Conference: AAIC 2026 | Dates: July 12-15, 2026 | Location: Excel London, UK
Synaptic loss is the strongest correlate of cognitive decline in Alzheimer's disease, and preserving synaptic function has emerged as a critical therapeutic strategy. AAIC 2026 features extensive programming on synaptic biology, including mechanisms of synaptic degeneration, protective interventions, and synaptic resilience approaches.
- Vesicle Cycling Impairment: Disruptions in synaptic vesicle release and recycling
- ** neurotransmitter depletion**: Reduced synthesis and packaging of neurotransmitters
- Calcium dysregulation: Altered calcium signaling affecting vesicle dynamics
- Receptor downregulation: Loss of AMPA, NMDA, and muscarinic receptors
- Dendritic spine loss: Structural alterations in postsynaptic compartments
- Synaptic plasticity deficits: Impaired LTP and LTD mechanisms
- BDNF/TrkB signaling: Brain-derived neurotrophic factor pathways
- Activity-dependent synaptic strengthening: How neuronal activity promotes synapse stability
- Synaptic scaffolding proteins: PSD-95, synapsin, and related molecules
- Mitochondrial dynamics: Preserving energy supply at synapses
- Synaptic glucose metabolism: Local energy requirements
- NAD+ metabolism: Sirtuin pathways in synaptic protection
- Synaptic genes: Variations affecting synapse stability
- Resilience alleles: Protective genetic variants
- APOE isoforms: Differential effects on synaptic function
- Cognitive reserve: How education and engagement protect synapses
- Synaptic plasticity throughout life: Activity-dependent maintenance
- Sleep and synaptic homeostasis: The role of sleep in synaptic repair
- AMPAkines: Positive allosteric modulators of AMPA receptors
- NMDA receptor modulators: Fine-tuning glutamatergic signaling
- Muscarinic agonists: M1-selective activation for synaptic plasticity
- BDNF mimetics: Small molecule analogs
- TrkB agonists: Receptor activation strategies
- GDNF family ligands: Supporting cholinergic neurons
- Passive immunization: Anti-alpha-synuclein antibodies
- Active vaccination: Synuclein-targeted vaccines
- Oligomer-targeting: Specific removal of toxic species
- Anti-tau immunotherapy: Preventing tau-mediated synaptic damage
- Anti-amyloid approaches: Reducing synaptic amyloid burden
¶ Gene Therapy and Cell-Based Approaches
- AAV-mediated BDNF delivery: Gene therapy for neurotrophic support
- Synaptic protein gene delivery: Replenishing critical molecules
- Regulated expression systems: Controllable therapeutic expression
- Cholinergic neuron transplantation: Replacing lost neurons
- Synaptic reconstitution: Engineering synaptic connections
- Organoid approaches: Three-dimensional neural tissues
- "Synaptic Failure in Alzheimer's Disease: Mechanisms and Therapeutic Targets"
- "Preserving Synaptic Function: From Biology to Clinical Translation"
- "Neurotrophic Factor Signaling in Cognitive Decline"
- "Measuring Synaptic Function in Clinical Trials"
- "Synaptic Biomarkers: PET, CSF, and Blood"
- "Translational Models of Synaptic Dysfunction"