The glial biology track at SfN Neuroscience 2026 represents one of the most rapidly evolving areas in neurodegenerative disease research. Once considered mere support cells, astrocytes, microglia, and oligodendrocytes are now recognized as active participants in disease pathogenesis and promising therapeutic targets.
This page catalogs the major glial biology sessions at SfN 2026, with a focus on how each glial cell type contributes to Alzheimer's disease (AD), Parkinson's disease (PD), and related disorders.
Microglia are the brain's resident immune cells and play a dual role in neurodegeneration—protective in early stages, pathogenic in chronic activation.
The concept of disease-associated microglia has revolutionized our understanding of neuroinflammation:
| DAM Stage |
Markers |
Function |
| Stage 1 |
Trem2-independent |
Early response, phagocytosis |
| Stage 2 |
Trem2-dependent |
Lipid metabolism, plaque clearance |
| Stage 3 |
Apolipoprotein signaling |
Late-stage, neurotoxic |
- TREM2 signaling pathways and TREM2 variants in AD risk
- CSF1R inhibition for microglial depletion strategies
- Complement system activation and synaptic pruning
- Microglial senescence and aging-related dysfunction
- Tau-mediated microglial activation
¶ Microglia and Alzheimer's Disease
flowchart TD
A["Amyloid-beta<br/>Deposition"] --> B["Microglial<br/>Activation"]
B -->|"Phase 1"| C["Protective<br/>Phagocytosis"]
B -->|"Phase 2"| D["Chronic<br/>Inflammation"]
D --> E["Pro-inflammatory<br/>Cytokines"]
E --> F["Neuronal<br/>Dysfunction"]
C --> G["Aβ<br/>Clearance"]
style A fill:#ffcdd2
style C fill:#c8e6c9
style D fill:#ffcdd2
style E fill:#fff9c4999
style F fill:#ffcdd2
style G fill:#c8e6c9
Key presentations will cover:
- TREM2 agonist development and clinical trials
- CD33 modulation and microglial phagocytosis
- GAL3 (galectin-3) as microglial activation marker
- CX3CR1 fractalkine signaling pathway
- Microglial metabolic reprogramming
¶ Microglia and Parkinson's Disease
In Parkinson's disease, microglia contribute to dopaminergic neuron death through:
- Alpha-synuclein clearance and misprocessing
- Neuroinflammation amplification loops
- Oxidative stress propagation
- LRRK2 kinase pathway interactions
Related pages:
Astrocytes undergo dramatic phenotypic changes in neurodegeneration:
flowchart LR
subgraph "Astrocyte Activation Spectrum"
A["Naive Astrocyte"] --> B["Reactive A1"]
A --> C["Reactive A2"]
B -->|"Pro-inflammatory"| D["Neurotoxic"]
C -->|"Pro-survival"| E["Neuroprotective"]
end
style A fill:#e6f2ff
style B fill:#ffcdd2
style C fill:#c8e6c9
style D fill:#fff9c4999
style E fill:#c8e6c9
A1 astrocytes (neurotoxic):
- Upregulate complement components
- Lose glutamate uptake function
- Promote synaptic dysfunction
A2 astrocytes (neuroprotective):
- Upregulate neurotrophic factors
- Promote tissue repair
- Support synaptic function
- GFAP as biomarker and therapeutic target
- AQP4 water channel dysregulation
- S100B release and neuronal toxicity
- Lactate shuttle disruption in AD
- Glutamate handling impairment
- Potassium buffering dysfunction
- ** tripartite synapse** disruption
- Perisynaptic astrocyte remodeling
- Calcium wave propagation
Related pages:
- Amyloid plaque-associated astrocyte reactivity
- Tau pathology propagation support
- Blood-brain barrier maintenance
- Alpha-synuclein uptake and processing
- Neuroinflammation amplification
- Dopaminergic neuron support
¶ Oligodendrocytes and Myelin
Oligodendrocyte loss and dysfunction contributes to neurodegeneration through:
- Demyelination and conduction deficits
- Axonal energy failure due to lack of metabolic support
- Vulnerability to oxidative stress
- 4R Tauopathies and oligodendrocyte pathology
- White matter changes in AD and PD
- Remyelination strategies and OPC activation
- Myelin lipid metabolism defects
Related pages:
¶ Glial Interactions and Network Effects
flowchart TD
subgraph "Neuroimmune Axis"
M["Microglia"] <--> A["Astrocytes"]
A <--> O["Oligodendrocytes"]
M <--> N["Neurons"]
A <--> N
O <--> N
end
subgraph "Signaling Molecules"
C["Cytokines"]
C --> M
C --> A
C --> N
end
style M fill:#ffcdd2
style A fill:#c8e6c9
style O fill:#e6f2ff
style N fill:#fff3e0
Key signaling pathways:
- Cytokine networks (IL-1β, TNF-α, IL-6)
- Complement cascade cross-activation
- ATP/P2X7 receptor signaling
- Notch and Wnt developmental pathways
| Session Type |
Focus Area |
| Symposia |
Glial biology in AD/PD (90 min) |
| Minisymposia |
Emerging research on glial interactions |
| Poster Sessions |
Microglia, astrocyte, oligodendrocyte studies |
| Special Lectures |
Keynote speakers on neuroinflammation |
The detailed scientific program for Neuroscience 2026 is expected to be published in spring 2026. This page will be updated with specific session titles, speakers, and abstracts as they become available from SfN.