; effects are typically over weeks–months. Avoid equating leaf extract with essential oil dosing due to thujone-associated neurotoxicity risk.

Clinical evidence status: Small double-blind RCT in mild–moderate AD (extract vs placebo) and additional placebo-controlled cognitive studies in non-AD populations; evidence is supportive but not definitive/disease-modifying.

-Sage contains compounds (e.g., rosmarinic acid, luteolin, carnosic acid) that inhibit acetylcholinesterase (AChE) and butyrylcholinesterase (BChE).This enhances acetylcholine levels, supporting memory and cognition — similar to drugs like donepezil.
-High in phenolic compounds (e.g., flavonoids, diterpenes) that scavenge reactive oxygen species (ROS).

-High doses of thujone (a compound in some sage oils) may be neurotoxic or hepatotoxic.

Salvia officinalis — AD / Neurodegeneration Pathway Map

RankPathway / AxisCellsTSFPrimary EffectNotes / Interpretation
1 AChE ↓ → ACh ↑ (cholinergic synapse) ACh ↑ (via AChE inhibition) P/R Improved synaptic cholinergic transmission Extract inhibits acetylcholinesterase → reduced ACh breakdown → increased synaptic ACh. Symptomatic mechanism analogous to donepezil-class drugs.
2Neuroinflammation (NF-κB / cytokines) ↓R/G Reduced inflammatory stress Extracts show anti-inflammatory signaling in cell/biochemical models; relevance to AD progression is supportive.
3ROS / lipid peroxidation ↓P/R Oxidative burden reduction Phenolics/diterpenes contribute to antioxidant effects; typically requires sustained intake for tissue adaptation.
4NRF2 antioxidant-response program ↔ / ↑ (context-dependent)R/G Stress-defense regulation Consider as a supportive axis; not always directly measured in human cognition trials.
5Ca²⁺ excitotoxicity interplay ↔P/R Not primary More relevant to essential-oil neurotoxicity discussions than leaf-extract cognition trials; include only with explicit Ca²⁺ endpoints.
6Aβ / tau-associated pathology ↔ (limited human evidence)G Not established clinically Any anti-amyloid/tau claims are largely preclinical; avoid over-weighting without biomarker-confirmed replication.
7Clinical Translation Constraint ↓ (constraint)— Safety + product variability Essential oil/thujone can be pro-convulsant; regulators specify limits for thujone exposure in herbal products. Extract standardization and duration (weeks–months) matter.

TSF legend: P: 0–30 min; R: 30 min–3 hr; G: >3 hr
CREB, cAMP Response Element Binding Protein: Click to Expand ⟱
Source:
Type: transcription factor
CREB is a transcription factor that binds to specific DNA sequences, known as cAMP response elements (CRE), in the promoter regions of target genes.
CREB is activated by phosphorylation, which allows it to bind to CRE and recruit other transcriptional coactivators.
CREB regulates the expression of genes involved in various cellular processes, including:
    Cell growth and differentiation
    Apoptosis
    Metabolism
    Neurotransmission

CREB is also involved in the regulation of genes involved in cancer, including:
    Cell cycle progression
    Angiogenesis
    Invasion and metastasis

CREB is often overexpressed in cancer tissues.
High levels of CREB expression are associated with poor prognosis, increased tumor aggressiveness, and resistance to therapy. CREB can promote the expression of genes involved in cell survival and proliferation.
Scientific Papers found: Click to Expand⟱
4217- Sage,  RosA,  Aroma,    Neuroprotective Potential of Aromatic Herbs: Rosemary, Sage, and Lavender
- Review, AD, NA - Review, Park, NA
*Inflam↓, *antiOx↑, *neuroP↑, *ERK↑, *CREB↑, *BDNF↑, *Aβ↑, *AChE↓, *memory↑, *cognitive↑,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,  

Core Metabolism/Glycolysis ⓘ

CREB↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   BDNF↑, 1,  

Protein Aggregation ⓘ

Aβ↑, 1,  

Functional Outcomes ⓘ

cognitive↑, 1,   memory↑, 1,   neuroP↑, 1,  
Total Targets: 10

Scientific Paper Hit Count for: CREB, cAMP Response Element Binding Protein
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#:338  Target#:798  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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