Database Query Results : Magnetic Fields, , neuroP

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


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⟱
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.

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.

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

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↑,
*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.

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

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↑,

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.

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↓,

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)
*ARG↑, 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


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 18

Results for Effect on Cancer/Diseased Cells:
Catalase↑,1,  
Total Targets: 1

Results for Effect on Normal Cells:
5HT↑,1,   Ach↑,1,   AChE↓,1,   Akt↓,1,   p‑Akt↓,1,   antiOx↑,3,   Apoptosis↓,3,   ARG↑,1,   Aβ↓,5,   BDNF↑,5,   cAMP↑,1,   Casp3↓,1,   Catalase↑,2,   CDK5↓,1,   cFos↑,1,   cognitive↑,8,   p‑CREB↑,1,   Dose↝,3,   eff↑,5,   ERK↓,1,   p‑ERK↓,1,   GPx1↑,1,   GPx4↑,1,   GSK‐3β↓,1,   Hif1a↝,1,   Hif1a∅,1,   HSP70/HSPA5↑,2,   p‑IKKα↓,1,   IL1↓,1,   IL10↑,2,   IL1β↓,2,   IL1β↑,1,   IL4↑,1,   IL6↓,1,   Inflam↓,7,   iNOS↓,2,   p‑IκB↓,1,   p‑JNK↓,1,   LDH↓,1,   MAPK↓,1,   MCP1↑,1,   memory↑,6,   MMP↑,1,   MMP-10↓,1,   MMP1↓,1,   MMP9↓,1,   motorD↑,2,   mTOR↓,2,   MyD88↓,1,   neuroP↑,18,   NF-kB↓,3,   NGF↑,1,   NO↓,2,   NO↑,2,   NRF2↑,1,   other↑,1,   other↝,2,   p‑p38↓,1,   p‑p65↓,1,   PI3K↓,1,   ROS↓,9,   SOD↑,2,   SOD1↑,1,   SOD2↑,1,   p‑tau↓,2,   TGF-β1↑,1,   TIMP1↑,1,   TIMP2↑,1,   TLR4↓,1,   TNF-α↓,3,   toxicity∅,2,   VEGF↑,1,   β-catenin/ZEB1↑,1,  
Total Targets: 73

Scientific Paper Hit Count for: neuroP, neuroprotective
18 Magnetic Fields
4 Magnetic Field Rotating
1 EMF
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:172  Target#:1105  State#:%  Dir#:%
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