Magnetic Fields / neuroP Cancer Research Results

MF, Magnetic Fields: Click to Expand ⟱
Features: Therapy

Magnetic Fields — externally applied static or time-varying magnetic fields used to alter cellular signaling, redox state, ion handling, membrane behavior, metabolism, or neural activity without introducing a chemical agent. They are a physical therapeutic modality and include static magnetic fields (SMF), extremely-low-frequency magnetic fields (ELF-MF), pulsed electromagnetic fields (PEMF), and other non-rotating oscillating/time-varying magnetic fields. Common abbreviations include MF, SMF, ELF-MF, EMF, and PEMF. Biological effects are strongly dependent on field strength, frequency, waveform, gradient, duty cycle, exposure duration, and tissue or cell type. Rotating magnetic fields are excluded here because they are represented separately as pid 192; magnetic-nanoparticle-dependent magnetothermal or magnetomechanical effects are also better assigned primarily to the magnetic nanoparticle product.

Primary mechanisms (ranked):

  1. Redox modulation and ROS perturbation, including radical-pair and mitochondrial mechanisms; cancer cells may develop sustained oxidative stress whereas normal cells frequently show adaptive antioxidant responses.
  2. Ca²⁺ and ion-channel modulation, particularly TRPC, voltage-gated channels, intracellular Ca²⁺ handling, and ER–mitochondrial Ca²⁺ communication.
  3. Mitochondrial and bioenergetic modulation, including membrane potential, electron transport, ATP production, mitochondrial permeability, and metabolic reprogramming.
  4. Cell proliferation, cell-cycle, apoptosis, and senescence signaling through pathways including EGFR/PI3K/AKT/mTOR, MAPK/ERK, caspases, PARP, Bax and survivin.
  5. Membrane permeability and drug-uptake modulation, producing context-dependent chemosensitization to agents including doxorubicin, etoposide and methotrexate.
  6. Inflammatory and stress-response modulation including NF-κB, cytokine signaling, HSPs, ER stress and adaptive antioxidant pathways.
  7. Migration, invasion, angiogenesis and tumor-microenvironment modulation; effects are field-parameter and tumor-model dependent.

Bioavailability / PK relevance: Conventional pharmacokinetic concepts do not apply because the intervention is a physical field rather than an absorbed drug. Relevant exposure variables are magnetic flux density, field gradient, frequency, waveform, pulse width, repetition rate, duty cycle, spatial distribution, treatment duration and tissue depth. Magnetic fields can penetrate tissue without the concentration gradients characteristic of drugs, but induced electric fields and biological coupling vary markedly with geometry and frequency.

In-vitro vs systemic exposure relevance: Effects are not concentration-driven. Many experimental results cannot be generalized between devices because apparently small differences in waveform, frequency, flux density, orientation, gradient and exposure duration can change the biological response. Static fields ranging from millitesla to tesla and PEMF/ELF protocols ranging from weak fields to substantially stronger stimulation should therefore be treated as distinct exposure regimens rather than as a single dose-response continuum.

Clinical evidence status: Cancer treatment remains predominantly preclinical, with cell-culture and animal evidence plus limited supportive or adjunctive human use. Evidence supports parameter-dependent anticancer effects and chemosensitization, but non-rotating magnetic-field exposure alone is not an established standard anticancer therapy. PEMF has established clinical use in several musculoskeletal applications and has been studied as supportive therapy in oncology. Repetitive transcranial magnetic stimulation has substantially stronger human evidence in neurological and psychiatric applications, including investigational use in Alzheimer’s disease, but should not be interpreted as evidence that generic magnetic-field exposure is an established systemic cancer treatment.

Magnetic Fields can be Static, or pulsed. The most common therapy is a pulsed magnetic field in the uT or mT range.
The main pathways affected are:
Calcium Signaling: -influence the activity of voltage-gated calcium channels.
Oxidative Stress and Reactive Oxygen Species (ROS) Pathways
Heat Shock Proteins (HSPs) and Cellular Stress Responses
Cell Proliferation and Growth Signaling: MAPK/ERK pathway.
Gene Expression and Epigenetic Modifications: NF-κB
Angiogenesis Pathways: VEGF (improving VEGF for normal cells)
PEMF was found to have a 2-fold increase in drug uptake compared to traditional electrochemotherapy in rat melanoma models

Pathways:
- most reports have ROS production increasing in cancer cells , while decreasing in normal cells.
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx,
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, VEGF↓(mostly regulated up in normal cells),
- cause Cell cycle arrest : TumCCA↑,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, GLUT1↓, LDH↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- Others: PI3K↓, AKT↓, STAT↓, Wnt↓, β-catenin↓, ERK↓, JNK, - SREBP (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, cytoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Magnetic Field Mechanisms in Cancer

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 ROS and redox homeostasis ↑ ROS (context-dependent); ↑ oxidative stress ↑ transient ROS followed by ↔ or ↓ ROS in adaptive protocols P, R, G Redox perturbation One of the most recurrent MF mechanisms. Direction is strongly field- and cell-dependent; sustained ROS elevation is reported in several cancer models and during chemotherapy sensitization.
2 Ca²⁺ and ion-channel signaling ↑ Ca²⁺ signaling or dysregulation; altered TRPC and voltage-sensitive channel activity ↑ transient signaling with homeostatic recovery (context-dependent) P, R Electrophysiological signal transduction Ca²⁺ is a major mechanistic bridge between membrane sensing, mitochondria, ROS, proliferation and apoptosis. Response depends strongly on waveform and frequency.
3 Mitochondrial function and membrane potential ↓ ΔΨm; altered respiration; ↑ mitochondrial stress ↔ or reversible modulation (context-dependent) P, R, G Bioenergetic destabilization Mitochondrial effects can arise downstream of ROS and Ca²⁺ signaling and contribute to apoptotic commitment.
4 Apoptosis and caspase signaling ↑ apoptosis; ↑ caspases; ↑ PARP cleavage; ↑ Bax; ↓ survivin ↔ or substantially weaker response in selective protocols R, G Programmed cell death Reported with several PEMF and time-varying field protocols and can be amplified when combined with chemotherapy.
5 EGFR PI3K AKT mTOR signaling ↓ EGFR/AKT/mTOR signaling (model-dependent) ↔ or mixed R, G Growth-signal suppression Particularly supported in static-field experiments; response varies with cell type, cell density and field intensity.
6 Cell cycle and proliferation ↓ proliferation; ↑ cell-cycle arrest or mitotic disruption ↔ or mixed G Growth suppression Effects are highly protocol-specific. Some exposures are neutral or can stimulate proliferation, so suppression should not be treated as universal.
7 DNA damage and DNA-damage response ↑ DNA damage; ↑ ATM/p53/p21 signaling (context-dependent) ↔ or mixed; protective responses reported with some protocols R, G Genotoxic stress and repair modulation Often secondary to ROS and particularly evident during combination treatment with chemotherapy or radiation. Magnetic fields alone are not consistently genotoxic, and some static-field protocols can reduce radiation-associated DNA damage.
8 Chemosensitization and drug uptake ↑ chemotherapy response; ↑ drug uptake or cytotoxicity ↔ or ↑ toxicity (drug-dependent) R, G Adjunctive anticancer effect Documented with doxorubicin, etoposide and other agents. Selectivity is not guaranteed; normal-cell toxicity must be evaluated for each field-drug combination.
9 Glutathione and antioxidant buffering ↓ GSH reserve or altered GSH/GSSG balance (context-dependent) ↑ GSH or antioxidant adaptation in some protocols R, G Redox buffering modulation GSH depletion is best interpreted as a consequence of oxidative load rather than a universal direct MF target.
10 NRF2 antioxidant response ↔ / mixed; inadequate adaptive response in some oxidative protocols ↑ NRF2 and antioxidant-response signaling in some protective protocols R, G Adaptive antioxidant defense NRF2 direction is not uniform enough to classify MF globally as either an NRF2 activator or inhibitor.
11 ER stress and unfolded protein response ↑ ER stress and UPR (model-dependent) ↑ adaptive stress response or ↔ R, G Proteostasis stress Can develop secondary to ROS, altered Ca²⁺ handling and mitochondrial dysfunction.
12 Mitochondrial permeability transition ↑ MPTP opening propensity ↔ or reversible opening R Mitochondrial death commitment Supported mechanistically for specific ELF-MF exposures through ROS-sensitive pathways; should not be generalized to all magnetic fields.
13 Glycolysis and cellular energetics ↓ glycolytic flux or altered ATP production (model-dependent) ↔ or metabolic adaptation R, G Metabolic reprogramming Some frequency-tuned exposures suppress glycolysis, but this is substantially less universal than ROS or Ca²⁺ modulation.
14 HIF-1α and angiogenic signaling ↓ HIF-1α / VEGF in selected models ↑ VEGF or tissue-repair signaling in some regenerative protocols G Angiogenesis modulation Potential cancer-versus-normal-tissue divergence is attractive but remains highly exposure- and model-specific.
15 NF-κB and inflammatory signaling ↓ NF-κB and inflammatory signaling in selected models ↓ inflammatory cytokines in many regenerative PEMF applications R, G Inflammation modulation Better established as an anti-inflammatory/regenerative PEMF effect than as a universal cancer-cell mechanism.
16 Migration invasion and angiogenesis ↓ migration; ↓ invasion; ↓ angiogenic signaling in selected models ↔ or pro-repair angiogenesis (context-dependent) G Metastatic phenotype modulation Direction varies substantially with field protocol and normal-versus-tumor context.
17 Radiosensitization ↑ radiation-induced ROS and DNA damage in selected protocols Mixed; radioprotection has also been reported with other protocols R, G Modification of radiation response Both radiosensitizing and radioprotective responses have been reported; field parameters and tissue context determine direction.
18 Clinical Translation Constraint Field-specific response; substantial tumor heterogeneity Potential tissue-specific physiological effects G Translation limitation No pharmacokinetic dose metric exists. Field strength, frequency, waveform, geometry, gradients, duration and induced electric fields must be specified. Most anticancer evidence remains preclinical and protocols are poorly standardized.

P: 0–30 min     R: 30 min–3 hr     G: >3 hr

MPTP: opening represents a mitochondrial commitment event integrating ROS and Ca²⁺ stress; sustained opening indicates irreversible bioenergetic failure.




Alzheimer’s disease relevance: Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive magnetic neuromodulation modality with randomized human evidence for modest improvement in global cognition in mild cognitive impairment and Alzheimer’s disease. The strongest recent evidence supports excitatory stimulation of cortical cognitive-network regions, particularly the dorsolateral prefrontal cortex. The mechanism is principally neural-network and synaptic modulation rather than the systemic ROS-based mechanism often discussed for low-intensity PEMF. Meta-analyses generally report cognitive benefit, but protocol heterogeneity, small trials and uncertain durability remain important limitations. rTMS should therefore be classified as investigational or adjunctive for AD rather than an established disease-modifying treatment.

Clinical evidence status: Multiple RCTs and meta-analyses support a modest short-term cognitive signal. Longer-term benefit remains less certain, optimal frequency/intensity/site protocols are not standardized, and evidence does not establish prevention or reversal of Alzheimer pathology.

Magnetic Stimulation in Alzheimer’s Disease

Rank Pathway / Axis Modulation TSF Primary Effect Notes / Interpretation
1 Cortical network excitability ↑ P, R Neuromodulation High-frequency rTMS and excitatory stimulation of cortical network hubs can increase cortical responsiveness.
2 Synaptic plasticity ↑ R, G Plasticity enhancement Repeated stimulation can produce LTP-like network effects and is a leading explanation for persistence beyond the stimulation session.
3 Cognitive-network connectivity ↑ G Network normalization DLPFC and related cortical networks are the most consistently studied targets.
4 Global cognition ↑ G Clinical cognitive improvement Recent meta-analyses show modest improvement in MMSE, MoCA or ADAS-Cog outcomes, although heterogeneity remains substantial.
5 Neuroinflammation and neurotrophic signaling ↓ inflammation; ↑ neurotrophic signaling (context-dependent) G Secondary neurobiological effects Supported mainly by mechanistic and preclinical studies; less directly established than cortical-network effects in human AD.
6 Clinical Translation Constraint ↔ G Protocol heterogeneity Optimal stimulation site, frequency, intensity, pulse count, session number and maintenance schedule remain unresolved; long-term disease modification has not been demonstrated.

P: 0–30 min     R: 30 min–3 hr     G: >3 hr
neuroP, neuroprotective: Click to Expand ⟱
Source:
Type:
Neuroprotective refers to the ability of a substance, intervention, or strategy to preserve the structure and function of nerve cells (neurons) against injury or degeneration.
-While cancer and neurodegenerative processes might seem distinct, there is significant overlap in terms of treatment-related neurotoxicity, shared molecular mechanisms, and the potential for therapies that provide neuroprotection during cancer treatment.
Scientific Papers found: Click to Expand⟱
3475- MF,    A Pulsed Electromagnetic Field Protects against Glutamate-Induced Excitotoxicity by Modulating the Endocannabinoid System in HT22 Cells
- in-vitro, Nor, HT22 - Review, AD, NA
*Apoptosis↓, PEMF exposure improved viability of HT22 cells after excitotoxicity and reduced lactate dehydrogenase release and cell death.
*LDH↓,
*neuroP↑, PEMF exposure indicated that the neuroprotective effects of PEMF were related to modulation of the eCB metabolic system.
*toxicity∅, Recent studies have shown that PEMF is a safe and non-invasive approach for management of several neurological diseases, including Alzheimer's disease
*IL1β↓, Previous studies have shown that PEMF could modulate inflammation after traumatic brain injury by inhibiting production of pro-inflammatory factor IL-1β
*Inflam↓, PEMF influences neuroinflammation via elevation of anti-inflammatory IL-10 and reduction of pro-apoptotic tumor necrosis factor
*IL10↑,
*TNF-α↓,

3476- MF,    Pulsed Electromagnetic Fields Stimulate HIF-1α-Independent VEGF Release in 1321N1 Human Astrocytes Protecting Neuron-like SH-SY5Y Cells from Oxygen-Glucose Deprivation
- in-vitro, Stroke, 1321N1 - in-vitro, Park, NA
*VEGF↑, PEMF exposure induced a time-dependent, HIF-1α-independent release of VEGF from 1321N1 cells
*eff↑, further corroborate their therapeutic potential in cerebral ischemia.
*neuroP↑, emerging evidence has identified PEMFs as an attractive non-invasive strategy also for the treatment of different neuropathological conditions
*other↑, PEMF stimulation have been studied in the context of Parkinson’s disease [2,3], Alzheimer’s disease [4], and neuropathic pain
*eff↑, PEMFs significantly reduced neuroinflammation and pro-apoptotic factors and determined a reduction of infarct size, implicating PEMFs as possible adjunctive therapy for stroke patients
*Inflam↓, anti-inflammatory effect of PEMFs in microglial cells
*Hif1a∅, PEMFs exposure did not modulate HIF-1α expression confirming that the PEMF-mediated VEGF production was independent by the activation of this transcriptional regulator of cellular response to hypoxia

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.

4148- MF,    Increase in Blood Levels of Growth Factors Involved in the Neuroplasticity Process by Using an Extremely Low Frequency Electromagnetic Field in Post-stroke Patients
- Human, Stroke, NA
*neuroP↑, We observed that ELF-EMF significantly increased growth factors and cytokine levels involved in neuroplasticity, as well as promoted an enhancement of functional recovery in post-stroke patients.
*BDNF↑, The increase of the BDNF level in the ELF-EMF group was about 200%
*Dose↝, magnetic induction of 5 mT, 40 Hz, rectangular and bipolar waveforms) was conducted in the ELF-EMF group

4147- MF,    PEMFs Restore Mitochondrial and CREB/BDNF Signaling in Oxidatively Stressed PC12 Cells Targeting Neurodegeneration
- in-vitro, AD, PC12
*ROS↓, PEMF treatment significantly counteracted H2O2- and Aβ-induced cytotoxicity by restoring cell viability, reducing reactive oxygen species production, and improving catalase activity.
*Catalase↑,
*MMP↑, PEMFs preserved the mitochondrial membrane potential and decreased caspase-3 activation and chromatin condensation
*Casp3↓,
*p‑ERK↓, Mechanistically, PEMFs inhibited ERK phosphorylation and enhanced cAMP levels, CREB phosphorylation, and BDNF expression
*cAMP↑,
*p‑CREB↑,
*BDNF↑,
*neuroP↑, PEMFs modulate multiple stress response systems, promoting neuroprotection under oxidative and amyloidogenic conditions.

4118- MF,    Effects of transcranial magnetic stimulation on neurobiological changes in Alzheimer's disease
- Review, AD, NA
*cognitive↑, TMS may increase brain cortical excitability, induce specific potentiation phenomena, and promote synaptic plasticity and recovery of impaired functions; thus, it may re-establish cognitive performance in patients with AD.
*BDNF↑, Notably, a number of studies have indicated an increase in endogenous neurotrophic content (BDNF) in the affected brain regions after TMS therapy
*neuroP↑, neuroprotective and neuroregenerative effects
*memory↑, 1 Hz LF-rTMS: reversed memory deficits, and improved spatial memory retrieval ability.
*ROS↓, 20 Hz HF-rTMS: Increased visual recognition memory functions, decreased oxidant status, increased anti-oxidant levels and improvement in familiarity-based cognition.
*antiOx↑,
*Aβ↓, Repeated electromagnetic field stimulation (3 mT; 75 Hz) Decreased Aβ toxicity
*eff↑, TMS parameters combined with short trains and long inter-train intervals carry a lower risk of side effects

4110- MF,    Pulsed Electromagnetic Fields: A Novel Attractive Therapeutic Opportunity for Neuroprotection After Acute Cerebral Ischemia
- Review, Stroke, NA
*ROS↓, PEMFs counteract hypoxia-induced apoptosis and ROS production in neuronal-like cells and exert a strong anti-inflammatory effect on microglial cells.
*Inflam↓, PEMFs exposure is able to reduce the size of the infarct area and decrease the levels of pro-inflammatory mediators.
*other↝, Pulsed electromagnetic fields (PEMFs) act as modulators of adenosine receptors (ARs); in particular, PEMF stimulation induces a significant upregulation of A2A and A3 ARs in different cell types.
*neuroP↑, PEMFs through the specific action on A2A and A3 ARs show great potential to be exploited also to control brain inflammation and to provide neuroprotection following brain damage.
*Apoptosis↓, PEMFs exposure significantly reduced apoptosis, partially restored hypoxia inducible factor-1α (HIF-1α) activation to normoxic conditions, and inhibited ROS production.
*Hif1a↝,

4106- MF,    Cognitive Decline: Current Intervention Strategies and Integrative Therapeutic Approaches for Alzheimer's Disease
- Review, AD, NA
*cognitive↑, Dragicevic and colleagues [52] efficiently showed that long-term exposure to high-frequency EMF treatment in Alzheimer’s transgenic (Tg) mice not only prevents cognitive impairment, but also reverses it and improves memory functioning in normal mice.
*memory↑,
*Aβ↓, EMF treatment was able to disaggregate amyloid-beta peptide (Aβ) oligomers, which are the form of Aβ that causes mitochondrial dysfunction in AD
*neuroP↑, EMF application has the capacity to selectively target microglia, eliciting neuroprotective effects against AD

8487- MF,    The effect of repetitive transcranial magnetic stimulation on immediate and long-term cognitive functions in Alzheimer's dementia and mild cognitive impairment: a meta-analysis
- Review, AD, NA
*cognitive↑, The results demonstrated that rTMS significantly improved immediate cognition (SMD = 0.93, 95% CI = 0.64 to 1.22, p < 0.001) and long-term cognition (SMD = 0.42, 95% CI = 0.13 to 0.70, p = 0.004) across all patients (including
*Dose↝, Thirty-three studies reported the effectiveness of rTMS stimulation frequency lesser than 20 Hz, sixteen studies presented the effectiveness of rTMS stimulation frequency greater than or equal to 20 Hz
*Dose↝, Twelve studies reported the effectiveness of rTMS stimulation duration/session lesser than 30 min,
*BDNF↑, upregulating brain-derived neurotrophic factor (BDNF)
*neuroP↑, These mechanisms work synergistically to enhance GABAergic neuron activity and neuroprotection

4105- MF,    Extremely low frequency electromagnetic fields stimulation modulates autoimmunity and immune responses: a possible immuno-modulatory therapeutic effect in neurodegenerative diseases
- Review, AD, NA
*Inflam↓, On the basis of in vitro and clinical studies on brain activity, modulation by ELF-EMFs could possibly counteract the aberrant pro-inflammatory responses present in neurodegenerative disorders reducing their severity and their onset.
*neuroP↑, TMS (60 Hz, 0.7 mT) applied to rats for 2 hours twice daily, can be neuroprotective
*NO↑, The growth curve of exposed bacteria was lower than the control, while field application increased NO levels
*ROS↓, A significant increase of free radical production has been observed after exposure to 50 Hz electromagnetic fields at a flux density of 1 mT to mouse macrophages
*NO↓, EMF represents a non-pharmacological inhibitor of NO and an inducer of MCP-1,
*MCP1/CCL2↑,
*HSP70/HSPA5↑, Tokalov and Gutzeit (2004) showed the effect of ELF-EMF on heat shock genes and demonstrated that even a low dose of ELF-EMF (10 mT) caused an increase in HSPs, especially hsp70
*antiOx↑, Whereas most environmental electromagnetic radiations cause oxidative stress in the brain (Sahin and Gumuslu, 2007), ELF-EMF seems to have an antioxidant and neuroprotective effect
*NRF2↑, ELF-EMF induces the antioxidant pathway Nrf2, which is closely associated with its protective effect against neurotoxicity induced by 3-nitropropionic acid (3-NP)
*NF-kB↓, Selective inhibition of the NF-κB signaling pathway by ELF-EMF may be involved in the decrease of chemokine production.

3728- MF,    Long-term exposure to ELF-MF ameliorates cognitive deficits and attenuates tau hyperphosphorylation in 3xTg AD mice
- in-vivo, AD, NA
*cognitive↑, ELF-MF exposure ameliorated cognitive deficits and increased synaptic proteins in 3xTg mice.
*neuroP↑, protective effects of ELF-MF exposure may have also been caused by the inhibition of apoptosis and/or decreased oxidative stress levels that were observed in the hippocampus tissues of treated mice.
*Apoptosis↓,
*ROS↓,
*p‑tau↓, tau hyperphosphorylation was decreased in vivo because of ELF-MF exposure, and this decrease was induced by the inhibition of GSK3β and CDK5 activities and activation of PP2Ac.
*GSK‐3β↓,
*CDK5↓,

3724- MF,  RF,    Electromagnetic Field in Alzheimer's Disease: A Literature Review of Recent Preclinical and Clinical Studies
- Review, AD, NA
*memory↑, recent evidence revealed that exposure to electromagnetic fields (EMF) can delay the development of AD and improve memory.
*neuroP↑,

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.

4096- MF,    Extremely Low‐Frequency and Low‐Intensity Electromagnetic Field Technology (ELF‐EMF) Sculpts Microtubules
- in-vitro, AD, NA
*p‑tau↓, 40 Hz and 1 G Reduces Tau Phosphorylation in the Microtubule Pellet
*neuroP↑, Complementing these preconditioning neuroprotective effects, concomitant 1 h treatment protocols comparing 3.9 or 40 Hz and 1 G exposure, indicated effects on Tau phosphorylation accentuated with 40 Hz
*Dose↝, circular horizontal coil (18 cm in diameter, 50 turns of copper wire) and a waveform generator with built in amplifier (BK Precision, Yorba Linda, CA, 4045B).

4094- MF,    EMAGINE-Study protocol of a randomized controlled trial for determining the efficacy of a frequency tuned electromagnetic field treatment in facilitating recovery within the subacute phase following ischemic stroke
- Study, Stroke, NA
*neuroP↑, low-intensity electromagnetic fields (ELF-EMF) stimulation (exposure to sham field, 3.93 Hz or 15.72 Hz, every second day, for 4 weeks) was associated in treated animals with decreased edema, increased white matter integrity, evidence of neural regen
*Dose↝, BQ 2.0; BrainQ Technologies Ltd., Jerusalem, Israel) delivers a non-invasive, extremely low-frequency (1–100 Hz) and intensity ( ≤ 1 Gauss), frequency-tuned electromagnetic field.

3488- MFrot,  MF,    Rotating magnetic field improves cognitive and memory impairments in APP/PS1 mice by activating autophagy and inhibiting the PI3K/AKT/mTOR signaling pathway
- in-vivo, AD, NA
*cognitive↑, RMF treatment significantly ameliorated their cognitive and memory impairments, attenuated neuronal damage, and reduced amyloid deposition.
*memory↑,
*neuroP↑,
*Aβ↓,
*PI3K↓, RMF improves cognitive and memory dysfunction in APP/PS1 mice by activating autophagy and inhibiting the PI3K/AKT/mTOR signaling pathway, thus highlighting the potential of RMF as a clinical treatment for hereditary AD.
*Akt↓,
*mTOR↓,

3745- MFrot,  MF,    The neurobiological foundation of effective repetitive transcranial magnetic brain stimulation in Alzheimer's disease
- Review, AD, NA
*neuroP↑, neuroprotective actions aimed at mitigatingoxidative stress and inflammation, and intense stimulation of neu-rotrophic factors
*ROS↓,
*Inflam↓,
*5HT↑, increase in serotoninand its metabolites and a change in the properties of serotonergicreceptors.
*cFos↑, in rats, a single session of bothLF- (1 Hz) and HF-rTMS (10 Hz) enhanced c-Fos expression in all exam-ined cortical areas
*Aβ↓, rTMS enhances neuronal viability and counteracts oxidative stressors, such as Aβ and glutamate toxicity, in vitro
*memory↑, downregulation results in memory impairments
*BDNF↑, long-term change in synaptic proteinexpression due to BDNF-TrkB pathway activation following rTMSprotocols
*Ach↑, rTMSincreases ACh levels by modulating AChE activity.
*AChE↓,
*cognitive↑, HF-rTMS (20 Hz) and LF-rTMS (1 Hz)—in termsof neurotransmitter circuits and neurogenic signaling. 142 While bothprotocols improved cognition-related behaviors
*BDNF↑, Notably, rTMS could enhance BDNF and NGF expression irrespec-tive of frequency,
*NGF↑,
*β-catenin/ZEB1↑, both LF-rTMS (1 Hz) and HF-rTMS (10 Hz)protocols enhanced cognitive performance through the activation of β-catenin via the regulation of glycogen synthase kinase-3β (GSK-3β) andTau
*p‑Akt↓, 3 weeks, iTBS reducedinflammation and increased anti-inflammatory molecules, specificallylinked to reversing the downregulation of phosphorylated forms ofAkt and the mammalian target of rapamycin.
*mTOR↓,
*MMP1↓, 6 months, patients showed significant reductions in plasma levels of MMP1, MMP9, and MMP10, along with increases in TIMP1 and TIMP2
*MMP9↓,
*MMP-10↓,
*TIMP1↑,
*TIMP2↑,

3567- MFrot,  MF,    The Effect of Extremely Low-Frequency Magnetic Field on Stroke Patients: A Systematic Review
- Review, Stroke, NA
*eff↑, All included studies showed a beneficial effect of ELF-MFs on stroke patients
*ROS↓, Improvements were observed in domains such as oxidative stress, inflammation, ischemic lesion size, functional status, depressive symptoms and cognitive abilities.
*Inflam↓,
*cognitive↑, An improvement in cognitive abilities reported in some of the included studies [25,26,27,28] is in line with other researchers’ finding
*Catalase↑, Cichoń et al. [27] also showed that catalase activity in erythrocytes and superoxide dismutase were significantly higher in the experimental group than in the control group.
*SOD↑,
*SOD1↑, similar effect was observed in regard to SOD1 and SOD2 mRNA levels.
*SOD2↑,
*GPx1↑, ELF-MFs impacted also the expression of GPx1 and GPx4 mRNA, which increased in the experimental group about 160% (p < 0.001) and 140% (p < 0.001), respectively.
*GPx4↑,
*IL1β↑, blood samples of IL-1β in the experimental group after 10 sessions of rehabilitation which involved ELF-MFs were significantly higher than in the control group
*neuroP↑, majority of the articles included in this study, a neuroprotective effect of ELF-MFs was indicated
*toxicity∅, Particularly noteworthy is the fact that none of the studies included in this review reported any negative side effects of ELF-MFs.

204- MFrot,  MF,    Rotating magnetic field improved cognitive and memory impairments in a sporadic ad model of mice by regulating microglial polarization
- in-vivo, AD, NA
*NF-kB↓, RMF improves memory and cognitive impairments in a sporadic AD model, potentially by promoting the M1 to M2 transition of microglial polarization through inhibition of the NF-кB/MAPK signaling pathway.
*MAPK↓,
*TLR4↓,
*memory↑,
*cognitive↑,
*TGF-β1↑, RMF treatment promoted the expression of anti-inflammatory cytokines (TGF-β1, Arg-1, IL-4, IL-10)
*ARG1/2↑, Arg-1
*IL4↑,
*IL10↑,
*IL6↓,
*IL1↓, IL-1β
*TNF-α↓,
*iNOS↓,
*ROS↓, in mice brain
*NO↓, in serum
*MyD88↓,
*p‑IKKα↓, phosphorylated IKKα/β, IкBα, NF-кB p65, JNK, p38,
*p‑IκB↓, IкBα
*p‑p65↓,
*p‑JNK↓,
*p‑p38↓,
*ERK↓,
*neuroP↑, RMF treatment resulted in reduced aluminum deposition in the brains of AD mice.
*Aβ↓, RMF treatment reduced Aβ deposition in the AD model mice


Showing Research Papers: 1 to 19 of 19

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 19

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↑, 1,  
Total Targets: 1

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3,   Catalase↑, 2,   GPx1↑, 1,   GPx4↑, 1,   NRF2↑, 1,   ROS↓, 9,   SOD↑, 2,   SOD1↑, 1,   SOD2↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cAMP↑, 1,   p‑CREB↑, 1,   LDH↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↓, 3,   Casp3↓, 1,   iNOS↓, 2,   p‑JNK↓, 1,   MAPK↓, 1,   p‑p38↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 1,   other↑, 1,   other↝, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

HSP70/HSPA5↑, 2,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

cFos↑, 1,   ERK↓, 1,   p‑ERK↓, 1,   GSK‐3β↓, 1,   mTOR↓, 2,   PI3K↓, 1,  

Migration(tgid=13) ⓘ

ARG1/2↑, 1,   CDK5↓, 1,   MMP-10↓, 1,   MMP1↓, 1,   MMP9↓, 1,   TGF-β1↑, 1,   TIMP1↑, 1,   TIMP2↑, 1,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↝, 1,   Hif1a∅, 1,   NO↓, 2,   NO↑, 2,   VEGF↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

p‑IKKα↓, 1,   IL1↓, 1,   IL10↑, 2,   IL1β↓, 2,   IL1β↑, 1,   IL4↑, 1,   IL6↓, 1,   Inflam↓, 7,   p‑IκB↓, 1,   MCP1/CCL2↑, 1,   MyD88↓, 1,   NF-kB↓, 3,   p‑p65↓, 1,   TLR4↓, 1,   TNF-α↓, 3,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1,   AChE↓, 1,   BDNF↑, 6,   NGF↑, 1,   p‑tau↓, 2,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 5,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 5,   eff↑, 5,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,   LDH↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 9,   memory↑, 6,   motorD↑, 2,   neuroP↑, 19,   toxicity∅, 2,  
Total Targets: 75

Scientific Paper Hit Count for: neuroP, neuroprotective
19 Magnetic Fields
4 Magnetic Field Rotating
1 EMF
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#:172  Target#:1105  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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