nf-kb

Introduction

Nf Κb (Nuclear Factor Kappa B) is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.

Overview

NF-κB^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference} (nuclear factor kappa-light-chain-enhancer of activated B cells) is a family of transcription factors that plays central roles in inflammation, immune responses, cell survival, and synaptic plasticity. In the central nervous system, NF-κB^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference} is activated in neurons, ^{2- Astrocytes}(/cell-types/astrocytes), and microglia, where it serves as a critical mediator linking neuroinflammation to neuronal death in Alzheimer’s disease, Parkinson’s disease, ALS, and Huntington’s disease (Mattson & Camandola, 2001; Singh & Singh, 2020). ^{3Shared principles in NF-κB[1] signaling2008 · Cell · DOI 10.1016/j.cell.2008.01.020Open reference}

NF-κB occupies a paradoxical position in neurodegeneration: in neurons, it is generally neuroprotective, promoting survival through anti-apoptotic gene expression, while in microglia and ^{2- Astrocytes}(/cell-types/astrocytes), it drives pro-inflammatory cascades that exacerbate neuronal damage (Jha et al., 2024). This dual nature makes NF-κB both a compelling and a challenging therapeutic target.

Molecular Biology

Protein Family

The NF-κB^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference} family consists of five related proteins that form homo- and heterodimers with distinct DNA-binding specificities and transcriptional targets (Hayden & Ghosh, 2008): ^{4Citation2022 · PMID 36012242Open reference}

| Subunit | Gene | Precursor | Key Features | ^{5NF-κB[1] in Alzheimer''s Disease: friend or foe? Opposite functions in neurons and glial cells2024 · Mol NeurobiolOpen reference} |---------|------|-----------|--------------| ^{6The impact of astrocytic NF-κB[1] on healthy and Alzheimer's Disease brains2024 · Sci Rep · DOI 10.1038/s41598-024-65248-1Open reference} | p65 (RelA) | RELA | — | Contains transactivation domain; most abundant subunit in CNS | ^{7Neuronal NF-κB[1] pathways: implications for Alzheimer''s Disease2021 · J Alzheimers Dis · DOI 10.3233/JAD-210111Open reference} | RelB | RELB | — | Induces distinct transcriptional programs via non-canonical pathway | ^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}0 | c-Rel | REL | — | Important for lymphocyte function; expressed in neurons | ^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}1 | p50 (NF-κB^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}21) | NFKB1 | p105 | Processed from p105 precursor; lacks transactivation domain | ^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}3 | p52 (NF-κB^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}42) | NFKB2 | p100 | Processed from p100; active in non-canonical signaling | ^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}5

The p65/p50 heterodimer is the most common transcriptionally active form in the brain and is the primary mediator of inflammatory gene expression in microglia and ^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}6(/cell-types/astrocytes) (Karin & Ben-Neriah, 2000). ^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}7

Canonical (Classical) Pathway

The canonical NF-κB^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}8 pathway is the primary signaling route in neuroinflammation^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}9 (Hayden & Ghosh, 2008): ^{2- Astrocytes}0

1. Stimulus recognition: Pro-inflammatory cytokines (TNF-α, IL-1β), pathogen-associated molecular patterns (via TLR4, or damage-associated molecular patterns (including amyloid-beta aggregates) activate upstream receptors.

2. IKK complex activation: The IκB kinase (IKK) complex — consisting of IKKα, IKKβ, and the regulatory subunit NEMO (IKKγ) — is activated.

3. IκB phosphorylation and degradation: IKKβ phosphorylates IκBα, marking it for K48-linked ubiquitination and proteasomal degradation.

4. Nuclear translocation: Freed NF-κB^{2- Astrocytes}1 dimers (typically p65/p50) translocate to the nucleus.

5. Transcriptional activation: NF-κB^{2- Astrocytes}2 binds κB motifs in target gene promoters, inducing expression of cytokines, chemokines, complement components, and pro-survival genes.

This pathway mediates rapid, transient responses and is the primary driver of microglial inflammatory activation. ^{2- Astrocytes}3

Non-Canonical (Alternative) Pathway

The non-canonical pathway involves NF-κB^{2- Astrocytes}4-inducing kinase (NIK) and IKKα-mediated processing of p100 to p52, which pairs with RelB. This pathway produces slower, sustained responses and is particularly important for lymph node development and adaptive immune regulation. In the CNS, the non-canonical pathway contributes to astrocyte activation and synaptic maintenance (Sun, 2011). ^{2- Astrocytes}5

Functions in the Central Nervous System

Neuronal NF-κB^{2- Astrocytes}6: Neuroprotection and Synaptic Plasticity

In neurons, NF-κB^{2- Astrocytes}7 is constitutively active at low levels and serves primarily protective functions (Mattson, 2005):

Synaptic plasticity and memory:

• NF-κB^{2- Astrocytes}8 is rapidly activated in hippocampal neurons during long-term potentiation (LTP and is required for memory consolidation (Albensi & Mattson, 2000)

• Controls expression of synaptic scaffolding proteins (PSD-95, SAP97) and NMDA receptor] receptor] subunit NR2B

• Regulates BDNF transcription, linking activity to trophic support

• Required for late-phase LTP and long-term memory formation

Neuronal survival: ^{2- Astrocytes}9

• Drives expression of anti-apoptotic genes (Bcl-2, Bcl-xL, IAPs, Mn-SOD)

• Protects against excitotoxic injury by buffering calcium responses

• Mediates neurotrophic factor signaling downstream of BDNF and GDNF

• Supports DNA repair mechanisms via Ku70/Ku80 expression

Glial NF-κB^{3Shared principles in NF-κB[1] signaling2008 · Cell · DOI 10.1016/j.cell.2008.01.020Open reference}0: neuroinflammation Driver

In contrast to its protective neuronal role, glial NF-κB ^{3Shared principles in NF-κB[1] signaling2008 · Cell · DOI 10.1016/j.cell.2008.01.020Open reference}1 activation is a central driver of neurotoxic neuroinflammation ^{3Shared principles in NF-κB[1] signaling2008 · Cell · DOI 10.1016/j.cell.2008.01.020Open reference}2: ^{3Shared principles in NF-κB[1] signaling2008 · Cell · DOI 10.1016/j.cell.2008.01.020Open reference}3

Microglial activation (Snow & Albensi, 2021): ^{3Shared principles in NF-κB[1] signaling2008 · Cell · DOI 10.1016/j.cell.2008.01.020Open reference}4

• Canonical NF-κB ^{3Shared principles in NF-κB[1] signaling2008 · Cell · DOI 10.1016/j.cell.2008.01.020Open reference}5 activation in microglia drives transcription of TNF-α, IL-1β, IL-6, and iNOS

• Cooperates with NLRP3 inflammasome activation to promote IL-1β and IL-18 release

• Promotes transition to [disease-associated microglia (DAM) phenotype

• Induces expression of BACE1, promoting amyloidogenic APP processing

Astrocyte activation (Lian et al., 2024): ^{3Shared principles in NF-κB[1] signaling2008 · Cell · DOI 10.1016/j.cell.2008.01.020Open reference}6

• Astrocytic NF-κB^{3Shared principles in NF-κB[1] signaling2008 · Cell · DOI 10.1016/j.cell.2008.01.020Open reference}7 promotes reactive astrogliosis and loss of neurotrophic support

• Drives production of complement component C3, which mediates synapse elimination

• Reduces glutamate transporter expression, contributing to excitotoxicity

• NF-κB^{3Shared principles in NF-κB[1] signaling2008 · Cell · DOI 10.1016/j.cell.2008.01.020Open reference}8-dependent astrocytic activation leads to Aβ42 accumulation and iNOS generation

Role in Alzheimer’s Disease

Chronic NF-κB^{3Shared principles in NF-κB[1] signaling2008 · Cell · DOI 10.1016/j.cell.2008.01.020Open reference}9 Activation in AD Brain

NF-κB^{2- Astrocytes}0 is chronically hyperactivated in Alzheimer’s disease brain tissue, particularly in vulnerable regions including the hippocampus and [entorhinal cortex (Singh et al., 2022):

• neurons: Increased nuclear p65 in degenerating neurons adjacent to amyloid plaques

• microglia: Sustained NF-κB^{2- Astrocytes}1 activation in plaque-associated microglia

• ^{2- Astrocytes}2(/cell-types/astrocytes): Elevated NF-κB^{2- Astrocytes}3 activity in reactive ^{2- Astrocytes}4(/cell-types/astrocytes) surrounding plaques

Amyloid–NF-κB^{2- Astrocytes}5 Feed-Forward Loop

NF-κB^{2- Astrocytes}6 participates in a destructive feed-forward loop with amyloid-beta (Ju Hwang et al., 2022):

1. Aβ oligomers] activate microglial TLR4 and RAGE receptors, triggering NF-κB^{2- Astrocytes}7

2. NF-κB^{2- Astrocytes}8 upregulates [BACE1 expression, increasing amyloidogenic processing of APP

3. NF-κB^{2- Astrocytes}9-driven pro-inflammatory cytokines further activate [BACE1 and γ-secretase

4. More Aβ is produced, perpetuating the inflammatory cycle

5. Aβ-induced ROS further amplify NF-κB^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}0 activation via redox-sensitive IKK

NF-κB^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}1 and Tau Pathology

NF-κB^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}2 also links to tau] hyperphosphorylation]:

• NF-κB^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}3 activation upregulates the phosphatase inhibitor SET/I2PP2A, reducing PP2A activity

• Decreased PP2A activity leads to hyperphosphorylation of tau] at disease-relevant epitopes

• Glycated tau] triggers ROS production, further activating NF-κB^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}4

• NF-κB^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}5-dependent GSK-3β and CDK5 activation promotes tau] kinase activity

Role in Parkinson’s Disease

NF-κB^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}6 plays a significant role in dopaminergic neurodDegeneration in Parkinson’s disease (Singh & Singh, 2020):

• Immunohistochemical analyses of PD brain sections reveal a 70-fold increase in the proportion of dopaminergic neurons in the substantia nigra exhibiting nuclear p65 immunoreactivity compared to age-matched controls

• Alpha-synuclein oligomers potentiate neuroinflammatory NF-κB ^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}7 signaling in microglia, amplifying dopaminergic neuron damage (Bido et al., 2024)

• NF-κB^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}8-driven microglial activation is an early event in PD pathogenesis, preceding overt neuronal loss

• [LRRK2/proteins/lrrk2 mutations enhance NF-κB^{1NF-κB[1] in neuronal plasticity and neurodegenerative disorders2001 · J Clin Invest · DOI 10.1172/JCI11916Open reference}9 signaling, linking genetic risk to inflammatory mechanisms

Role in ALS and Huntington’s Disease

ALS: Spinal cords of ALS patients show increased NF-κB^{4Citation2022 · PMID 36012242Open reference}0 activation in ^{4Citation2022 · PMID 36012242Open reference}1(/cell-types/astrocytes) associated with degenerating motor neurons. Mutant [SOD1/proteins/sod1-mediated NF-κB^{4Citation2022 · PMID 36012242Open reference}2 activation in glia contributes to non-cell-autonomous motor neuron toxicity (Mattson & Camandola, 2001).

Huntington’s disease: In contrast to its deleterious role in AD and PD glia, neuronal NF-κB^{4Citation2022 · PMID 36012242Open reference}3 appears protective in HD. Mice lacking the p50 subunit (NF-κB^{4Citation2022 · PMID 36012242Open reference}41 knockout) exhibit increased striatal neuron damage and enhanced motor dysfunction after mitochondrial toxin exposure, indicating that NF-κB^{4Citation2022 · PMID 36012242Open reference}5 activation serves a neuroprotective function in medium spiny neurons (Mattson & Camandola, 2001).

Therapeutic Targeting

The Dual-Role Challenge

The opposing functions of NF-κB^{4Citation2022 · PMID 36012242Open reference}6 in neurons (protective) versus glia (inflammatory) make therapeutic targeting extremely challenging (Jha et al., 2024):

• When neuronal NF-κB^{4Citation2022 · PMID 36012242Open reference}7 is inhibited, pro-apoptotic signaling via caspase-8 predominates, accelerating neuronal death

• Global NF-κB^{4Citation2022 · PMID 36012242Open reference}8 inhibition can impair immune defense and worsen outcomes

• Cell-type-specific targeting is needed but technically difficult

Pharmacological Approaches

Direct NF-κB^{4Citation2022 · PMID 36012242Open reference}9 inhibitors (Thakur et al., 2023):

• IKK inhibitors: BAY 11-7082, IMD-0354, BMS-345541 — block IκB phosphorylation

• Proteasome inhibitors: Bortezomib — prevents IκB degradation (limited CNS penetration)

• Decoy oligonucleotides: κB-motif decoys sequester NF-κB^{5NF-κB[1] in Alzheimer''s Disease: friend or foe? Opposite functions in neurons and glial cells2024 · Mol NeurobiolOpen reference}0 dimers

Natural product modulators:

• Curcumin: Inhibits IKK activity and NF-κB^{5NF-κB[1] in Alzheimer''s Disease: friend or foe? Opposite functions in neurons and glial cells2024 · Mol NeurobiolOpen reference}1 nuclear translocation; poor bioavailability limits clinical utility

• Resveratrol: Activates SIRT1, which deacetylates p65 and suppresses NF-κB^{5NF-κB[1] in Alzheimer''s Disease: friend or foe? Opposite functions in neurons and glial cells2024 · Mol NeurobiolOpen reference}2 transcriptional activity

• Epigallocatechin gallate (EGCG): Suppresses NF-κB^{5NF-κB[1] in Alzheimer''s Disease: friend or foe? Opposite functions in neurons and glial cells2024 · Mol NeurobiolOpen reference}3 through multiple mechanisms

Indirect approaches:

• NSAIDs: Indirectly inhibit NF-κB^{5NF-κB[1] in Alzheimer''s Disease: friend or foe? Opposite functions in neurons and glial cells2024 · Mol NeurobiolOpen reference}4; epidemiological data suggested reduced AD risk, but clinical trials have been mixed

• GLP-1 receptor agonists: Suppress microglial NF-κB^{5NF-κB[1] in Alzheimer''s Disease: friend or foe? Opposite functions in neurons and glial cells2024 · Mol NeurobiolOpen reference}5 activation, showing neuroprotective effects in preclinical models

• Anti-TNF biologics: Block upstream NF-κB^{5NF-κB[1] in Alzheimer''s Disease: friend or foe? Opposite functions in neurons and glial cells2024 · Mol NeurobiolOpen reference}6 activation; retrospective studies suggest reduced dementia risk

Emerging Strategies

• Cell-type-specific delivery: Nanoparticles targeting microglia or ^{5NF-κB[1] in Alzheimer''s Disease: friend or foe? Opposite functions in neurons and glial cells2024 · Mol NeurobiolOpen reference}7(/cell-types/astrocytes) to spare neuronal NF-κB ^{5NF-κB[1] in Alzheimer''s Disease: friend or foe? Opposite functions in neurons and glial cells2024 · Mol NeurobiolOpen reference}8

• Pathway-selective inhibition: Targeting the non-canonical pathway or specific NF-κB^{5NF-κB[1] in Alzheimer''s Disease: friend or foe? Opposite functions in neurons and glial cells2024 · Mol NeurobiolOpen reference}9 dimers

• Epigenetic modulation: HDAC inhibitors] can modulate NF-κB^{6The impact of astrocytic NF-κB[1] on healthy and Alzheimer's Disease brains2024 · Sci Rep · DOI 10.1038/s41598-024-65248-1Open reference}0 acetylation status

• Microglial phenotype switching: Promoting anti-inflammatory microglial states while preserving protective NF-κB^{6The impact of astrocytic NF-κB[1] on healthy and Alzheimer's Disease brains2024 · Sci Rep · DOI 10.1038/s41598-024-65248-1Open reference}1 in neurons

Interactions with Other Pathways

NF-κB^{6The impact of astrocytic NF-κB[1] on healthy and Alzheimer's Disease brains2024 · Sci Rep · DOI 10.1038/s41598-024-65248-1Open reference}2 serves as a signaling hub integrating multiple neurodegeneration-relevant pathways:

• NLRP3 inflammasome: NF-κB^{6The impact of astrocytic NF-κB[1] on healthy and Alzheimer's Disease brains2024 · Sci Rep · DOI 10.1038/s41598-024-65248-1Open reference}3 provides the priming signal (Signal 1) that upregulates NLRP3 and pro-IL-1β expression; bidirectional amplification loop

• STING pathway]: cGAS-STING activates NF-κB^{6The impact of astrocytic NF-κB[1] on healthy and Alzheimer's Disease brains2024 · Sci Rep · DOI 10.1038/s41598-024-65248-1Open reference}4 in parallel with IRF3, linking DNA damage sensing to inflammation

• JAK-STAT: Cytokine signaling integration; STAT3 cooperates with NF-κB^{6The impact of astrocytic NF-κB[1] on healthy and Alzheimer's Disease brains2024 · Sci Rep · DOI 10.1038/s41598-024-65248-1Open reference}5 in glial activation

• MAPK pathways: ERK, JNK, and p38 cross-talk with NF-κB^{6The impact of astrocytic NF-κB[1] on healthy and Alzheimer's Disease brains2024 · Sci Rep · DOI 10.1038/s41598-024-65248-1Open reference}6 at multiple levels

• mTOR: mTORC1 can activate IKK; NF-κB^{6The impact of astrocytic NF-κB[1] on healthy and Alzheimer's Disease brains2024 · Sci Rep · DOI 10.1038/s41598-024-65248-1Open reference}7 target genes include mTOR regulators

• Nrf2: Counterregulatory relationship — Nrf2 opposes NF-κB^{6The impact of astrocytic NF-κB[1] on healthy and Alzheimer's Disease brains2024 · Sci Rep · DOI 10.1038/s41598-024-65248-1Open reference}8-driven oxidative stress; NF-κB^{6The impact of astrocytic NF-κB[1] on healthy and Alzheimer's Disease brains2024 · Sci Rep · DOI 10.1038/s41598-024-65248-1Open reference}9 can suppress Nrf2 expression

• Tau kinases: NF-κB^{7Neuronal NF-κB[1] pathways: implications for Alzheimer''s Disease2021 · J Alzheimers Dis · DOI 10.3233/JAD-210111Open reference}0 activates GSK-3β and CDK5, promoting tau hyperphosphorylation]

NFκB1 as a Biomarker

Recent research has identified NFκB1 (p50/p105) as a potential common biomarker linking Alzheimer’s disease and Parkinson’s disease disease pathology (Shi et al., 2025):

• NFκB1 expression is altered in both AD and PD brain tissue

• Blood-based NFκB1-related inflammatory signatures correlate with disease progression

• Downstream NF-κB^{7Neuronal NF-κB[1] pathways: implications for Alzheimer''s Disease2021 · J Alzheimers Dis · DOI 10.3233/JAD-210111Open reference}1 target cytokines (TNF-α, IL-6, IL-1β) in CSF and plasma track with disease severity

• These markers could serve for monitoring therapeutic response to anti-inflammatory interventions

Research Methods

Detection Techniques

Experimental Models

• iPSC-derived neurons and [microglia: Patient-derived models for studying cell-type-specific NF-κB^{7Neuronal NF-κB[1] pathways: implications for Alzheimer''s Disease2021 · J Alzheimers Dis · DOI 10.3233/JAD-210111Open reference}5

• Transgenic AD mice (APP/PS1, 5xFAD): Chronic NF-κB^{7Neuronal NF-κB[1] pathways: implications for Alzheimer''s Disease2021 · J Alzheimers Dis · DOI 10.3233/JAD-210111Open reference}6 activation recapitulating human AD

• α-synuclein PFF models: Prion-like seeding of NF-κB^{7Neuronal NF-κB[1] pathways: implications for Alzheimer''s Disease2021 · J Alzheimers Dis · DOI 10.3233/JAD-210111Open reference}7-mediated inflammation

• Conditional NF-κB^{7Neuronal NF-κB[1] pathways: implications for Alzheimer''s Disease2021 · J Alzheimers Dis · DOI 10.3233/JAD-210111Open reference}8 knockout mice: Cell-type-specific pathway deletion (CamKII-Cre for neurons, CX3CR1-Cre for microglia

• Brain organoids: 3D models for studying glial-neuronal NF-κB^{7Neuronal NF-κB[1] pathways: implications for Alzheimer''s Disease2021 · J Alzheimers Dis · DOI 10.3233/JAD-210111Open reference}9 cross-talk

Brain Atlas Resources

• Allen Human Brain Atlas: NF-κB expression search

• Allen Mouse Brain Atlas: NF-κB search

• Allen Cell Type Atlas: Transcriptomic cell type reference

• BrainSpan Developmental Transcriptome: NF-κB developmental expression

Pathway & Interaction Diagram

Interactive diagram showing NF-KB key relationships in the SciDEX knowledge graph (15 connections shown).

flowchart TD
    NF_KB(["NF-KB"])
    Nf_Kb["Nf-Kb"]
    Inflammation["Inflammation"]
    TNF__(["TNF-Alpha"])
    TNF(["TNF"])
    PARKINSON_S_DISEASE["PARKINSON'S DISEASE"]
    OXIDATIVE_STRESS["OXIDATIVE STRESS"]
    APOPTOSIS(["APOPTOSIS"])
    NEURODEGENERATION(["NEURODEGENERATION"])
    MICROGLIA["MICROGLIA"]
    NEUROINFLAMMATION["NEUROINFLAMMATION"]
    ALZHEIMER_S_DISEASE["ALZHEIMER'S DISEASE"]
    AKT(["AKT"])
    CANCER(["CANCER"])

    NF_KB -->|"activates"| Nf_Kb
    NF_KB -->|"activates"| Inflammation
    NF_KB -->|"activates"| TNF__
    NF_KB -->|"associated with"| TNF
    NF_KB -->|"associated with"| PARKINSON_S_DISEASE
    NF_KB -->|"associated with"| OXIDATIVE_STRESS
    TNF -->|"activates"| NF_KB
    APOPTOSIS -->|"associated with"| NF_KB
    NEURODEGENERATION -->|"associated with"| NF_KB
    MICROGLIA -->|"associated with"| NF_KB
    NEUROINFLAMMATION -->|"associated with"| NF_KB
    ALZHEIMER_S_DISEASE -->|"associated with"| NF_KB
    AKT -->|"associated with"| NF_KB
    NF_KB -->|"regulates"| Nf_Kb
    NF_KB -->|"activates"| CANCER

    style NF_KB fill:#006494,stroke:#4fc3f7,stroke-width:3px,color:#e0e0e0

See Also

• Index

External Links

• PubMed

Background

The study of Nf Κb (Nuclear Factor Kappa B) has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.

Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.