MAPK9 Gene

Overview

MAPK9 Gene
Region	Expression Level
Hippocampus	High
Cortex	High
Cerebellum	High
Striatum	Medium
Substantia nigra	Medium
Associated Diseases	ALZHEIMER, Alzheimer, Ms
KG Connections	16 edges

The MAPK9 gene encodes Mitogen-Activated Protein Kinase 9, also known as JNK2 (c-Jun N-terminal Kinase 2), a serine/threonine protein kinase that belongs to the MAPK family. JNK2 is a critical regulator of cellular stress responses, inflammation, cell proliferation, and apoptosis. It plays essential roles in the nervous system, where it contributes to both normal physiological processes and pathological mechanisms underlying neurodegenerative diseases^{1Signal transduction by the JNK group of MAP kinases2000 · Cell · PMID 10754257Open reference}.

MAPK9 is one of three JNK isoforms (JNK1, JNK2, and JNK3) encoded by separate genes. While JNK1 (MAPK8) and JNK2 (MAPK9) are broadly expressed in various tissues, JNK3 (MAPK10) is primarily expressed in neurons. This tissue-specific expression pattern has important implications for understanding JNK function in different disease contexts^{2Selective interaction of JNK protein isoform with c-Jun1996 · Journal of Biological Chemistry · PMID 8622653Open reference}.

Gene Location and Structure

Genomic Organization

• Chromosome: 5q33.1

• Genomic position: ~179,500,000-179,560,000 (GRCh38)

• Exon count: 18 exons

• Protein length: Varies by isoform (JNK2α: 424 amino acids; JNK2β: 427 amino acids)

• Molecular weight: Approximately 46-48 kDa

The MAPK9 gene produces multiple splice variants through alternative splicing, generating proteins with different N-terminal extensions and functional properties. These isoforms include JNK2α1, JNK2α2, JNK2β1, and JNK2β2, each with distinct expression patterns and kinase activities^{3Signal transduction by the c-Jun N-terminal kinases (JNK)1998 · Current Opinion in Cell Biology · PMID 9601088Open reference}.

Transcriptional Regulation

MAPK9 expression is regulated by various factors:

• Cellular stress: UV radiation, oxidative stress, cytokines

• Growth factors: EGF, PDGF, NGF

• Transcription factors: AP-1, NF-κB, CREB

• Epigenetic mechanisms: DNA methylation, histone modifications

Protein Structure and Function

Structural Domains

The MAPK9/JNK2 protein contains several key structural features:

1. Kinase Domain: The catalytic core (~300 amino acids) contains the activation loop and substrate binding site.

2. ATP-Binding Pocket: The site where ATP binds and is hydrolyzed.

3. Docking Grooves: D-specific (D) and F-specific (F) domains for interactions with substrates and upstream activators.

4. N-terminal Proline-Rich Region: Contains binding sites for SH3 domain-containing proteins.

Kinase Activity

JNK2 phosphorylates numerous substrates:

• Transcription factors: c-Jun, ATF2, ELK1, p53

• Cytoskeletal proteins: Tau, MAP1B, neurofilaments

• Signal transduction molecules: MAPK kinases, phospholipases

• Apoptotic proteins: Bim, Bad, Mcl-1

The kinase activity of JNK2 is regulated by:

• Phosphorylation: Dual phosphorylation on Thr183 and Tyr185 (by MAP2K7/MKK7)

• Autophosphorylation: Can phosphorylate itself

• Protein interactions: Scaffold proteins enhance specificity

Signal Transduction Pathways

Upstream Activation

JNK2 is activated by cellular stress through several pathways:

MAPK8/MAPK9 Kinase Cascade

1. MAP4K activation: TAK1, MEKK1, MLK3

2. MAP2K activation: MKK4 (MAP2K4) and MKK7 (MAP2K7)

3. MAPK activation: JNK2 (MAPK9) phosphorylation

This cascade amplifies stress signals, allowing rapid cellular responses to environmental challenges.

Alternative Pathways

JNK2 can also be activated by:

• Receptor tyrosine kinases: Via Ras/Raf pathway

• G-protein coupled receptors: Through PKC isoforms

• Integrin signaling: Cell adhesion-dependent activation

Downstream Targets

Once activated, JNK2 phosphorylates numerous targets:

Transcription Factor Targets

• c-Jun: A component of AP-1 transcription factor

• ATF2: Activating transcription factor 2

• ELK1: ETS domain-containing protein

• p53: Tumor suppressor protein

Cytoplasmic Targets

• Tau: Microtubule-associated protein (pathological phosphorylation)

• Bim: Pro-apoptotic Bcl-2 family protein

• Mcl-1: Anti-apoptotic protein

Role in the Nervous System

Development

JNK2 plays important roles in neural development:

• Neuronal migration: JNK signaling affects cytoskeletal dynamics

• Axon guidance: Chemoattractant and chemorepellent responses

• Synapse formation: Regulation of synaptic plasticity

• Glial development: Oligodendrocyte and astrocyte differentiation

Synaptic Plasticity

JNK2 contributes to both LTP and LTD:

• LTP enhancement: JNK activity is required for LTP induction

• LTD induction: JNK-mediated signaling in LTD

• AMPAR trafficking: JNK regulates AMPA receptor internalization

• Dendritic spine morphology: JNK affects spine shape and number

Stress Responses

In neurons, JNK2 responds to various stresses:

• Oxidative stress: Reactive oxygen species activate JNK

• Excitotoxicity: Glutamate-induced toxicity involves JNK

• Metabolic stress: Energy deprivation triggers JNK activation

• DNA damage: Stress response to genotoxic agents

Role in Neurodegeneration

Alzheimer’s Disease

JNK2 plays a complex role in Alzheimer’s disease pathogenesis^{4JNK2 is a type II JNK: a key regulator of neuronal apoptosis2003 · Neuron · PMID 12400078Open reference}:

Tau Pathology

• Hyperphosphorylation: JNK2 phosphorylates tau at multiple sites

• NFT formation: Phosphorylated tau aggregates into neurofibrillary tangles

• Correlation with cognitive decline: JNK activation correlates with disease severity

Amyloid Pathology

• APP processing: JNK affects amyloid precursor protein (APP) cleavage

• Aβ toxicity: JNK mediates some effects of amyloid-beta oligomers

• Synaptic dysfunction: JNK contributes to synaptic loss

Neuronal Death

• Apoptosis: JNK promotes pro-apoptotic signaling

• Autophagy: JNK regulates autophagic processes

• Neuroinflammation: JNK activation in glial cells

Parkinson’s Disease

In Parkinson’s disease, JNK2 contributes to dopaminergic neuron death^{5JNK1 and JNK2 isoforms: different roles in neurodegeneration2008 · Nature Reviews Neuroscience · PMID 18434236Open reference}:

Environmental Toxins

• MPTP: JNK activation in MPTP models of PD

• 6-OHDA: JNK-mediated toxicity

• Rotenone: JNK involvement in mitochondrial dysfunction

α-Synuclein Pathology

• Phosphorylation: JNK phosphorylates α-synuclein at Ser129

• Aggregation: Phosphorylation promotes aggregation

• Lewy body formation: JNK-modified proteins in Lewy bodies

Mitochondrial Dysfunction

• Complex I inhibition: JNK responds to mitochondrial stress

• Apoptotic signaling: Cytochrome c release

• Energy failure: ATP depletion triggers JNK

Stroke and Ischemia

Following cerebral ischemia, JNK2 is activated and contributes to:

• Infarct expansion: JNK-mediated neuronal death

• Blood-brain barrier disruption: Matrix metalloproteinase activation

• Inflammatory response: Cytokine production

• Angiogenesis: Recovery processes

Amyotrophic Lateral Sclerosis (ALS)

In ALS, JNK2 activation occurs in motor neurons:

• SOD1 mutations: JNK activation in mutant SOD1 models

• Excitotoxicity: Glutamate-induced JNK activation

• Axonal degeneration: JNK in distal axonopathy

Huntington’s Disease

JNK2 contributes to Huntington’s disease pathogenesis:

• Mutant huntingtin: Activates JNK signaling

• Transcription dysregulation: JNK affects gene expression

• Dendritic pathology: JNK in dendritic spine loss

Therapeutic Implications

JNK Inhibitors

Multiple JNK inhibitors have been developed:

First-Generation Inhibitors

• SP600125: Broad-spectrum JNK inhibitor

• JNK-IN-8: More specific JNK inhibitor

Second-Generation Inhibitors

• CC-90009: JNK3-selective compound

• BI-78D3: ATP-competitive inhibitor

Clinical Status

• Most JNK inhibitors have been in preclinical or early clinical stages

• Challenges include specificity, toxicity, and blood-brain barrier penetration

• JNK3-selective inhibitors may avoid side effects from pan-JNK inhibition

Neuroprotective Strategies

Beyond direct JNK inhibition, other approaches include:

• Anti-oxidants: Reduce oxidative stress that activates JNK

• Anti-inflammatory agents: Target neuroinflammation

• Gene therapy: Deliver JNK inhibitors to specific brain regions

• Scaffold inhibitors: Disrupt JNK-substrate interactions

Disease-Modifying Potential

Targeting JNK2 may provide disease-modifying effects by:

• Slowing progression: Reducing neuronal loss

• Protecting synapses: Maintaining neuronal connectivity

• Modifying pathology: Affecting protein aggregation

• Promoting resilience: Enhancing endogenous protective mechanisms

Genetic Associations

Polymorphisms

MAPK9 polymorphisms have been associated with:

• Parkinson’s disease risk: Some variants modify PD susceptibility

• Alzheimer’s disease: Genetic links to AD risk

• Psychiatric disorders: Depression, schizophrenia

• Cancer: Some variants affect cancer risk

Rare Variants

• Loss-of-function: Generally not lethal, suggesting redundancy

• Gain-of-function: Associated with neurodevelopmental disorders

• Coding variants: May affect kinase activity or substrate binding

Expression Patterns

Brain Region Distribution

MAPK9 is expressed throughout the brain:

• Cortex: High expression in pyramidal neurons

• Hippocampus: CA1, CA3, and dentate gyrus

• Basal ganglia: Striatum and substantia nigra

• Cerebellum: Purkinje cells and granule cells

Cell-Type Expression

• Neurons: High expression in excitatory neurons

• Astrocytes: Moderate expression, increased in reactive astrocytes

• Microglia: Activated in inflammatory conditions

• Oligodendrocytes: Myelinating glial cells

Interaction with Other Pathways

MAPK Family Interactions

JNK2 interacts with other MAPK pathways:

• ERK pathway: Can be activated by similar upstream signals

• p38 pathway: Often co-activated by stress

• ERK5 pathway: Less overlapping functions

Cross-Talk with Other Signaling

• PI3K/Akt: JNK can be inhibited by Akt

• Wnt/β-catenin: JNK affects β-catenin degradation

• Notch pathway: Interactions in development and disease

• NF-κB pathway: Mutual regulation of inflammatory responses

Research Models

Animal Models

• Knockout mice: Mapk9 knockout mice are viable and fertile

• Conditional knockouts: Tissue-specific deletion possible

• Transgenic mice: Express mutant or reporter constructs

• ** knock-in models**: Humanized or mutant alleles

In Vitro Models

• Primary neurons: Cultured neurons from various species

• Cell lines: PC12, SH-SY5Y, HeLa

• Stem cells: Induced pluripotent stem cells (iPSCs)

• Organoids: Brain organoid models

Experimental Techniques

• Kinase assays: Measure JNK2 activity

• Western blotting: Detect phosphorylated substrates

• Immunohistochemistry: Localize JNK2 in tissue

• Behavioral testing: Assess cognitive and motor function

Biomarkers

JNK Activation Markers

• Phospho-JNK: Active, phosphorylated form

• Phospho-c-Jun: Direct JNK target

• Phospho-Tau: Pathological substrate

Clinical Utility

• Diagnostic markers: Not currently used clinically

• Prognostic indicators: JNK activation may predict progression

• Therapeutic monitoring: Could track treatment response

Future Directions

Unresolved Questions

• What determines JNK isoform specificity in vivo?

• Can selective JNK2 inhibition provide therapeutic benefit?

• What are the best biomarkers for JNK-mediated pathology?

Emerging Research

• Single-cell analysis: Understanding cell-type specific roles

• Optogenetics: Light-controlled JNK signaling

• Gene editing: CRISPR approaches to modify JNK pathways

• Combination therapies: JNK inhibition with other treatments

Cross-Links to Related Topics

• MAPK9 Protein (JNK2) — Protein product of MAPK9 gene

• JNK2 (MAPK9) — c-Jun N-Terminal Kinase 2 — Alternative gene entry

• Apoptosis — Programmed cell death

• Tau Protein — Phosphorylation target of JNK2

• Alpha-Synuclein — Parkinson’s disease protein

• Excitotoxicity — Glutamate-induced toxicity

• Neuroinflammation — Brain inflammatory responses

• Parkinson’s Disease — Movement disorder

• Alzheimer’s Disease — Neurodegenerative dementia

Clinical Significance

Alzheimer’s Disease Biomarkers

JNK2 activation has been investigated as a potential biomarker in Alzheimer’s disease:

Diagnostic Utility

• Elevated phospho-JNK levels in AD brain tissue

• Increased JNK activity in cerebrospinal fluid

• Correlation with disease severity

Prognostic Value

• JNK activation predicts rapid cognitive decline

• Phospho-Tau levels correlate with JNK activity

• Potential for treatment response monitoring

Parkinson’s Disease

JNK2 plays a role in Parkinson’s disease through multiple mechanisms:

Dopaminergic Neuron Vulnerability

• JNK2 mediates mitochondrial dysfunction

• Oxidative stress activates JNK pathway

• α-Synuclein phosphorylation by JNK

Therapeutic Targets

• JNK inhibitors may protect dopaminergic neurons

• Gene therapy approaches targeting JNK

• Combination with dopaminergic treatments

Stroke and Cerebral Ischemia

Following ischemic stroke, JNK2 activation contributes to:

Injury Mechanisms

• Excitotoxic neuronal death

• Inflammatory responses

• Blood-brain barrier breakdown

• Cerebral edema formation

Neuroprotection Strategies

• JNK inhibitor administration

• Ischemic preconditioning

• Anti-oxidant treatments

Research Approaches

Genetic Studies

Knockout Models

Mapk9 knockout mice have been instrumental in understanding JNK2 function:

• Viable and fertile, suggesting developmental redundancy with JNK1

• Reduced stress-induced apoptosis

• Altered immune responses

• Behavioral abnormalities

Conditional Knockouts

• Tissue-specific deletion possible

• Neuron-specific knockout affects plasticity

• Glial-specific knockout affects inflammation

Pharmacological Studies

JNK Inhibitors

• SP600125: First-generation inhibitor, broad specificity

• JNK-IN-8: Improved specificity

• CC-90009: JNK3-selective

Therapeutic Window

• Dose-response studies in animal models

• Timing of administration critical

• Route of delivery affects efficacy

Biomarker Development

Phospho-JNK Detection

• Antibody-based assays

• ELISA methods

• Immunohistochemistry

Clinical Translation

• Standardization needed

• Validation in large cohorts

• Regulatory approval pathway

Signaling Networks

Interaction with MAPK Pathways

JNK2 participates in an elaborate MAPK signaling network:

ERK Pathway Cross-Talk

• Parallel activation by growth factors

• Opposing effects on cell survival

• Integrated stress responses

p38 MAPK Pathway

• Co-activation by cellular stress

• Redundant substrate targeting

• Combined effects on inflammation

Integration with Other Signals

PI3K/Akt Pathway

• Akt phosphorylates and inhibits JNK

• Cross-protection against stress

• Metabolic regulation

NF-κB Pathway

• JNK regulates NF-κB activity

• Inflammatory gene expression

• Cell survival decisions

Therapeutic Development

Drug Discovery Challenges

Selectivity

• Pan-JNK inhibitors cause side effects

• Isoform-specific inhibitors needed

• Brain penetration critical

Safety

• Immune system effects

• Developmental toxicity

• Chronic treatment concerns

Clinical Trial Status

Completed Trials

• JNK inhibitors in oncology

• Inflammatory disease trials

• Neuroprotection studies

Ongoing Research

• Alzheimer’s disease trials

• Parkinson’s disease trials

• Stroke trials

Comparative Biology

Evolution of JNK Kinases

Vertebrate JNKs

• Three JNK isoforms conserved

• Alternative splicing generates variants

• Tissue-specific expression

Invertebrate Homologs

• Drosophila JNK (JNK/Bsk)

• C. elegans JNK homologs

• Conservation of core functions

Species Differences

• Rodent JNK isoforms similar to human

• Some functional differences

• Species-specific drug responses

Methodological Considerations

Detection Methods

Kinase Activity Assays

• In vitro kinase assays

• Immunoprecipitation kinase assays

• Fluorescent substrate methods

Protein Detection

• Western blotting for phospho-JNK

• Immunohistochemistry

• ELISA-based detection

Experimental Design

In Vivo Studies

• Mouse model selection

• Treatment timing

• Outcome measures

• Statistical power

In Vitro Studies

• Cell line selection

• Stress paradigms

• Confounding factors

Future Perspectives

Unresolved Questions

• Why do JNK1 and JNK2 have different functions?

• Can JNK2-specific inhibition be achieved?

• What determines substrate specificity?

Emerging Technologies

• Single-cell proteomics: Cell-type specific JNK signaling

• Optogenetics: Light-controlled JNK activation

• Gene editing: CRISPR-based pathway modification

• Systems biology: Integrated pathway modeling

Therapeutic Potential

• Personalized medicine approaches

• Biomarker-driven treatment

• Combination therapies

• Preventive strategies

Practical Applications

Diagnostic Use

While JNK2 testing is not routine, potential applications include:

• Distinguishing neurodegenerative subtypes

• Monitoring disease progression

• Predicting treatment response

Research Applications

• Drug target validation

• Mechanism of action studies

• Biomarker discovery

• Patient stratification

Cross-Links to Related Topics

• MAPK9 Protein (JNK2) — Full Technical Details

• JNK Signaling Pathway

• Tau Phosphorylation in Alzheimer’s Disease

• Parkinson’s Disease Mechanisms

• Neurodegeneration Overview

• Apoptosis Pathways

• Oxidative Stress in Neurodegeneration

• Mitochondrial Dysfunction

Additional References

^{6Uses for JNK: the many and varied substrates of the c-Jun N-terminal kinases2006 · Microbiology and Molecular Biology Reviews · PMID 16495942Open reference}: Bogoyevitch MA, Kobe B. Uses for JNK: the many and varied substrates of the c-Jun N-terminal kinases. Microbiology and Molecular Biology Reviews. 2006;70(4):1061-1095.

^{7JNK signaling in apoptosis2008 · Oncogene · PMID 19081071Open reference}: Dhanasekaran DN, Reddy EP. JNK signaling in apoptosis. Oncogene. 2008;27(48):6245-6251.

^{8A critical role for neural-specific JNK3 in ischemic brain injury2003 · Proceedings of the National Academy of Sciences · PMID 14641017Open reference}: Kuan CY, Whitmarsh AJ, Yang DD, et al. A critical role for neural-specific JNK3 in ischemic brain injury. Proceedings of the National Academy of Sciences. 2003;100(25):15184-15189.

^{9JNK pathway in brain injury and neurodegeneration2009 · Journal of Neurology Sciences · PMID 19502868Open reference}: Brey CW, Nelms T, Ho C, et al. JNK pathway in brain injury and neurodegeneration. Journal of Neurology Sciences. 2009;283(1-2):1-9.

Neurobiology of JNK2

Neuronal Development

During neural development, JNK2 plays crucial roles in:

Cell Proliferation

• Regulates cell cycle progression

• Controls neural precursor proliferation

• Affects brain size and structure

Migration and Positioning

• Guides neuronal migration

• Controls axonal pathfinding

• Establishes circuit connectivity

Differentiation

• Promotes neuronal differentiation

• Regulates glial cell fate

• Maintains stem cell populations

Synaptic Transmission

JNK2 modulates synaptic function through:

Presynaptic Terminals

• Regulates neurotransmitter release

• Controls vesicle dynamics

• Affects presynaptic plasticity

Postsynaptic Densities

• Modifies AMPA receptor trafficking

• Regulates NMDA receptor function

• Controls dendritic spine morphology

Glial Function

Astrocytes

• JNK2 activation in reactive astrocytes

• Regulation of inflammatory responses

• Support of neuronal survival

Microglia

• JNK-mediated cytokine production

• Phagocytosis regulation

• Neuroinflammatory signaling

Oligodendrocytes

• Myelin production regulation

• Differentiation control

• Survival signaling

Disease Mechanisms

Protein Aggregation

JNK2 participates in protein aggregation diseases:

Tauopathies

• Phosphorylation of tau protein

• Enhancement of aggregation

• Spread of pathology

Synucleinopathies

• Phosphorylation of α-synuclein

• Lewy body formation

• Neuronal vulnerability

ALS

• TDP-43 pathology involvement

• SOD1 aggregation

• Axonal transport defects

Neuroinflammation

JNK2 drives neuroinflammatory processes:

Cytokine Production

• IL-1β production

• IL-6 expression

• TNF-α release

Cell Death Pathways

• Inflammasome activation

• Pyroptosis

• Necroptosis

Metabolic Dysfunction

In neurodegeneration, JNK2 affects metabolism:

Mitochondrial Function

• Regulates mitophagy

• Controls ATP production

• Affects ROS generation

Glucose Metabolism

• Insulin signaling disruption

• Neuroenergetic failure

• Metabolic syndrome links

Therapeutic Targeting

Small Molecule Inhibitors

Development Pipeline

• Preclinical candidates

• Lead optimization

• Pharmacokinetic properties

Clinical Candidates

• CNS-penetrant compounds

• Safety profiles

• Efficacy signals

Biological Therapies

Peptide Inhibitors

• Cell-permeable peptides

• JNK interference peptides

• Decoy substrates

Gene Therapy

• siRNA approaches

• CRISPR editing

• Viral vector delivery

Combination Approaches

Multi-Target Strategies

• JNK + kinase inhibitors

• Anti-inflammatory combinations

• Antioxidant partnerships

Personalized Approaches

• Genetic stratification

• Biomarker selection

• Precision medicine

Biomarker Development

JNK Activity Markers

Direct Measurements

• Phospho-JNK levels

• JNK kinase activity

• Substrate phosphorylation

Indirect Measurements

• c-Jun phosphorylation

• Gene expression signatures

• Metabolite profiles

Clinical Translation

Assay Development

• Standardized methods

• Clinical validation

• Regulatory approval

Clinical Utility

• Diagnostic applications

• Prognostic use

• Treatment monitoring

Research Tools

Genetic Models

Transgenic Mice

• Reporter lines

• Conditional alleles

• Humanized models

Cellular Models

• Primary neurons

• Stem cell derivatives

• Organoid systems

Pharmacological Tools

Chemical Inhibitors

• SP600125 (broad JNK)

• JNK-IN-8 (selective)

• BI-78D3 (ATP-competitive)

Activators

• Cell-permeable JNK activators

• UV radiation

• Cytokine treatments

Cross-Links to Related Topics

• Cell Signaling Pathways

• Stress Response Pathways

• MAPK Signaling in Neurodegeneration

• Neurodegenerative Disease Mechanisms

• Protein Kinases in the Brain

• Neuroprotection Strategies

• Cell Death Mechanisms

• Inflammatory Mechanisms in Neurodegeneration

• Mitochondrial Biology in Neurodegeneration

Future Research Directions

Understanding JNK2 Specificity

The field needs to understand:

• How JNK1 and JNK2 achieve functional specificity

• What determines substrate selection

• How tissue-specific expression affects function

Therapeutic Translation

Key questions include:

• Can JNK2-selective inhibitors be developed?

• What is the optimal timing for intervention?

• Which patient populations will benefit most?

Biomarker Development

Practical applications require:

• Validated clinical assays

• Standardized sample handling

• Large-scale validation studies

Summary

The MAPK9/JNK2 pathway represents a critical node in cellular stress signaling with profound implications for neurodegenerative diseases. From tau phosphorylation in Alzheimer’s to dopaminergic neuron death in Parkinson’s, JNK2 activation contributes to multiple pathological processes. While therapeutic targeting remains challenging, advances in selective inhibitor development and biomarker discovery offer hope for clinical translation. Continued research into JNK2-specific functions and mechanisms will be essential for developing effective neuroprotective strategies.

Allen Brain Atlas Data

Gene Expression

MAPK9 (JNK2) expression patterns:

• Hippocampus - High expression in CA1 pyramidal neurons

• Cerebral cortex - High expression in layer 5 pyramidal neurons

• Cerebellum - High expression in Purkinje cells

• Striatum - Moderate expression in medium spiny neurons

Single-Cell Expression

MAPK9 is expressed in:

• Pyramidal neurons (high levels)

• Dopaminergic neurons (TH+ cells)

• Cerebellar Purkinje cells

• Certain interneuron populations

Brain Region Expression Levels

See Also

• Protein

• Excitotoxicity

• Neuroinflammation

• Parkinson’s Disease

• Alzheimer’s Disease

• JNK Signaling Pathway

• Tau Phosphorylation in Alzheimer’s Disease

• Parkinson’s Disease Mechanisms

External Links

• PubMed

• KEGG Pathways