PSD95 Cancer Research Results

PSD95, Postsynaptic density protein 95: Click to Expand ⟱
Source:
Type:
PSD95 (Postsynaptic density protein 95) is a critical scaffolding protein in excitatory synapses, particularly abundant in the postsynaptic density (PSD) of neurons. It plays a key role in synaptic signaling and plasticity, including anchoring NMDA receptors and organizing signaling complexes.
-↓ PSD95 levels in hippocampus and cortex in AD patients and models.
-Loss of PSD95 impairs synaptic plasticity (e.g., LTP) and memory formation
-Hyperphosphorylated tau disrupts PSD95-mediated signaling.
-Agents that preserve or restore PSD95 levels show cognitive benefits in models
Scientific Papers found: Click to Expand⟱
3797- CUR,    Curcumin reverses cognitive deficits through promoting neurogenesis and synapse plasticity via the upregulation of PSD95 and BDNF in mice
- in-vitro, NA, NA
*cognitive↑, Our results showed that curcumin administration rescued the impaired cognition of mice, shown as enhanced BrdU+ and dendritic spine in hippocampus.
*BDNF↑, At the molecular level, curcumin was found to promote the expression of brain-derived neurotrophic factor (BDNF) and postsynaptic density protein 95 (PSD95).
*PSD95↑,
*memory↑, Studies have shown that curcumin improves the spatial learning and memory abilities of the Alzheimer’s disease model mice

4213- Hup,    Huperzine A-Liposomes Efficiently Improve Neural Injury in the Hippocampus of Mice with Chronic Intermittent Hypoxia
- in-vivo, NA, NA
*cognitive↑, HuA-LIP significantly ameliorated cognitive dysfunction and neuronal damage in CIH mice.
*SOD↑, HuA-LIP elevated T-SOD and GSH-Px abilities and decreased MDA content to resist oxidative stress damage induced by CIH.
*GPx↑,
*MDA↓,
*ROS↓,
*Iron↓, HuA-LIP reduced brain iron levels by downregulating TfR1, hepcidin, and FTL expression.
*TfR1/CD71↓,
*FTL↓,
*ERK↑, HuA-LIP activated the PKAα/Erk/CREB/BDNF signaling pathway and elevated MAP2, PSD95, and synaptophysin to improve synaptic plasticity.
*PKA↑,
*CREB↑,
*BDNF↑,
*PSD95↑,
*neuroP↑, HuA-LIP showed a superior performance against neuronal damage induced by CIH.

4209- Hup,    Huperzine A, reduces brain iron overload and alleviates cognitive deficit in mice exposed to chronic intermittent hypoxia
- in-vivo, NA, NA
*ROS↓, HuA improves synaptic plasticity and decreases ROS level in CIH mice
*cognitive↑, HuA significantly improved cognitive impairment and neuronal damage in the hippocampus of CIH mice via increasing the ratio of Bcl-2/Bax and inhibiting caspase-3 cleavage.
*neuroP↑,
*Bax:Bcl2↓,
*Casp3↑,
*NADPH↓, HuA considerably decreased ROS levels by downregulating the high levels of NADPH oxidase (NOX 2, NOX 4) mediated by CIH.
*NOX↓,
*TfR1/CD71↓, Decreased levels of TfR1 and FTL proteins observed in HuA treated CIH group, could reduce iron overload in hippocampus. HuA increased PSD 95 protein expression, CREB activation and BDNF protein expression
*Iron↓,
*PSD95↑,
*BDNF↑,

7784- ISL,    Isoliquiritigenin attenuates lipopolysaccharide-induced cognitive impairment through antioxidant and anti-inflammatory activity
- in-vivo, AD, NA
*Learn↑, ISL pretreatment reversed these deficits as well as LPS-induced decreases in the hippocampal expression levels of synaptophysin, postsynaptic density-95, brain-derived neurotrophic factor, superoxide dismutase, glutathione peroxidase, and BCL-2.
*PSD95↑,
*BDNF↑,
*SOD↑,
*GPx↑,
*Bcl-2↑,
*SYP↑,
*Bax:Bcl2↓, ISL pretreatment also reversed LPS-induced increases in TUNEL-positive (apoptotic) cells, BAX/BCL-2 ratio, and expression levels of tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and C-C motif chemokine ligand 3.
*TNF-α↓,
*IL1β↓,
*IL6↓,
*MIP‑1α/CCL3↓,
*p‑GSK‐3β↑, Pretreatment with ISL increased the expression levels of phosphorylated (p)-GSK-3β, nuclear NRF2, HO-1 mRNA, and NQO1 mRNA, and reversed LPS-induced nuclear translocation of nuclear factor (NF)-κB
*NRF2↑,
*HO-1↑,
*NQO1↑,
*cognitive↑, ISL protects against LPS-induced cognitive impairment and neuronal injury by promoting or maintaining antioxidant capacity and suppressing neuroinflammation, likely through phosphorylation-dependent inactivation of GSK-3β, enhanced expression of NRF
*Inflam↓,

7865- isoO,    Isoorientin inhibits oxidative stress to ameliorate cognitive dysfunction in type 2 diabetes mice via GSK3β/Nrf2 axis
- in-vivo, Diabetic, NA
*cognitive↑, ISO improved systemic glucose metabolism and alleviated hepatic steatosis, and reversed cognitive deficits.
*PSD95↑, ISO restored synaptic proteins (PSD-95, BDNF, soluble α-synuclein), exerted anti-apoptotic effects (increased Bcl-2/Bax ratio, decreased cleaved caspase-3), and attenuated oxidative stress and mitochondrial damage.
*BDNF↑,
*Bax:Bcl2↓,
*cl‑Casp3↓,
*ROS↓,
*mtDam↓,
*GSK‐3β↓, Mechanistically, ISO inhibited GSK3β activity, promoted Nrf2 nuclear accumulation, upregulated HO-1 expression, and reduced tau phosphorylation at Ser396
*NRF2↑,
*HO-1↑,
*p‑tau↓,
*neuroP↑, ISO exerts a neuroprotective effect in TDACD model by inhibiting oxidative stress via GSK3β/Nrf2 pathway, and highlight ISO as a potential therapeutic candidate for TDACD.

4231- Lut,    Luteolin and its antidepressant properties: From mechanism of action to potential therapeutic application
- Review, AD, NA
*PSD95↑, upregulating the expression of synaptophysin, postsynaptic density protein 95, brain-derived neurotrophic factor, B cell lymphoma protein-2, superoxide dismutase, and glutathione S-transferase; and decreasing the expression of malondialdehyde, caspa
*BDNF↑,
*SOD↑,
*GSTA1↑,
*MDA↑,
*Casp3↓,
*Mood↑, antidepressant effects of luteolin are mediated by various mechanisms, including anti-oxidative stress, anti-apoptosis, anti-inflammation, anti-endoplasmic reticulum stress, dopamine transport, synaptic protection, hypothalamic–pituitary–adrenal axi
*antiOx↑,
*Apoptosis↓,
*Inflam↓,
*ER Stress↓,

4227- Lyco,    Lycopene Alleviates Depression-Like Behavior in Chronic Social Defeat Stress-Induced Mice by Promoting Synaptic Plasticity via the BDNF-TrkB Pathway
- in-vivo, NA, NA
*BDNF↑, suggesting that lycopene may enhance synaptic plasticity via the BDNF–TrkB/pTrkB signaling pathway.
*TrkB↑,
*PSD95↑, mRNA expression levels of PSD‐95 and Syn in the hippocampus of the CSDS + LYC group mice were substantially upregulated compared to the model group

3740- MF,    Gamma rhythm low field magnetic stimulation alleviates neuropathologic changes and rescues memory and cognitive impairments in a mouse model of Alzheimer's disease
- in-vivo, AD, NA
*cognitive↑, DMS treatment enhances cognitive performances, attenuates Aβ load, upregulates postsynaptic density protein 95 level, and promotes hippocampal long-term potentiation in 5XFAD mouse brain.
*Dose↝, Successive trains of DMS for 40 minutes were administered daily for continuous 8 weeks.
*Aβ↓, When DMS was administered, the average area occupied by Aβ positive plaques was decreased in 5XFAD mice.
*PSD95↑, DMS could restore PSD95 expression in the brain of 5XFAD mice

3835- Moringa,    Moringa Oleifera Alleviates Aβ Burden and Improves Synaptic Plasticity and Cognitive Impairments in APP/PS1 Mice
- in-vivo, AD, NA
*antiOx↑, multiple effects such as Moringa oleifera (MO) that have strong anti-oxidative, anti-inflammatory, anticholinesterase, and neuroprotective virtues.
*Inflam↓,
*AChE↓,
*neuroP↑,
*Mood↑, MO improved behavioral deficits such as anxiety-like behavior and hyperactivity and cognitive, learning, and memory impairments.
*cognitive↑,
*memory↑,
*Aβ↓, MO treatment abrogated the Aβ burden to wild-type control mice levels via decreasing BACE1 and AEP and upregulating IDE, NEP, and LRP1 protein levels.
*BACE/β-secretase↓,
*AEP↓,
*IDE↑,
*NEP↑,
*LRP1↑,
*PSD95↑, MO improved synaptic plasticity by improving the decreased GluN2B phosphorylation, the synapse-related proteins PSD95 and synapsin1 levels, the quantity and quality of dendritic spines, and neurodegeneration in the treated mice
*STEP↓, These results suggest that MO modulates the PP2B/DARPP-32/PP1 axis to downregulate STEP activity thereby improving GluN2B Tyr1472 phosphorylation in APP/PS1 mice.
*APP↓, data suggest that MO downregulates the amyloidogenic processing of APP as well as improves Aβ clearance to decrease the Aβ burden in these mice.

3922- PTS,    Pterostilbene attenuates amyloid-β induced neurotoxicity with regulating PDE4A-CREB-BDNF pathway
- in-vivo, AD, NA
*BioAv↑, Pterostilbene (PTS), a kind of resveratrol analog which showed higher scores on BBB and OB, could overcome Aβ-induced neurotoxicity in vitro and in vivo.
*BBB↑, PTS exhibited a much higher BBB index than Resveratrol, which meant a higher compound concentration in the brain
*memory↑, Behavioral tests further confirmed PTS’ potential of overcoming memory deficits in APP/PS1 mice (AD model).
*p‑CREB↑, PTS increased the pVASP, pCREB, BDNF, and PSD95 expression.
*BDNF↑,
*PSD95↑,
*neuroP↑, PTS would be a qualified natural product for alleviating Aβ-induced neurotoxicity in AD.

3798- RES,    Resveratrol reverses hippocampal synaptic markers injury and SIRT1 inhibition against developmental Pb exposure
- in-vivo, NA, NA
*SIRT1↑, Resveratrol attenuated a decrease in the expression levels of SIRT1 and BDNF induced by Pb
*BDNF↑,
*PSD95↑, Moreover, resveratrol treatment reversed the decrease in PSD-95 and NL-1 expression induced by Pb.
*memory↑, Resveratrol improved spatial learning and memory deficits in Pb- exposed rats

7902- VT,    Vitexin Protects Against Scopolamine-Induced Cognitive Impairment by Preserving Synaptic Integrity and Modulating Nrf2/HO-1 and NF-κB Signaling Pathways
- in-vivo, AD, NA
*Dose↝, Sco (2 mg/kg/day, i.p.), Sco + vitexin (30 mg/kg/day, oral), Sco + donepezil (1.5 mg/kg/day, i.p.), vitexin alone, and donepezil alone
*Learn↑, co significantly impaired spatial learning and memory while increasing anxiety-like behaviors. Vitexin treatment markedly improved these deficits, with efficacy comparable to donepezil
*memory↑,
*AChE↓, Sco elevated acetylcholinesterase activity, lipid peroxidation, and oxidative/nitrosative stress markers (TOS, OSI, MDA, Peroxynitrite, NO, and NOS) while decreasing total antioxidant status (TAS). Vitexin reversed these changes.
*lipid-P↓,
*TOS↓,
*MDA↓,
*ONOO↓,
*NO↓,
*NOS2↓,
*TAC↑,
*BDNF↑, Sco reduced hippocampal BDNF, GDNF, PSD95, and synaptophysin levels and increased GFAP, IL-6, TNF-α, NF-κB p65, and COX-2 expression. Vitexin restored neurotrophic and synaptic proteins, suppressed astrocyte activation and inflammatory signaling, a
*GDNF↑,
*PSD95↑,
*GFAP↓,
*NF-kB↓,
*COX2/PTGS2↓,
*NRF2↑, and activated the Nrf2/HO-1 pathway.
*HO-1↑,
*neuroP↑, vitexin exerts significant neuroprotective and synaptoprotective effects against Sco-induced cognitive impairment by simultaneously restoring redox balance
*NeuroI↓, suppressing neuroinflammation, and preserving synaptic integrity.


Showing Research Papers: 1 to 12 of 12

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

GDNF↑, 1,   GFAP↓, 1,   Learn↑, 2,   NeuroI↓, 1,   ONOO↓, 1,   SYP↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   GPx↑, 2,   GSTA1↑, 1,   HO-1↑, 3,   Iron↓, 2,   lipid-P↓, 1,   MDA↓, 2,   MDA↑, 1,   NQO1↑, 1,   NRF2↑, 3,   ROS↓, 3,   SOD↑, 3,   TAC↑, 1,   TOS↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

FTL↓, 1,   TfR1/CD71↓, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

mtDam↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

CREB↑, 1,   p‑CREB↑, 1,   NADPH↓, 1,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,   Bax:Bcl2↓, 3,   Bcl-2↑, 1,   Casp3↓, 1,   Casp3↑, 1,   cl‑Casp3↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 1,  

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

ERK↑, 1,   GSK‐3β↓, 1,   p‑GSK‐3β↑, 1,  

Migration(tgid=13) ⓘ

APP↓, 1,   LRP1↑, 1,   PKA↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 3,   MIP‑1α/CCL3↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Cellular Microenvironment(tgid=17) ⓘ

NOX↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 2,   BDNF↑, 10,   PSD95↑, 12,   p‑tau↓, 1,   TrkB↑, 1,  

Protein Aggregation(tgid=19) ⓘ

AEP↓, 1,   Aβ↓, 2,   BACE/β-secretase↓, 1,   IDE↑, 1,   NEP↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   Dose↝, 2,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,   NOS2↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 7,   memory↑, 5,   Mood↑, 2,   neuroP↑, 6,   STEP↓, 1,  
Total Targets: 69

Scientific Paper Hit Count for: PSD95, Postsynaptic density protein 95
2 Huperzine A/Huperzia serrata
1 Curcumin
1 Isoliquiritigenin
1 isoorientin
1 Lutein
1 Lycopene
1 Magnetic Fields
1 Moringa oleifera
1 Pterostilbene
1 Resveratrol
1 Vitexin
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

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