concept

EXCITOTOXICITY

Entity Detail — Knowledge Graph Node

Understanding Entity Pages

This page aggregates everything SciDEX knows about EXCITOTOXICITY: its mechanistic relationships (Knowledge Graph edges), hypotheses targeting it, analyses mentioning it, and supporting scientific papers. The interactive graph below shows its immediate neighbors. All content is AI-synthesized from peer-reviewed literature.

363Connections

3Hypotheses

12Analyses

50Outgoing

50Incoming

0Experiments

14Debates

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💡 Concept Info

Name	EXCITOTOXICITY
Key Genes/Proteins	AKT, AMPK, AMYLOID, AMYLOID-BETA, amyotrophic lateral sclerosis
Related Diseases	ALS, ALZHEIMER, Alzheimer'S Disease, ALZHEIMER'S DISEASE, AMYOTROPHIC LATERAL SCLEROSIS

Wiki Pages (1)

Knowledge base pages for this entity

Canonical Page

Excitotoxicity in Neurodegeneration

mechanism · 4129 words

→

Pathway Diagram

graph TD
    EXCITOTOXICITY["EXCITOTOXICITY"]
    EXCITOTOXICITY -->|"causes"| Neurotoxicity["Neurotoxicity"]
    EXCITOTOXICITY -->|"causes"| STIM1["STIM1"]
    EXCITOTOXICITY -->|"causes"| NEURODEGENERATION["NEURODEGENERATION"]
    EXCITOTOXICITY -->|"inhibits"| FOXO3["FOXO3"]
    EXCITOTOXICITY -->|"activates"| NEURON["NEURON"]
    EXCITOTOXICITY -->|"activates"| STING["STING"]
    EXCITOTOXICITY -->|"promotes"| HIPPOCAMPUS["HIPPOCAMPUS"]
    EXCITOTOXICITY -->|"promotes"| OXIDATIVE_STRESS["OXIDATIVE STRESS"]
    EXCITOTOXICITY -->|"regulates"| MITOCHONDRIAL_DYSFUNCTION["MITOCHONDRIAL DYSFUNCTION"]
    glutamate_receptors["glutamate receptors"] -->|"causes"| EXCITOTOXICITY
    Glutamate["Glutamate"] -->|"causes"| EXCITOTOXICITY
    Glutamate_receptors["Glutamate receptors"] -->|"mediates"| EXCITOTOXICITY
    NAD_metabolism["NAD metabolism"] -->|"participates in"| EXCITOTOXICITY
    GLUTAMATE["GLUTAMATE"] -->|"causes"| EXCITOTOXICITY
    glutamate["glutamate"] -->|"causes"| EXCITOTOXICITY
    ginsenosides["ginsenosides"] -->|"inhibits"| EXCITOTOXICITY
    inflammation["inflammation"] -->|"causes"| EXCITOTOXICITY
    GLUTAMATE_RECEPTORS["GLUTAMATE_RECEPTORS"] -->|"causes"| EXCITOTOXICITY

Outgoing (162)

Target	Relation	Type	Str
Ischemic Stroke	contributes_to	disease	0.90
Stroke	contributes_to	disease	0.90
Alzheimer's disease pathogenesis	associated_with	disease	0.90
Neurotoxicity	causes	process	0.90
Calcium Overload	associated_with	process	0.90
AD pathogenesis	associated_with	disease	0.90
Motor Neuron Death	causes	process	0.90
Motor Neuron Degeneration	contributes_to	phenotype	0.85
ferroptosis	activates	pathway	0.70
Amyotrophic lateral sclerosis	associated_with	disease	0.70
CELL DEATH	activates	phenotype	0.70
ERK	regulates	gene	0.70
motor neuron death	causes	phenotype	0.70
Ferroptosis	activates	pathway	0.70
FERROPTOSIS	causes	phenotype	0.65
AXONAL DEGENERATION	activates	phenotype	0.65
NECROPTOSIS	regulates	phenotype	0.65
AMPK	activates	gene	0.65
UBIQUITIN	degrades	protein	0.65
FERROPTOSIS	inhibits	phenotype	0.65
FERROPTOSIS	targets	phenotype	0.65
FERROPTOSIS	activates	phenotype	0.65
NECROPTOSIS	activates	phenotype	0.65
STIM1	causes	protein	0.64
SST	activates	gene	0.60
STIM1	activates	gene	0.60
neuroinflammation	associated_with	process	0.60
TRKB	associated_with	gene	0.60
MIRO1	associated_with	gene	0.60
oxidative stress	regulates	process	0.60
PARKINSON'S DISEASE	participates_in	disease	0.55
TFEB	activates	gene	0.55
ULK1	activates	gene	0.55
TET2	activates	gene	0.55
VGLUT1	inhibits	gene	0.55
HK2	activates	gene	0.55
SPINAL CORD	associated_with	brain_region	0.55
RIPK3	co_discussed	entity	0.50
LOCUS COERULEUS	co_discussed	entity	0.50
OLIGODENDROCYTE	co_discussed	entity	0.50
OLIGODENDROCYTES	co_discussed	entity	0.50
Proteins	interacts_with	protein	0.50
Parkinson's Disease	associated_with	disease	0.50
STING	co_discussed	entity	0.50
OXIDATIVE STRESS	co_discussed	entity	0.50
HIPPOCAMPUS	co_discussed	entity	0.50
NEURON	co_discussed	cell_type	0.50
RIPK1	co_discussed	entity	0.50
NMDA	co_discussed	entity	0.50
Proteins	inhibits	protein	0.50

Incoming (201)

Source	Relation	Type	Str
NPY	protects_against	protein	0.95
41302199	is a convergent hallmark of	paper	0.90
Glutamate	causes	entity	0.90
Glutamate receptors	mediates	receptor	0.90
Astrocyte	mediates	cell_type	0.90
glutamate receptors	causes	protein	0.90
39602529	were neuroprotective against	paper	0.90
Oligodendrocyte	mediates	cell_type	0.90
Glutamate Receptor Accumulation	contributes_to	process	0.85
Glutamate Receptor Accumulation	causes	mechanism	0.85
Astrocytes	contributes_to	cell_type	0.85
CYTOKINES	associated_with	protein	0.85
SOD1	mediates	protein	0.80
NPY	alleviates	gene	0.80
NAD metabolism	participates_in	process	0.80
HMGCR	inhibits	gene	0.80
GLUTAMATE	causes	drug	0.72
ginsenosides	inhibits	drug	0.70
glutamate clearance deficit	causes	process	0.70
NPTX2 downregulation	causes	mechanism	0.70
NMDAR dysregulation	causes	mechanism	0.70
CDK5	causes	gene	0.70
MCU deletion	protective_against	intervention	0.70
SYNAPTIC PLASTICITY	causes	phenotype	0.70
glutamate	causes	protein	0.70
Alpha-beta pathology	causes	phenotype	0.70
TREM2 upregulation in DAM cells	causes	mechanism	0.70
GABA	inhibits	phenotype	0.70
SLC7A11	causes	protein	0.70
inflammation	causes	process	0.70
JNK3	causes	gene	0.70
GABA	protects_against	phenotype	0.70
system xC-	causes	protein	0.70
VGLUT1 terminals	vulnerable_to	cell_type	0.70
CX3CR1 deficiency	causes	gene	0.70
AΒ	causes	gene	0.70
NR2B	causes	protein	0.70
GLUTAMATE_RECEPTORS	causes	protein	0.68
glutamate_receptors	causes	protein	0.68
STROKE	causes	disease	0.65
ASTROCYTES	exacerbates	cell_type	0.65
ASTROCYTE	causes	cell_type	0.65
LOCUS COERULEUS	causes	brain_region	0.65
KYNURENINE PATHWAY	activates	pathway	0.65
ALZHEIMER'S DISEASE	implicated_in	disease	0.65
ROS	inhibits	phenotype	0.65
BDNF	activates	gene	0.65
SLC1A2	protects_against	gene	0.60
SLC1A3	protects_against	gene	0.60
ALZHEIMER'S DISEASE	activates	disease	0.58

Targeting Hypotheses (3)

Hypotheses where this entity is a therapeutic target

Hypothesis	Score	Disease	Analysis
Closed-loop optogenetic targeting of PV interneurons to rest	0.633	als	-
Subtle NMDAR Inhibition Attenuates Excitotoxicity-Driven Tau	0.620	neurodegeneration	Investigate prion-like spreading of tau
Synaptic NMDAR Subtype Targeting Prevents Excitotoxicity	0.520	neurodegeneration	Test Preregistration Analysis

Mentioning Analyses (12)

Scientific analyses that reference this entity

Does tau dendritic missorting persist independently after Aβ clearance, maintain

neurodegeneration | 2026-04-25 | 7 hypotheses Top: 0.740

Is ferroptosis the primary driver of motor neuron death in ALS or an epiphenomen

neurodegeneration | 2026-04-18 | 4 hypotheses Top: 0.538

Ferroptosis in ALS and motor neuron disease: GPX4, lipid peroxidation, and iron

neurodegeneration | 2026-04-16 | 7 hypotheses Top: 0.680

Proteomics Differential Expression in AD CSF and Brain Tissue

neurodegeneration | 2026-04-16 | 1 hypotheses Top: 0.865

How can circuit-level neurodegeneration mechanisms be identified without complet

research methodology | 2026-04-11 | 0 hypotheses

Experiments (0)

Experimental studies targeting or related to this entity

Experiment	Type	Disease	Score	Feasibility	Model	Status	Est. Cost
No experiments found

Related Papers (0)

Scientific publications cited in analyses involving this entity

Title & PMID	Authors	Journal	Year	Citations
No papers found

Debates (14)

Multi-agent debates referencing this entity

Does tau dendritic missorting persist independently after Aβ clearance, maintain

closed · Rounds: 4 · Score: 0.65 · 2026-04-25

While the study establishes TDP-43 triggers mtDNA release via mPTP to activate c

closed · Rounds: 4 · Score: 0.73 · 2026-04-21

The debate raised this developmental hypothesis but couldn't resolve the mechani

closed · Rounds: 4 · Score: 0.71 · 2026-04-21

AD patients with TDP-43 pathology show worse cognitive impairment, but how TDP-4

closed · Rounds: 4 · Score: 0.73 · 2026-04-21

Mechanistic validation of SEA-AD differential expression hypotheses: Complement

closed · Rounds: 0 · Score: 0.66 · 2026-04-21

Mechanistic validation of SEA-AD differential expression hypotheses: Complement

closed · Rounds: 0 · Score: 0.64 · 2026-04-21

Do these mechanistic hypotheses from the SEA-AD Atlas bundle explain layer-speci

closed · Rounds: 4 · Score: 0.30 · 2026-04-21

Which proteins are differentially expressed in AD CSF and brain tissue, and do t

closed · Rounds: 4 · Score: 0.70 · 2026-04-21

The abstract claims Cdk5 activation is the primary cause of AD, contradicting th

closed · Rounds: 4 · Score: 0.50 · 2026-04-20

The debate generated therapeutic hypotheses targeting different cell types but n

closed · Rounds: 4 · Score: 1.00 · 2026-04-20

Related Research

Hypotheses and analyses mentioning EXCITOTOXICITY in their description or question text

No additional research found

EXCITOTOXICITY

Understanding Entity Pages

Wiki Pages (1)

Excitotoxicity in Neurodegeneration

Pathway Diagram

Outgoing (162)

Incoming (201)

Targeting Hypotheses (3)

Mentioning Analyses (12)

Does tau dendritic missorting persist independently after Aβ clearance, maintain

Is ferroptosis the primary driver of motor neuron death in ALS or an epiphenomen

Ferroptosis in ALS and motor neuron disease: GPX4, lipid peroxidation, and iron

Proteomics Differential Expression in AD CSF and Brain Tissue

How can circuit-level neurodegeneration mechanisms be identified without complet

Which neural cell types exhibit the most pronounced gene expression alterations

What evidence supports Cdk5 activation as THE primary cause of AD versus other e

Do these mechanistic hypotheses from the SEA-AD Atlas bundle explain layer-speci

Mechanistic validation of SEA-AD differential expression hypotheses: Complement

What mechanisms underlie TDP-43's contribution to cognitive impairment severity

Do perinatal immune challenges create persistent epigenetic modifications that p

What determines the specificity of TDP-43-induced mitochondrial DNA release for

Experiments (0)

Related Papers (0)

Debates (14)

Does tau dendritic missorting persist independently after Aβ clearance, maintain

While the study establishes TDP-43 triggers mtDNA release via mPTP to activate c

The debate raised this developmental hypothesis but couldn't resolve the mechani

AD patients with TDP-43 pathology show worse cognitive impairment, but how TDP-4

Mechanistic validation of SEA-AD differential expression hypotheses: Complement

Mechanistic validation of SEA-AD differential expression hypotheses: Complement

Do these mechanistic hypotheses from the SEA-AD Atlas bundle explain layer-speci

Which proteins are differentially expressed in AD CSF and brain tissue, and do t

The abstract claims Cdk5 activation is the primary cause of AD, contradicting th

The debate generated therapeutic hypotheses targeting different cell types but n

Related Research