BDNF Cancer Research Results
BDNF, brain-derived neurotrophic factor: Click to Expand ⟱
| Source: |
| Type: |
Brain-Derived Neurotrophic Factor (BDNF) is a key neurotrophin (a type of growth factor) involved in brain health, and its role in Alzheimer’s Disease (AD) has been extensively studied.
-AD patients often have lower BDNF levels in key brain regions, such as the hippocampus and cortex.
-This reduction correlates with cognitive decline and brain atrophy.
-BDNF normally protects neurons from Aβ toxicity
-Exercise and cognitive training have been shown to boost BDNF levels and may slow cognitive decline.
- natural compounds (like curcumin or flavonoids) may also upregulate BDNF.
|
Scientific Papers found: Click to Expand⟱
| - |
in-vivo, |
AD, |
NA |
|
|
|
- |
in-vivo, |
Park, |
NA |
|
|
|
*neuroP↑, Chicoric acid attenuated neuron damage in d-gal-treated mice as revealed through histological examination in the hippocampus region of the mouse brain.
*TNF-α↓, The levels of inflammatory mediators, such as TNF-α and IL-1β, as well as malondialdehyde levels, were markedly reduced after chicoric acid treatment.
*IL1β↓,
*MDA↓,
*Catalase↑, activity of CAT and the level of GSH were significantly elevated in serum by chicoric acid
*GSH↑,
*NRF2↑, chicoric acid treatment noticeably activated the Nrf2 antioxidative defense system
*mtDam↓, reversing mitochondrial dysfunction, decreasing inflammation, and neuron apoptosis caused by oxidative stress.
*Inflam↓,
*Apoptosis↓,
*ROS↓, chicoric acid significantly quenched intracellular ROS to the normal level
*cognitive↑, suggested that chicoric acid supplementation ameliorated cognitive impairment induced by d-gal and SH-SY5Y cell apoptosis induced by H2O2
*Aβ↓, chicoric acid inhibited d-gal-induced Aβ1-42 accumulation in hippocampus of mice brain.
*BDNF∅, suggesting chicoric acid treatment did not restore the expression of BDNF in the hippocampus of aging mice.
*APP↓, chicoric acid treatment markedly decreased the expression of APP and BACE1 in the whole brain, which partly explains the inhibition by chicoric acid of Aβ1-42 accumulation in the cortex and hippocampus.
*BACE↓,
*memory↑, CA prevented LPS-induced memory impairment and neuronal loss through behavioral tests and histological examination.
*Aβ↓, CA prevented LPS-induced increases in amyloid β (1-42 specific) (Aβ1-42) accumulation, levels of amyloid precursor protein, and neuronal β-secretase 1 (BACE1), as well as the equilibrium cholinergic system in mouse brain.
*BACE↓,
*MAPK↓, CA down-regulated LPS-induced glial overactivation by inhibiting the MAPK and NF-κB pathway
*NF-kB↓,
*NF-kB↓, CA reduced the levels of NF-κB transcriptionally regulated inflammatory mediators and cytokines such as iNOS, cyclooxygenase-2 (COX-2), IL-1β, and TNF-α in both mouse brain and BV2 microglial cells.
*iNOS↓,
*COX2↓,
*IL1β↓,
*TNF-α↓,
*BDNF∅, we found that BDNF, NGF, NT3, and NT4 mRNA expressions of neurotrophic factors exhibited no changes after CA treatment
*MMPs↓, CA also down-regulated the mRNA levels of MMPs in LPS-treated mice, which might provide another clue for the explanation of the anti-amyloidosis effects of CA (
*BDNF∅, Our results have evidenced that a six-week consumption of Ginkgo biloba extract did not result in an increase in basal BDNF content.
*neuroP↑, TQ significantly increases the number of hippocampal neurons.
*Casp3↓, TQ significantly decreases the amount of Caspase-3 expression and the cleavage of poly ADP ribose polymerase, indicating a decrease in apoptosis.
*Apoptosis↓,
*ERK↑, ERK, GSK-3, JNK, CREB, and iNOS proteins are found to be positively regulated by TQ.
*JNK↑,
*CREB↑,
*iNOS↑,
*BDNF∅, gene expression of synapsin, synaptophysin, NGF, AKT, Bax, NFkB, and p53 and the protein expression of BDNF and nNOS are not affected by TQ.
*other↑, After 10 weeks, mean 25(OH)D levels increased from 46 to 81 nmol/L in the vitamin D group with no change in the placebo group.
*BDNF∅, There was no effect of vitamin D on muscle power, function or BDNF.
*BDNF∅, There was no association of vitamin D with NGF, GDNF, or BDNF levels.
*BDNF∅, Zinc supplementation may not significantly increase BDNF levels. However, the small number of included articles and significant heterogeneity between them can increase the risk of a false negative result;
Showing Research Papers: 1 to 7 of 7
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7
Pathway results for Effect on Cancer / Diseased Cells:
Total Targets: 0
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
Catalase↑, 1, GSH↑, 1, MDA↓, 1, NRF2↑, 1, ROS↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
mtDam↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
CREB↑, 1,
Cell Death(tgid=5) ⓘ
Apoptosis↓, 2, Casp3↓, 1, iNOS↓, 1, iNOS↑, 1, JNK↑, 1, MAPK↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↑, 1,
Migration(tgid=13) ⓘ
APP↓, 1, MMPs↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2↓, 1, IL1β↓, 2, Inflam↓, 1, NF-kB↓, 2, TNF-α↓, 2,
Synaptic & Neurotransmission(tgid=18) ⓘ
BDNF∅, 7,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 2, BACE↓, 2,
Functional Outcomes(tgid=23) ⓘ
cognitive↑, 1, memory↑, 1, neuroP↑, 2,
Total Targets: 28
Scientific Paper Hit Count for: BDNF, brain-derived neurotrophic factor
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#:1356 State#:% Dir#:6
wNotes=on sortOrder:rid,rpid
Home Page